Fiona Geekie, a nurse from Croydon who is apractitioner for TheCentral London Community Healthcare NHS Trust, donated bone marrow to a person she had never met earlier this year.

According to Fiona (49), about 2,000 people in the UK require a bone marrow or stem cell transplant every year.

For most of them its their last chance of surviving blood cancer, she added.

The nurse, who is a member of the Merton enhanced rapid intervention team,described why she went on the register to donate through the Anthony Nolan Trust 15 years ago.

Three quarters cant find a matching donor in their family so rely upon the generosity of a complete stranger already on the bone marrow register. So I joined up, it was simple.

Last Christmas Fiona was called for blood tests as she was a possible match for someone.

I was surprised to be called in the first place and I must confess I was a little apprehensive, Fiona admitted.

However, she continued: But then I thought what if someone in my family needed a bone marrow transplant. Its the most fantastic gift you can give to total stranger.

After donating, Fiona said she felt quite emotional and wanted the recipient to get well again.

She concluded: Overall, it was a wonderful experience and I have no hesitation in recommending all young people aged 16-30 to consider joining the bone marrow donor register.

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Nurse goes the extra mile and donates bone marrow to a complete stranger through the Anthony Nolan Trust - Sutton Guardian

Bone Marrow Stem Cells Comments Off on Nurse goes the extra mile and donates bone marrow to a complete stranger through the Anthony Nolan Trust – Sutton Guardian | June 29th, 2017

Important pieces of the puzzle to understand what drives diseases such as Alzheimer's and Parkinson's are still missing today. One crucial obstacle for researchers is that it is impossible to examine a living brain cell in someone who is affected by the disease. With the help of a new method for cell conversion, researchers at Lund University in Sweden have found a way to produce diseased, aging brain cells on a large scale in a cell culture dish.

After performing a biopsy on the patient, the skin cells are transformed into brain cells that effectively imitate the disease and the age of the patient. The fact that the cells can now be produced in large quantities enables researchers to carry out a series of experiments that were previously not possible.

A few years ago, Malin Parmar's research team was one of the first in the world to convert human skin cells directly into brain cells without passing the stem cell state. The discovery shocked the researchers and was perceived as almost impossible. The team is now approaching a point where the discovery is about to bear fruit on a wide scale. By following a new method that involves slightly changing the genetic code that triggers cell conversion, the researchers were able to multiply the production of disease-specific brain cells.

"Primarily, we inhibited a protein, REST, involved in establishing identity in cells that are not nerve cells. After limiting this protein's impact in the cells during the conversion process, we've seen completely different results. Since then, we've been playing around with changing the dosage of the other components in the previous method, which also proved effective. Overall, the efficiency is remarkable. We can now generate almost unlimited amounts of neurons from one skin biopsy", says Malin Parmar, professor of developmental and regenerative neurobiology at Lund University.

The increase in production will have far-reaching effects. The new volumes enable research projects that were simply not viable before. Among other things, it opens up research areas linked to new drug testing, the establishment of more accurate disease models and the development of diagnostics to detect the diseases at an earlier stage.

The new cells are not only able to imitate the disease but also the patient's age. By studying the cell in the culture dish, the researchers can now monitor the mechanisms of the disease in an "old" brain cell over time. Neurodegenerative diseases are commonly referred to as "aging brain diseases" and in order to understand them, we must better appreciate how the age specifically affects the course of the disease. The Lund researchers' discovery can hopefully contribute a crucial piece to the puzzle with regard to the connection between the onset of disease and cell aging, something which previous research based on animal experiments and stem cells has failed to provide.

"This takes us one step closer to reality, as we can now look inside the human neurons and see what goes on inside the cell in these diseases. If all goes well, this could fundamentally change the field of research, as it helps us better understand the real mechanisms of the disease. We believe that many laboratories around the world would like to start testing on these cells to get closer to the diseases", says Johan Jakobsson, leader of the molecular neurogenetics research group at Lund University.

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Large-scale Production of Living Brain Cells Enables Entirely New Research - Laboratory Equipment

Skin Stem Cells Comments Off on Large-scale Production of Living Brain Cells Enables Entirely New Research – Laboratory Equipment | June 28th, 2017

If youve ever been concerned about hair loss in the past, this could be your lucky day. A new experiment carried out by Michael Rosenblum, assistant professor of dermatology at the University of California has proved just how useful regulatory T cells (tregs) are when it comes to hair loss. Previously scientists were led to believe that these cells single task was to inform other cells when to attack. However, what Rosenblum discovered when he shaved the mouse he was experimenting on, he noticed that the hair never grew back.

From the study, Rosenblum and team discovered that tregs in the skin had high levels of Jagged 1 (Jag1) which has the duty of calling in the stem cells through a process called Notch signaling. Removing the tregs reduced the notch signaling and when Jag1 was added the stem cells were called which then activated the process of follicle regeneration.

This study will be of particular interest to one type of hair loss sufferer: those with alopecia areata. This is an autoimmune disease that impedes hair follicle regeneration and affects as many as 1.7 percents of the U.S. population. Until now, very little has been known about what causes hair loss, but this research will give doctors and scientists everywhere new direction and a potential cure.

As well as hair regeneration, this process could be used to correct other skin related problems such as wound repair. What we found here is that stem cells, and immune cells have to work together to make regeneration possible, says Rosenblum. So dont despair if youre losing your hair, help is on the way!

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Say Goodbye to Hair Loss and Hello to Body Regeneration - TrendinTech

Skin Stem Cells Comments Off on Say Goodbye to Hair Loss and Hello to Body Regeneration – TrendinTech | June 26th, 2017

One of the coolest things about working in the beauty industry is being in the know and having the ability to tell readers, friends and family about a new product or brand that really works the way it claims. When Beauty Pie, the self-professed Buyers Club for Beauty Addicts came onto the scene and the cosmetic line was just as good as it promised, it was an exciting discovery. Most luxury beauty products retail for about 10x what they actually cost to make, is one of Beauty Pies mantras, and now the "Netflix of Beauty" is out to revolutionize the skin carebuying process the same way it did with makeup when it launched six months ago.

You May Also Like: I Tried the Netflix of Beauty and the $2$4 Products Are Totally Legit

The digital-only, UK-based brand was started by Marcia Kilgore, founder of other notable brands like Bliss Spa and Soap & Glory, so its no wonder that the membership club has now ventured into skin care, too. Now, a monthly membership of just $10 allows you to not only buy high-quality $7 foundations, $3 mascaras and $5 lipsticks, but you can also get all of your skin care needs meet for less than $13.

For the launch of its new skin care line, Beauty Pie has tapped the best Swiss suppliers and leading cosmetic chemists to create a line with ingredients and formulations that rival high-end luxury brands. The 11 newly released products range from the hydrating Swiss-Korean Jeju Daily Antioxidant Superinfusion Essence Serum ($8 for members/ $80 for nonmembers) and the creamy Double-Phase Daily Deep Rinse-Off Cleanser ($5 for members/ $32 for nonmembers) to a Fruitzyme Five Minute Facial ($6 for members/ $60 for nonmembers).

With ingredients like kiwiberry stem cells, meadowfoam seed oils, pomegranate enzymes and oil-absorbing kaolin clay, were excited to try the serums, masks, moisturizer, cleanser and eye cream and judge for ourselves whether the products stand up to their makeup counterparts. Beauty Pie's concept of luxury products at factory prices is a concept that will never get old and one worthy of throuougly exploring.

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$5 High-Quality Skin Care ExistsHere's the Proof - NewBeauty Magazine (blog)

Skin Stem Cells Comments Off on $5 High-Quality Skin Care ExistsHere’s the Proof – NewBeauty Magazine (blog) | June 26th, 2017

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Stem Cell Research is an amazing field right now, and promises to be a powerful and potent tool to help us live longer and healthier lives. Just last month, for example, Stem Cell Therapy was used to restore sight in patients with severe retinal deterioration, allowing them to see clearer than they had in years, or even decades.

Now, there is another form of Stem Cell Treatment on the horizonthis one of a very different form. Stem Cells have now been used as a mechanism to deliver medical treatment designed to eliminate cancer cells, even in hard to reach places. One issue with current cancer treatments is that, treatments that are effective at treating tumors on the surface of the brain cannot be performed safely when the tumor is deeper within the brains tissues.

Stem Cells have the fantastic ability to transform into any other kind of cell within the human body, given the appropriate stimulation. As of today, most of these cells come from Embryonic Lines, but researchers are learning how to backwards engineer cells in the human body, reverting them back to their embryonic state. These cells are known as Induced Pluripotent Stem Cells.

How Does This Stem Cell Cancer Treatment Work?

Using genetic engineering, it is possible to create stem cells that are designed to release a chemical known as Pseudomonas Exotoxin, which has the ability to destroy certain tumor cells in the human brain.

What is Pseudomonas Exotoxin?

Pseudomonas Exotoxin is a compound that is naturally released by a form of bacteria known as Pseudomonas Aeruginosa. This chemical is toxic to brain tumor cells because it prevents polypeptides from growing longer, essentially preventing the polypeptides from growing and reproducing. When used in a specific manner, this toxin has the ability to destroy cancerous and malignant tissue without negatively impacting healthy tissue. In addition to its potential as a cancer treatment, there is also evidence that the therapy could be used for the treatment of Hepatitis B.

PE and Similar Toxins Have been Used Therapeutically in the Past

As of now, this chemical, which we will refer to for the rest of the article as PE, has been used as a cancer treatment before, but there are major limitations regarding the use of PE for particular cancers, not because of the risks of the treatment, but because of the lack of an effective method to deliver the medication to where it is needed.

For example, similar chemicals have been highly effective in the treatment of a large number of blood cancers, but havent been nearly as effective in larger, more inaccessible tumors. The chemicals break down or become metabolized before they can fully do their job.

How do Stem Cells Increase the Effectiveness of PE Cancer Treatment

Right now, PE has to be created in a laboratory before it is administered, which is not very effective for these embedded cancers. By using Stem Cells as an intermediary, it is possible to deliver the medication to deeper areas of the brain more effectively, theoretically highly increasing the efficacy of the treatment.

The leader of this Stem Cell Research is Harvard researcher Dr. Khalis Shah. His goal was to find an effective means to treat these deep brain tumors which are not easily treated by methods available today. In utilizing Stem Cells, Dr. Shah has potentially found a means by which the stem cells can constantly deliver this Cancer Toxin to the tumor area. The cells remain active and are fed by the body, which allows them to provide a steady stream of treatment that is impossible to provide via any other known method.

This research is still in its early stages, and has not yet reached human trials, but in mice, the PE Toxin worked exactly as hypothesized and was able to starve out tumors by preventing them from replicating effectively.

Perhaps this might seem a bit less complicated than it actually is. One of the major hurdles that had to be overcome was that this Toxin would normally be strong enough to kill the cell that hosted it. In order for the Stem Cells to release the cancer, they had to be able to withstand the effects of PE, themselves. Using genetic engineering, Dr. Shah and his associates were able to create a cell that is capable of both producing and withstanding the effects of the toxin.

Stem Cell delivered medical therapy is a 21st century form of medical treatment that researchers are just beginning to learn how to effectively utilize. Essentially, this treatment takes a stem cell and converts it into a unique symbiotic tool capable of feeding off of the host for energy in order to perform a potentially life-saving function. Its really quite fascinating.

How Does PE Not Damage or Kill Brain Cells Indiscriminately?

You might be concerned about the idea of a patient having a toxin injected into the brain to cure a disease. It sounds almost like a dangerous, tribal, homeopathic remedy. In reality, the researchers have been able to harness the destructive power of the toxin and re-engineer it so that it directly targets cancer cells while having limited negative effects on healthy, non-cancerous tissue.

The toxin does its damage after it has been absorbed by a cell. By retooling the toxin so that it does not readily absorb into healthy cells, the dangers associated with having such a potentially dangerous toxin in the brain are seriously and significantly mitigated.

Beyond that, Dr. Shah and his associates have been able to take steps to effectively turn off PE while it is inside the host stem cell, and only activates when it has entered the cancerous tissue. Dr. Shah explains that, although this research has only been conducted in animal subjects, there is no known reason why the effectiveness and safety of the treatment would not be applicable to human patients.

In this treatment, surgeons remove as much of the tumor as possible from the brain, and insert the engineered Stem Cells submerged in a sterile gel in the area where the tumor was removed or partially still exists. Researchers found that, when they used this treatment on laboratory rats, they could tell through imaging and analysis that the modified PE toxin effectively killed the cancer cells, and that this cancer treatment effectively lengthened the life of the rat, as compared to control subjects.

Whats the Next Step?

Of course, cancer treatment is far more complex than a single treatment, no matter how effective that treatment may be. Because human cancer treatment is a comprehensive therapy approach, the end goal of this research is to create a form of therapy in which the method used in animal subjects is combined with other existing approaches, increasing and maximizing the effectiveness of the comprehensive treatment.

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A recent change in how well we understand stem cells may make it easier for scientists and researchers to gather stem cells for use in scientific research as well as medical application. A new study was released in the research publication, Cell, which was performed by representatives from the University of California San Francisco.

One of the issues which hinder the use of stem cells as a more widespread treatment or field of research is that researchers and patients have a bottleneck of available healthy stem cell lines which can be used for research. Researchers hope that this new discovery will allow future scientific discoveries and applications in the areas of creating new and healthy tissue for patients with kidney failure or any other form of organ tissue failure. The future of medical therapy lies with Stem Cell Research, but many other forms of treatment, including Hormone Replacement Therapy, are already in practice today.

Researchers have discovered that it is possible to essentially flip a switch in an adult cell, reverting it back to the preliminary state at which cells existed in one of the earliest stages of developmentthe embryonic stem cell. Medical researchers hypothesize that Stem Cell treatments could be used for a variety of medical health issues which plague the world today, including kidney failure, liver disease, and Type-1 and Type-2 Diabetes.

Use of Embryonic Stem Cells Contentious

There is an ethical issue in Stem Cell Research today. Many Pro-Life Advocates are vociferously against the use of Embryonic Stem Cells harvested from procedures such as fertility treatments designed for conception. They believe that the use of embryonic stem cells harvested from donors and couples looking to conceive is unethical.

Using current research, it may be possible to bypass this ethical quandary completely by using adult cells and converting them into embryonic stem cells. Furthermore, because these stem cells are genetic derivatives of the patient from which the adult cells were harvested, this potentially paves the way for patient-specific medical treatments using stem cells.

After adult cells have been converted back into Embryonic Stem Cells, it will be possible to convert them into any possible cell that the patient needs or would benefit from.

Hijacking the Blueprint of the Cell Allows Scientists to Revert Adult Cells to their Earliest State

Researchers have increased the capacity to produce Embryonic Stem Cells by identifying previously unrecognized biochemical processes which tell human cells how to develop. In essence, researchers have discovered how the body blueprints cells, and can change the blueprints so that a new cell is made.

By utilizing these newly recognized pathways, it is possible to create new stem cells more quickly than ever before. One of the researchers explains the implications of this research. Dr. Miguel Ramalho-Santos is an associate professor of obstetrics, medicine, and cancer research at the University of California San Francisco. Dr. Ramalho-Santos is also a member of the Broad Center of Regenerative Medicine and Stem Cell Research.

He explains that these stem cell discoveries have the ability to alter the way that the medical sciences can take advantage of stem cells with regard to both cancer research and regenerative medicine. Dr. Ramalho-Santos was the lead researcher for this study, and the research was largely funded by the Director of the National Institutes of Health New Innovator Award, granted to promising young researchers which are leading highly innovative and promising medical research studies.

Dr. Ramalho-Santos research builds off of earlier research which discovered that it was possible to take adult cells and turn them back into embryonic stem cells. These stem cells dont have any inherent aging processes, and they can be turned into any other kind of tissue. In the process of this conversion, the adult cells lose all of their unique characteristics, leaving them in an ultimately immature and malleable state.

This earlier research was conducted by researchers from UC San Francisco in partnership with Dr. Shinya Yamanaka from Kyoto University and Gladstone Institutes. These entities all gained a piece of the Nobel Prize in Physiology or Medicine from their part in the study.

Pluripotent Stem Cells vs. Embryonic Stem Cells

Thus far, weve described these cells as Embryonic Stem Cells, but in fact, the more accurate term for these cells are Induced Pluripotent Stem Cells (IPS). These cells are biologically and functionally similar to Embryonic Stem Cells, but have a different name because they are sourced from adult cells. The difference between Induced Pluripotent Stem Cells and Embryonic Stem Cells is that Induced Pluripotent Stem Cells do seem to retain some of the characteristics of their previous state, which appears to limit their ability to convert into any other type of cell. This new research identifies new pathways by which it may be possible to increase the number of cells that an individual IPS Cell can turn into, perhaps allowing them to convert into any other kind of human cell.

Induced Pluripotent Stem Cells are not explicitly considered an alternative to Embryonic Stem Cells, but are considered a different approach to produce similar cells. If researchers fully uncover the mechanisms of how to reprogram these cells, it will lower many barriers to stem cell research and the availability of stem cell treatments.

As of today, researchers have figured out how to make these Induced Pluripotent Stem Cells, but the percentage of adult cells which are reverted successfully is quite low, and frequently, these cells still show some aspects of specialization, which limits their use.

How Do Scientists Make Stem Cells From Adult Cells?

There are genes within every cell which have the ability to induce pluripotency, reverting the cell to an earlier stage of specialization. The initial stage of this process is the result of activating Yamanaka Factors, specific genes that initiate this reversion process.

As of today, this process of de-maturation is not completely understood, and researchers realized from the start that the cells they created were not truly identical to Embryonic Stem Cells, because they still showed signs of their former lives, which often prevented them from being successfully reprogrammed.

The new research conducted by Dr. Ramalho-Santos appears to increase our knowledge regarding how these cells work, and how to program them more effectively. Dr. Ramalho-Santos and his team discovered more genes associated with these programming/reprogramming processes, and by manipulating them, they have increased the viability and range of particular stem cells.

It appears that these genetic impulses are constantly at play to maintain the structure and function of a cell, and that by systematically removing these safeguards, it is possible to increase the ability to alter these cells.

This research increases researchers ability to produce these stem cells, by increasing the ability of medical scientists to produce adequate numbers of stem cells, while also increasing the range of potential treatment options by more effectively inducing the total pluripotency which is available in Embryonic Stem Cells. This research may also help scientists treat certain forms of cancer which are the result of malfunctions of these genes.

Introduction

[Note: Many of the medical and scientific terms used in this summary are found in the NCI Dictionary of Genetics Terms. When a linked term is clicked, the definition will appear in a separate window.]

[Note: Many of the genes described in this summary are found in the Online Mendelian Inheritance in Man (OMIM) database. When OMIM appears after a gene name or the name of a condition, click on OMIM for a link to more information.]

The genetics of skin cancer is an extremely broad topic. There are more than 100 types of tumors that are clinically apparent on the skin; many of these are known to have familial components, either in isolation or as part of a syndrome with other features. This is, in part, because the skin itself is a complex organ made up of multiple cell types. Furthermore, many of these cell types can undergo malignant transformation at various points in their differentiation, leading to tumors with distinct histology and dramatically different biological behaviors, such as squamous cell carcinoma (SCC) and basal cell cancer (BCC). These have been called nonmelanoma skin cancers or keratinocytic cancers.

Figure 1 is a simple diagram of normal skin structure. It also indicates the major cell types that are normally found in each compartment. Broadly speaking, there are two large compartmentsthe avascular cellular epidermis and the vascular dermiswith many cell types distributed in a largely acellular matrix.[1]

Figure 1. Schematic representation of normal skin. The relatively avascular epidermis houses basal cell keratinocytes and squamous epithelial keratinocytes, the source cells for BCC and SCC, respectively. Melanocytes are also present in normal skin and serve as the source cell for melanoma. The separation between epidermis and dermis occurs at the basement membrane zone, located just inferior to the basal cell keratinocytes.

The outer layer or epidermis is made primarily of keratinocytes but has several other minor cell populations. The bottom layer is formed of basal keratinocytes abutting the basement membrane. The basement membrane is formed from products of keratinocytes and dermal fibroblasts, such as collagen and laminin, and is an important anatomical and functional structure. As the basal keratinocytes divide and differentiate, they lose contact with the basement membrane and form the spinous cell layer, the granular cell layer, and the keratinized outer layer or stratum corneum.

The true cytologic origin of BCC remains in question. BCC and basal cell keratinocytes share many histologic similarities, as is reflected in the name. Alternatively, the outer root sheath cells of the hair follicle have also been proposed as the cell of origin for BCC.[2] This is suggested by the fact that BCCs occur predominantly on hair-bearing skin. BCCs rarely metastasize but can invade tissue locally or regionally, sometimes following along nerves. A tendency for superficial necrosis has resulted in the name rodent ulcer.[3]

Some debate remains about the origin of SCC; however, these cancers are likely derived from epidermal stem cells associated with the hair follicle.[4] A variety of tissues, such as lung and uterine cervix, can give rise to SCC, and this cancer has somewhat differing behavior depending on its source. Even in cancer derived from the skin, SCC from different anatomic locations can have moderately differing aggressiveness; for example, SCC from glabrous (smooth, hairless) skin has a lower metastatic rate than SCC arising from the vermillion border of the lip or from scars.[3]

Additionally, in the epidermal compartment, melanocytes distribute singly along the basement membrane and can transform into melanoma. Melanocytes are derived from neural crest cells and migrate to the epidermal compartment near the eighth week of gestational age. Langerhans cells, or dendritic cells, are a third cell type in the epidermis and have a primary function of antigen presentation. These cells reside in the skin for an extended time and respond to different stimuli, such as ultraviolet radiation or topical steroids, which cause them to migrate out of the skin.[5]

The dermis is largely composed of an extracellular matrix. Prominent cell types in this compartment are fibroblasts, endothelial cells, and transient immune system cells. When transformed, fibroblasts form fibrosarcomas and endothelial cells form angiosarcomas, Kaposi sarcoma, and other vascular tumors. There are a number of immune cell types that move in and out of the skin to blood vessels and lymphatics; these include mast cells, lymphocytes, mononuclear cells, histiocytes, and granulocytes. These cells can increase in number in inflammatory diseases and can form tumors within the skin. For example, urticaria pigmentosa is a condition that arises from mast cells and is occasionally associated with mast cell leukemia; cutaneous T-cell lymphoma is often confined to the skin throughout its course. Overall, 10% of leukemias and lymphomas have prominent expression in the skin.[6]

Epidermal appendages are also found in the dermal compartment. These are derivatives of the epidermal keratinocytes, such as hair follicles, sweat glands, and the sebaceous glands associated with the hair follicles. These structures are generally formed in the first and second trimesters of fetal development. These can form a large variety of benign or malignant tumors with diverse biological behaviors. Several of these tumors are associated with familial syndromes. Overall, there are dozens of different histological subtypes of these tumors associated with individual components of the adnexal structures.[7]

Finally, the subcutis is a layer that extends below the dermis with varying depth, depending on the anatomic location. This deeper boundary can include muscle, fascia, bone, or cartilage. The subcutis can be affected by inflammatory conditions such as panniculitis and malignancies such as liposarcoma.[8]

These compartments give rise to their own malignancies but are also the region of immediate adjacent spread of localized skin cancers from other compartments. The boundaries of each skin compartment are used to define the staging of skin cancers. For example, an in situ melanoma is confined to the epidermis. Once the cancer crosses the basement membrane into the dermis, it is invasive. Internal malignancies also commonly metastasize to the skin. The dermis and subcutis are the most common locations, but the epidermis can also be involved in conditions such as Pagetoid breast cancer.

The skin has a wide variety of functions. First, the skin is an important barrier preventing extensive water and temperature loss and providing protection against minor abrasions. These functions can be aberrantly regulated in cancer. For example, in the erythroderma associated with advanced cutaneous T-cell lymphoma, alterations in the regulations of body temperature can result in profound heat loss. Second, the skin has important adaptive and innate immunity functions. In adaptive immunity, antigen-presenting cells engender a TH1, TH2, and TH17 response.[9] In innate immunity, the immune system produces numerous peptides with antibacterial and antifungal capacity. Consequently, even small breaks in the skin can lead to infection. The skin-associated lymphoid tissue is one of the largest arms of the immune system. It may also be important in immune surveillance against cancer. Immunosuppression, which occurs during organ transplant, is a significant risk factor for skin cancer. The skin is significant for communication through facial expression and hand movements. Unfortunately, areas of specialized function, such as the area around the eyes and ears, are common places for cancer to occur. Even small cancers in these areas can lead to reconstructive challenges and have significant cosmetic and social ramifications.[1]

While the appearance of any one skin cancer can vary, there are general physical presentations that can be used in screening. BCCs most commonly have a pearly rim (see Figure 3) or can appear somewhat eczematous. They often ulcerate (see Figure 3). SCCs frequently have a thick keratin top layer (see Figure 4). Both BCCs and SCCs are associated with a history of sun-damaged skin. Melanomas are characterized by asymmetry, border irregularity, color variation, a diameter of more than 6 mm, and evolution (ABCDE criteria). (Refer to What Does Melanoma Look Like? on NCIs website for more information about the ABCDE criteria.) Photographs representing typical clinical presentations of these cancers are shown below.

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Figure 2. Superficial basal cell carcinoma (left panel) and nodular basal cell carcinoma (right panel).

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Figure 3. Ulcerated basal cell carcinoma (left panel) and ulcerated basal cell carcinoma with characteristic pearly rim (right panel).

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Figure 4. Squamous cell carcinoma on the face with thick keratin top layer (left panel) and squamous cell carcinoma on the leg (right panel).

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Figure 5. Melanomas with characteristic asymmetry, border irregularity, color variation, and large diameter.

Basal cell carcinoma (BCC) is the most common malignancy in people of European descent, with an associated lifetime risk of 30%.[1] While exposure to ultraviolet (UV) radiation is the risk factor most closely linked to the development of BCC, other environmental factors (such as ionizing radiation, chronic arsenic ingestion, and immunosuppression) and genetic factors (such as family history, skin type, and genetic syndromes) also potentially contribute to carcinogenesis. In contrast to melanoma, metastatic spread of BCC is very rare and typically arises from large tumors that have evaded medical treatment for extended periods of time. BCCs can invade tissue locally or regionally, sometimes following along nerves. A tendency for superficial necrosis has resulted in the name rodent ulcer. With early detection, the prognosis for BCC is excellent.

Sun exposure is the major known environmental factor associated with the development of skin cancer of all types. There are different patterns of sun exposure associated with each major type of skin cancer (BCC, squamous cell carcinoma [SCC], and melanoma).

While there is no standard measure, sun exposure can be generally classified as intermittent or chronic, and the effects may be considered acute or cumulative. Intermittent sun exposure is obtained sporadically, usually during recreational activities, and particularly by indoor workers who have only weekends or vacations to be outdoors and whose skin has not adapted to the sun. Chronic sun exposure is incurred by consistent, repetitive sun exposure, during outdoor work or recreation. Acute sun exposure is obtained over a short time period on skin that has not adapted to the sun. Depending on the time of day and a persons skin type, acute sun exposure may result in sunburn. In epidemiology studies, sunburn is usually defined as burn with pain and/or blistering that lasts for 2 or more days. Cumulative sun exposure is the additive amount of sun exposure that one receives over a lifetime. Cumulative sun exposure may reflect the additive effects of intermittent sun exposure, chronic sun exposure, or both.

Specific patterns of sun exposure appear to lead to different types of skin cancer among susceptible individuals. Intense intermittent recreational sun exposure has been associated with melanoma and BCC,[2,3] while chronic occupational sun exposure has been associated with SCC. Given these data, dermatologists routinely counsel patients to protect their skin from the sun by avoiding mid-day sun exposure, seeking shade, and wearing sun-protective clothing, although evidence-based data for these practices are lacking. The data regarding skin cancer risk reduction by regular sunscreen use are variable. One randomized trial of sunscreen efficacy demonstrated statistically significant protection for the development of SCC but no protection for BCC,[4] while another randomized study demonstrated a trend for reduction in multiple occurrences of BCC among sunscreen users [5] but no significant reduction in BCC or SCC incidence.[6]

Level of evidence (sun-protective clothing, avoidance of sun exposure): 4aii

Level of evidence (sunscreen): 1aii

Tanning bed use has also been associated with an increased risk of BCC. A study of 376 individuals with BCC and 390 control subjects found a 69% increased risk of BCC in individuals who had ever used indoor tanning.[7] The risk of BCC was more pronounced in females and individuals with higher use of indoor tanning.[8]

Environmental factors other than sun exposure may also contribute to the formation of BCC and SCC. Petroleum byproducts (e.g., asphalt, tar, soot, paraffin, and pitch), organophosphate compounds, and arsenic are all occupational exposures associated with cutaneous nonmelanoma cancers.[9-11]

Arsenic exposure may occur through contact with contaminated food, water, or air. While arsenic is ubiquitous in the environment, its ambient concentration in both food and water may be increased near smelting, mining, or coal-burning establishments. Arsenic levels in the U.S. municipal water supply are tightly regulated; however, control is lacking for potable water obtained through private wells. As it percolates through rock formations with naturally occurring arsenic, well water may acquire hazardous concentrations of this material. In many parts of the world, wells providing drinking water are contaminated by high levels of arsenic in the ground water. The populations in Bangladesh, Taiwan, and many other locations have high levels of skin cancer associated with elevated levels of arsenic in the drinking water.[12-16] Medicinal arsenical solutions (e.g., Fowlers solution and Bells asthma medication) were once used to treat common chronic conditions such as psoriasis, syphilis, and asthma, resulting in associated late-onset cutaneous malignancies.[17,18] Current potential iatrogenic sources of arsenic exposure include poorly regulated Chinese traditional/herbal medications and intravenous arsenic trioxide utilized to induce remission in acute promyelocytic leukemia.[19,20]

Aerosolized particulate matter produced by combustion of arsenic-containing materials is another source of environmental exposure. Arsenic-rich coal, animal dung from arsenic-rich regions, and chromated copper arsenatetreated wood produce airborne arsenical particles when burned.[21-23] Burning of these products in enclosed unventilated settings (such as for heat generation) is particularly hazardous.[24]

Clinically, arsenic-induced skin cancers are characterized by multiple recurring SCCs and BCCs occurring in areas of the skin that are usually protected from the sun. A range of cutaneous findings are associated with chronic or severe arsenic exposure, including pigmentary variation (poikiloderma of the skin) and Bowen disease (SCC in situ).[25]

However, the effect of arsenic on skin cancer risk may be more complex than previously thought. Evidence from in vivo models indicate that arsenic, alone or in combination with itraconazole, can inhibit the hedgehog pathway in cells with wild-type or mutated Smoothened by binding to GLI2 proteins; in this way, these drugs demonstrated inhibition of BCC growth in these animal models.[26,27] Additionally, the effect of arsenic on skin cancer risk may be modified by certain variants in nucleotide excision repair genes (xeroderma pigmentosum [XP] types A and D).[28]

The high-risk phenotype consists of individuals with the following physical characteristics:

Specifically, people with more highly pigmented skin demonstrate lower incidence of BCC than do people with lighter pigmented skin. Individuals with Fitzpatrick skin types I or II were shown to have a twofold increased risk of BCC in a small case-control study.[29] (Refer to the Pigmentary characteristics section in the Melanoma section of this summary for a more detailed discussion of skin phenotypes based upon pigmentation.) Blond or red hair color was associated with increased risk of BCC in two large cohorts: the Nurses Health Study and the Health Professionals Follow-Up Study.[30]

Immunosuppression also contributes to the formation of nonmelanoma (keratinocyte) skin cancers. Among solid-organ transplant recipients, the risk of SCC is 65 to 250 times higher, and the risk of BCC is 10 times higher than in the general population.[31-33] Nonmelanoma skin cancers in high-risk patients (i.e., solid-organ transplant recipients and chronic lymphocytic leukemia patients) occur at a younger age and are more common, more aggressive, and have a higher risk of recurrence and metastatic spread than nonmelanoma skin cancers in the general population.[34,35] Among patients with an intact immune system, BCCs outnumber SCCs by a 4:1 ratio; in transplant patients, SCCs outnumber BCCs by a 2:1 ratio.

This increased risk has been linked to the level of immunosuppression and UV exposure. As the duration and dosage of immunosuppressive agents increases, so does the risk of cutaneous malignancy; this effect is reversed with decreasing the dosage of, or taking a break from, immunosuppressive agents. Heart transplant recipients, requiring the highest rates of immunosuppression, are at much higher risk of cutaneous malignancy than liver transplant recipients, in whom much lower levels of immunosuppression are needed to avoid rejection.[31,36] The risk appears to be highest in geographic areas of high UV radiation exposure: when comparing Australian and Dutch organ transplant populations, the Australian patients carried a fourfold increased risk of developing SCC and a fivefold increased risk of developing BCC.[37] This speaks to the importance of rigorous sun avoidance among high-risk immunosuppressed individuals.

Individuals with BCCs and/or SCCs report a higher frequency of these cancers in their family members than do controls. The importance of this finding is unclear. Apart from defined genetic disorders with an increased risk of BCC, a positive family history of any skin cancer is a strong predictor of the development of BCC.

A personal history of BCC or SCC is strongly associated with subsequent BCC or SCC. There is an approximate 20% increased risk of a subsequent lesion within the first year after a skin cancer has been diagnosed. The mean age of occurrence for these nonmelanoma skin cancers is the mid-60s.[38-43] In addition, several studies have found that individuals with a history of skin cancer have an increased risk of a subsequent diagnosis of a noncutaneous cancer;[44-47] however, other studies have contradicted this finding.[48-51] In the absence of other risk factors or evidence of a defined cancer susceptibility syndrome, as discussed below, skin cancer patients are encouraged to follow screening recommendations for the general population for sites other than the skin.

Mutations in the gene coding for the transmembrane receptor protein PTCH1, or PTCH, are associated with basal cell nevus syndrome (BCNS) and sporadic cutaneous BCCs. PTCH1, the human homolog of the Drosophila segment polarity gene patched (ptc), is an integral component of the hedgehog signaling pathway, which serves many developmental (appendage development, embryonic segmentation, neural tube differentiation) and regulatory (maintenance of stem cells) roles.

In the resting state, the transmembrane receptor protein PTCH1 acts catalytically to suppress the seven-transmembrane protein Smoothened (Smo), preventing further downstream signal transduction.[52] Stoichiometric binding of the hedgehog ligand to PTCH1 releases inhibition of Smo, with resultant activation of transcription factors (GLI1, GLI2), cell proliferation genes (cyclin D, cyclin E, myc), and regulators of angiogenesis.[53,54] Thus, the balance of PTCH1 (inhibition) and Smo (activation) manages the essential regulatory downstream hedgehog signal transduction pathway. Loss-of-function mutations of PTCH1 or gain-of-function mutations of Smo tip this balance toward constitutive activation, a key event in potential neoplastic transformation.

Demonstration of allelic loss on chromosome 9q22 in both sporadic and familial BCCs suggested the potential presence of an associated tumor suppressor gene.[55,56] Further investigation identified a mutation in PTCH1 that localized to the area of allelic loss.[57] Up to 30% of sporadic BCCs demonstrate PTCH1 mutations.[58] In addition to BCC, medulloblastoma and rhabdomyosarcoma, along with other tumors, have been associated with PTCH1 mutations. All three malignancies are associated with BCNS, and most people with clinical features of BCNS demonstrate PTCH1 mutations, predominantly truncation in type.[59]

Truncating mutations in PTCH2, a homolog of PTCH1 mapping to chromosome 1p32.1-32.3, have been demonstrated in both BCC and medulloblastoma.[60,61] PTCH2 displays 57% homology to PTCH1, differing in the conformation of the hydrophilic region between transmembrane portions 6 and 7, and the absence of C-terminal extension.[62] While the exact role of PTCH2 remains unclear, there is evidence to support its involvement in the hedgehog signaling pathway.[60,63]

BCNS, also known as Gorlin Syndrome, Gorlin-Goltz syndrome, and nevoid basal cell carcinoma syndrome, is an autosomal dominant disorder with an estimated prevalence of 1 in 57,000 individuals.[64] The syndrome is notable for complete penetrance and extremely variable expressivity, as evidenced by evaluation of individuals with identical genotypes but widely varying phenotypes.[59,65] The clinical features of BCNS differ more among families than within families.[66] BCNS is primarily associated with germline mutations in PTCH1, but families with this phenotype have also been associated with alterations in PTCH2 and SUFU.[67-69]

As detailed above, PTCH1 provides both developmental and regulatory guidance; spontaneous or inherited germline mutations of PTCH1 in BCNS may result in a wide spectrum of potentially diagnostic physical findings. The BCNS mutation has been localized to chromosome 9q22.3-q31, with a maximum logarithm of the odd (LOD) score of 3.597 and 6.457 at markers D9S12 and D9S53.[64] The resulting haploinsufficiency of PTCH1 in BCNS has been associated with structural anomalies such as odontogenic keratocysts, with evaluation of the cyst lining revealing heterozygosity for PTCH1.[70] The development of BCC and other BCNS-associated malignancies is thought to arise from the classic two-hit suppressor gene model: baseline heterozygosity secondary to germline PTCH1 mutation as the first hit, with the second hit due to mutagen exposure such as UV or ionizing radiation.[71-75] However, haploinsufficiency or dominant negative isoforms have also been implicated for the inactivation of PTCH1.[76]

The diagnosis of BCNS is typically based upon characteristic clinical and radiologic examination findings. Several sets of clinical diagnostic criteria for BCNS are in use (refer to Table 1 for a comparison of these criteria).[77-80] Although each set of criteria has advantages and disadvantages, none of the sets have a clearly superior balance of sensitivity and specificity for identifying mutation carriers. The BCNS Colloquium Group proposed criteria in 2011 that required 1 major criterion with molecular diagnosis, two major criteria without molecular diagnosis, or one major and two minor criteria without molecular diagnosis.[80] PTCH1 mutations are found in 60% to 85% of patients who meet clinical criteria.[81,82] Most notably, BCNS is associated with the formation of both benign and malignant neoplasms. The strongest benign neoplasm association is with ovarian fibromas, diagnosed in 14% to 24% of females affected by BCNS.[74,78,83] BCNS-associated ovarian fibromas are more likely to be bilateral and calcified than sporadic ovarian fibromas.[84] Ameloblastomas, aggressive tumors of the odontogenic epithelium, have also been proposed as a diagnostic criterion for BCNS, but most groups do not include it at this time.[85]

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IPS Cell Therapy IPS Cell Therapy - genetherapy.me

IPS Cell Therapy Comments Off on IPS Cell Therapy IPS Cell Therapy – genetherapy.me | June 25th, 2017

SOUTH SAN FRANCISCO, CA--(Marketwired - June 22, 2017) - VistaGen Therapeutics Inc.(NASDAQ: VTGN), a clinical-stage biopharmaceutical company focused on developing new generation medicines for depression and other central nervous system (CNS) disorders, announced today a peer-reviewed publication in the Scandinavian Journal of Pain of two Phase 1 clinical studies of the effects of AV-101 (4-Cl-KYN), the Company's CNS prodrug candidate, as a potential non-opioid treatment for neuropathic pain. Safety data from both the single and multi-dose Phase 1 studies indicated that oral AV-101 was extremely safe and well tolerated, with no meaningful difference in adverse events (AEs) at any dose between AV-101 and placebo. Recently published statistically-significant positive results in four well-established preclinical models of pain associated with tissue inflammation and nerve injury, together with the excellent clinical safety profile, pharmacokinetic (PK) characteristics and consistent reductions in three pain measures (allodynia, mechanical and heat hyperalgesia) demonstrated by these studies, support future Phase 2 clinical studies of AV-101 as a potential new non-opioid treatment alternative for neuropathic pain.

The publication, titled "Randomized, Double-Blind, Placebo Controlled, Dose-Escalation Study: Investigation of the Safety, Pharmacokinetics, and Antihyperalgesic Activity of L-4 chlorokynurenine in Healthy Volunteers," by lead author, Mark Wallace, MD, and co-authors, Alexander White, MD, Kathy A Grako, PhD, Randal Lane, Allen (Jo) Cato, PhD and H. Ralph Snodgrass, PhD, was recently published in the Scandinavian Journal of Pain (DOI: 10.1016/j.sjpain.2017.05.004) and is available online at http://www.scandinavianjournalpain.com/article/S1877-8860(17)30128-3/fulltext.

"The excellent safety data and consistent reductions in allodynia pain and mechanical and heat hyperalgesia during the two Phase 1 clinical studies of AV-101 support our belief in its potential to treat neuropathic pain without the negative side-effects experienced with most of the drugs used today to treat pain. Additional clinical trials of AV-101 in neuropathic pain are warranted," reported Mark Wallace, MD, Distinguished Professor of Clinical Anesthesiology at the University of California, San Diego.

"The positive results published in these studies further support our belief that AV-101 has the potential to reduce pain effectively and safely, without causing burdensome side effects like gabapentin and many other neuropathic pain treatments, such as opiates, on the market today. The opioid epidemic, which stems in part from prescribing opiate analgesics for outpatient procedures, makes it imperative that we find new analgesics devoid of abuse potential. Importantly, AV-101 does not bind to opioid receptors, and yet may still have efficacy in neuropathic pain," stated Mark A. Smith, MD, PhD, Chief Medical Officer, VistaGen Therapeutics. "Additionally, a key observation from these Phase 1 studies in normal volunteers was spontaneous reports of 'feelings of well-being' in subjects exposed to AV-101, especially those in the highest dose group of 1440 mg, while none of the subjects on placebo reported any such feelings. Importantly, these feelings were NOT characterized as feeling intoxicated or psychotic as has been often reported by subjects taking ketamine for major depressive disorder. We are optimistic about AV-101's potential as a new treatment alternative for major depressive disorder, without ketamine-like side effects, and for neuropathic pain, without gabapentin-like side effects or opioid abuse potential."

Study Summary and Key Findings:

Two Phase 1 Clinical Studies -

About AV-101AV-101 (4-CI-KYN) is an oral CNS prodrug candidate in Phase 2 development in the U.S., initially as a new generation treatment for major depressive disorder (MDD). AV-101 also has broad potential utility in several other CNS indications where modulation of NMDA receptors, activation of AMPA pathways and/or key active metabolites of AV-101 may achieve therapeutic benefit, including neuropathic pain and epilepsy, as well as addressing symptoms associated with neurodegenerative diseases, such as Parkinson's disease and Huntington's disease.

AV-101 is currently being evaluated in a Phase 2 monotherapy study in MDD, a study being fully funded by the U.S. National Institute of Mental Health (NIMH) and conducted by Dr. Carlos Zarate Jr., Chief, Section on the Neurobiology and Treatment of Mood Disorders and Chief of Experimental Therapeutics and Pathophysiology Branch at the NIMH, as Principal Investigator.

VistaGen is preparing to advance AV-101 into a 180-patient, U.S. multi-center, Phase 2 adjunctive treatment study in MDD patients with an inadequate response to standard FDA-approved antidepressants, with Dr. Maurizio Fava of Harvard University as Principal Investigator.

About VistaGenVistaGen Therapeutics, Inc. (NASDAQ: VTGN), is a clinical-stage biopharmaceutical company focused on developing new generation medicines for depression and other central nervous system (CNS) disorders. VistaGen's lead CNS product candidate, AV-101, is in Phase 2 development, initially as a new generation oral antidepressant drug candidate for major depressive disorder (MDD). AV-101's mechanism of action is fundamentally differentiated from all FDA-approved antidepressants and atypical antipsychotics used adjunctively to treat MDD, with potential to drive a paradigm shift towards a new generation of safer and faster-acting antidepressants. AV-101 is currently being evaluated by the U.S. National Institute of Mental Health (NIMH) in a Phase 2 monotherapy study in MDD being fully funded by the NIMH and conducted by Dr. Carlos Zarate Jr., Chief, Section on the Neurobiology and Treatment of Mood Disorders and Chief of Experimental Therapeutics and Pathophysiology Branch at the NIMH. VistaGen is preparing to launch a 180-patient Phase 2 study of AV-101 as an adjunctive treatment for MDD patients with inadequate response to standard, FDA-approved antidepressants. Dr. Maurizio Fava of Harvard University will be the Principal Investigator of the Company's Phase 2 adjunctive treatment study. AV-101 may also have the potential to treat multiple CNS disorders and neurodegenerative diseases in addition to MDD, including chronic neuropathic pain, epilepsy, Huntington's disease, and L-Dopa-induced dyskinesias associated with Parkinson's disease and, other disorders where modulation of NMDA receptors, activation of AMPA pathways and/or key active metabolites of AV-101 may achieve therapeutic benefit.

VistaStem Therapeutics is VistaGen's wholly owned subsidiary focused on applying human pluripotent stem cell technology, internally and with collaborators, to discover, rescue, develop and commercialize proprietary new chemical entities (NCEs), including small molecule NCEs with regenerative potential, for CNS and other diseases, and cellular therapies involving stem cell-derived blood, cartilage, heart and liver cells. In December 2016, VistaGen exclusively sublicensed to BlueRock Therapeutics LP, a next generation regenerative medicine company established by Bayer AG and Versant Ventures, rights to certain proprietary technologies relating to the production of cardiac stem cells for the treatment of heart disease.

For more information, please visit http://www.vistagen.com and connect with VistaGen on Twitter, LinkedIn and Facebook.

Forward-Looking StatementsThe statements in this press release that are not historical facts may constitute forward-looking statements that are based on current expectations and are subject to risks and uncertainties that could cause actual future results to differ materially from those expressed or implied by such statements. Those risks and uncertainties include, but are not limited to, risks related to the successful launch, continuation and results of the NIMH's Phase 2 (monotherapy) and/or the Company's planned Phase 2 (adjunctive therapy) clinical studies of AV-101 in MDD, and other CNS diseases and disorders, including neuropathic pain and L-DOPA-induced dyskinesia associated with Parkinson's disease, protection of its intellectual property, and the availability of substantial additional capital to support its operations, including the Phase 2 clinical development activities described above. These and other risks and uncertainties are identified and described in more detail in VistaGen's filings with the Securities and Exchange Commission (SEC). These filings are available on the SEC's website at http://www.sec.gov. VistaGen undertakes no obligation to publicly update or revise any forward-looking statements.

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VistaGen Announces Peer-Reviewed Publication in the Scandinavian Journal of Pain Highlighting Orally-Available AV ... - Markets Insider

Cardiac Stem Cells Comments Off on VistaGen Announces Peer-Reviewed Publication in the Scandinavian Journal of Pain Highlighting Orally-Available AV … – Markets Insider | June 23rd, 2017

A BRAVE Barrow girl is delighted to be back at school after eight months away fighting leukemia and recovering from complications following a stem cell transplant.

Bubbly Aimee Robinson returned to St James' CE Junior School this week to a warm welcome from her friends and teachers, who have all missed having her at the Barrow primary.

The eleven-year-old last attended the Blake Street school for three weeks in September as she is a patient at the Royal Manchester Children's Hospital, where she has battled leukemia.

Following aggressive chemotherapy, Aimee had a stem cell transplant using umbilical cord blood. She did well following the transplant and spent time in isolation. But she later developed graft versus host disease. This is when particular types of white blood cell in the donated bone marrow or stem cells attack a bodies own cells.

Aimee had to spend further time in isolation as she recovered from GVHD.

Aimee, who was first diagnosed with leukemia in January 2016, is now in remission and the treatment for GVHD is also working. She was eventually allowed home to Barrow last month, but she has treatment at the Manchester hospital every fortnight.

Medics then gave her the okay to return to school this week to complete her final year of primary school, Year Six, before she prepares to attend Furness Academy in September.

Aimee, who is a house captain and school council member at St James' school, said: "It feels great to be at school with my friends. St James' is the best school ever."

Her great friend Abbie Gelling, 11, said it is really great to have Aimee back, as they had to keep in touch through FaceTime, texts and letters.

Angela Rawlinson, the headteacher at St James' CE Junior School, said: "We are so thrilled to have Aimee back at school. It's such great news. Aimee loves school and learning.

"It was very important for Aimee to get back to school before they all move on to secondary school."

The St James' school community raised 3,000 to help Aimee and her family who have spent so much time away from home. The community also fundraised to support the pupil.

Aimee has been doing her schooling at hospital with input from St James' school.

Aimee's mum Joanne Robinson, said: "Aimee has been raring to get back to school, she missed all her friends and teachers. She wanted to go back as soon as possible.

"Nothing bothers Aimee, she just gets on with it. She is a superstar.

"There is no sign of the leukemia now, her bone marrow is working brilliantly."

Mrs Robinson thanked all the medics, the St James' community and the wider community.

She said: "Thank you to everyone for the love and support they have given our family over the past 18 months and for the support we continue to receive."

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Brave Aimee delighted to be back at Barrow school after months in hospital - NW Evening Mail

Bone Marrow Stem Cells Comments Off on Brave Aimee delighted to be back at Barrow school after months in hospital – NW Evening Mail | June 23rd, 2017

June 23, 2017

Imagine being able to take cells from your skin, transform them into other types of cells, such as lung, brain, heart or muscle cells, and use those to cure your ailments, from diabetes to heart disease or macular degeneration. To realise this, however, challenges still remain, Professor Janet Rossant, a pioneer in the field, says.

All across the world, scientists have begun clinical trials to try and do just that, by making use of the incredible power and versatility of stem cells, which are special cells that can make endless copies of themselves and transform into every other type of cell.

While human embryos contain embryonic stem cells, which help them to develop, the use of those cells has been controversial. The scientists are using induced pluripotent stem cells instead, which are other cells that have been reprogrammed to behave like stem cells.

"There are still significant challenges that we need to overcome, but in the long run we might even be able to create organs from stem cells taken from patients. That would enable rejection-free transplants," said Professor Janet Rossant, a pioneer in the field.

The mouse that changed everything

A speaker at the recent Commonwealth Science Conference 2017 held in Singapore and organised by Britain's Royal Society and Singapore's National Research Foundation, Prof Rossant gave an overview of stem cells' origins, history, uses and potential.

Now a senior scientist at The Hospital for Sick Children (also known as Sick Kids) in Toronto, Canada, after a decade as its chief of research, she was the first scientist to demonstrate the full power of stem cells in mice.

In the early 1990s, scientists believed that stem cells could only become certain types of cells and carry out limited functions. Based on her own research and that of others, however, Prof Rossant believed that they were capable of far more.

Working with other scientists, she created an entire mouse out of stem cells in 1992, upending the conventional wisdom. "We went on to create many baby mice that were completely normal, and completely derived from stem cells grown in a petri dish," she said.

"That was an amazing experiment, and it was instrumental in making people believe that human embryonic stem cells could have the full potential to make every cell type in the body," she added.

When scientists learned how to remove stem cells from human embryos in 1998, however, controversy ensued. Many lobbied against the cells' use in medical research and treatment due to the moral implications of destroying even unwanted embryos to gain the cells.

In Canada, Prof Rossant chaired the working group of the Canadian Institutes of Health Research on Stem Cell Research, establishing guidelines for the field. These guidelines helped to keep the field alive in Canada, and were influential well beyond the country's borders.

In 2006, Japanese researchers succeeded in taking skin cells from adult mice and reprogramming them to behave like embryonic stem cells. These revolutionary, induced pluripotent stem (IPS) cells allowed scientists to sidestep the ongoing controversy.

The challenges in the way

While stem cells have been used for medical treatment in some cases bone marrow transplants, for example, are a form of stem cell therapy there are several challenges that need to be overcome before they can be used more widely to treat diseases and injuries.

"We need to get better at turning stem cells into the fully mature cells that you need for therapy. That's going to take more work. Another issue is that of scale-up. If you're going to treat a patient, you need to be able to grow millions of cells," said Prof Rossant.

She added: "Safety is another concern. One of the most exciting things about pluripotent stem cells is that they can divide indefinitely in the culture dish. But that's also one of the most scary things about them, because that's also how cancer works.

"Furthermore, because we need to genetically manipulate cells to get IPS cells, it's very hard to know whether we've got completely normal cells at the end of the day. These are all issues that need to be resolved."

She noted that some scientists are working on making "failsafe" IPS cells, which have a built-in self-destruct option if they become dangerous. "Bringing stem cells into regenerative medicine is going to require interdisciplinary, international collaboration," she said.

In the meantime, stem cells have been a boon to medical research, as scientists can use them to create an endless supply of different cells to study diseases and injuries, and test drugs. "That's the biggest use of IPS cells right now," Prof Rossant said.

Sick kids and how to help them

At SickKids, which is Canada's largest paediatric research hospital, she has been using stem cells to study cystic fibrosis, a frequently fatal genetic disorder that causes mucus to build up and clog some organs such as the lungs. It affects primarily children and young adults.

SickKids discovered the CFTR gene that, when mutated, causes the disease. It was also the first to produce mature lung cells, from stem cells, that can be used to study the disease and test drugs against it.

Even better, Prof Rossant and her team were able to turn skin cells from cystic fibrosis patients into IPS cells and then into lung cells with the genetic mutation specific to each of them. This is critical to personalising treatment for each patient.

"Drugs for cystic fibrosis are extraordinarily expensive, and patients can have the same mutation and yet respond differently to the same drug," Prof Rossant explained. "With our work, we can make sure that each patient gets the right drug at the right time."

In 1998, Prof Rossant also discovered a new type of stem cell in mice, now called the trophoblast stem cell. These surround an embryo and attach it to the uterine wall, eventually becoming the placenta. She is using such cells to study placenta defects and pregnancy problems.

By using IPS cells to create heart cells and other cells, pharmaceutical companies can also test their new drugs' effectiveness and uncover potential side effects, as well as develop personalised medicines.

"There are still huge amounts of opportunities in pluripotent stem cells," said Prof Rossant, who has won numerous awards for her research, including the Companion of the Order of Canada and the 2016 Friesen International Prize in Health Research.

She is also president and scientific director of the Toronto-based Gairdner Foundation, which recognises outstanding biomedical research worldwide, and a professor at the University of Toronto's molecular genetics, obstetrics and gynaecology departments.

"Meetings like the Commonwealth Science Conference are a fantastic opportunity for scientists to come together, learn about each other's work and establish new relationships, which will help to push science forward, including in stem cell research," she said.

She noted: "The world of science is becoming increasingly interdisciplinary, so this kind of meeting of minds across nations, cultures and scientific fields is really the way of the future."

Explore further: Cardiac stem cells from heart disease patients may be harmful

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Stem cells: the future of medicine - Medical Xpress

Skin Stem Cells Comments Off on Stem cells: the future of medicine – Medical Xpress | June 23rd, 2017

11:59 Thursday 22 June 2017

A cancer survivor and transplant athlete from Warwick has issued a fresh plea for people to sign up to be an organ donor as he heads off to Malaga for the World Transplant Games.

Simon Perkin was diagnosed with blood cancer in 1991 at the age of 26 and after years of treatment and his deteriorating health, was left with no alternative but to have a bone marrow transplant in July 2012, when a donor match was found.

Since the operation, Simons health has steadily improved.

A major part of his recovery has been keeping himself in the best possible shape, which included taking part in the London Marathon just 18 months after his transplant.

In July 2016 Simon took part in the British Transplant Games in Liverpool, which is a qualifier for the World Transplant Games, where he won four gold medals.

Simon was selected for Team GB at this years World Transplant Games, and is part of the countrys largest ever team at the event, with 200 transplant athletes, including 20 juniors, 10 live donors, and 200-plus supporters.

The Games take place every two years, this year starting on the 25 June, and are supported by the International Olympic Committee.

They represent the largest organ donor awareness event in the world, featuring a week of 17 sporting events, 1000 transplant athletes, from 60 countries across the globe.

All of Team GBs athletes have survived either a heart, lung, kidney, pancreas, liver, small bowel or bone marrow transplant.

Simon has now launched a fresh plea to get more people to sign up to the Organ Donation Register.

He said: Every twenty minutes someone in the UK finds out they have a blood cancer.

Around 2,000 people in the UK are in need of a bone marrow or stem cell transplant every year. Like me, this is usually their last chance of survival

I was diagnosed with blood cancer in 1991 at the age of 26 and after years of treatment and deteriorating health, my only option was a bone marrow transplant. I was lucky as the Anthony Nolan Trust found a donor match in July 2012, and so my recovery began.

As training for the World Transplant Games enters its final phase, its a reminder of how far I have come and all I have achieved. It makes me feel so proud to be alive and representing Team GB at the Games.

To cover his own costs of getting to the World Transplant Games and raise money for Transplant Sport UK, Simon has launched a fundraising campaign that has so far, raised 2,030 of his of 2,500 target.

Warwickshire law firm Lodders has already donated 600 to Simons fundraising, making it his largest supporter to date.

Lynne Holt, Team GB Manager added: In spite of the constant training, fitting in work, school, exams, and hospital clinic appointments, these athletes receive no government support, and have to raise the funding themselves.

Sadly, many could not accept their place on the team, because of the heavy financial burden.

The team are supported by management, coaches, captains and a medical/physio team, all who are volunteers and are also self-financing.

Their motivation to be Fit for Life, the opportunity to represent their country, celebrate life and pay tribute to their donors who gave them life, is the goal.

These athletes certainly deserve the same recognition as the recent Olympic and Para Olympic Games. Not only are they ambassadors for our country, but they are also representing the charity, Transplant Sport, and hope to raise awareness here in the UK and globally, of the need for more people to sign on to the Organ Donor Register and discuss their wishes with their family and friends.

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Warwick man's plea for more organ donors as he heads to World Transplant Games - Warwick Courier

Bone Marrow Stem Cells Comments Off on Warwick man’s plea for more organ donors as he heads to World Transplant Games – Warwick Courier | June 22nd, 2017

Matthew Medinas doctors diagnosed him with a rare blood disease a few months ago and told him he would probably die without a bone marrow transplant.

With that prognosis came another: The 40-year-old Los Angeles police officer had a less than 50% chance of finding a donor because he is not white.

Most successful matches for bone marrow transplants involve a donor and patient of the same ethnicity. But the majority of the 25 million registered donors nationwide are white, and Medina is Filipino. So far, no match has been found.

Youre basically looking for a genetic twin, said Athena Mari Asklipiadis, who runs Mixed Marrow, an L.A.-based organization that is trying to increase diversity in the bone marrow donor registry. Its not like we have more of a chance we would get a disease, or that were harder to match, its just that theres not representation in the national registry.

Its a familiar problem for any nonwhite person who has needed a bone marrow transplant.

A white American of European descent has a 75% chance of finding a perfect match in the national donor registry, compared with a 40% chance for Filipinos. Few Filipinos in the U.S. have signed up as potential donors, and there is no registry in the Philippines.

Researchers are experimenting with ways to perform bone marrow transplants on people who cant find matches. But while those treatments are being perfected, thousands of people are diagnosed every year with leukemia, lymphomas and other blood diseases whose only hope for a cure is a marrow transplant. And for them, it can come down to ethnicity.

Medinas wife, Angelee, has watched dozens of people at sign-up events across Southern California, particularly in the Filipino community, volunteer to donate bone marrow with the hope of curing her husband. Were very thankful for that, she said. Were hoping something comes up.

For now, Medina is being kept alive with transfusions.

All you want is for that loved one to have a chance, said Officer Dante Pagulayan, Medinas partner at the LAPD and a childhood friend. Thats what were praying for.

Medina went to the doctor in March because he had a rash. His blood work revealed something far more dangerous.

Medina was diagnosed with aplastic anemia, a disease in which the bone marrow stops working. Bone marrow is spongy material inside bones that produces the essential components of blood white blood cells, red blood cells and platelets.

Between 600 and 900 Americans are diagnosed with aplastic anemia each year, according to the Aplastic Anemia and MDS International Foundation. The disease can be caused by exposure to toxic chemicals or a virus, but most cases, including Medinas, are unexplained.

One day he wakes up and the doctor tells him he has this. It could happen to anyone, said Pagulayan, who went to high school and Cal State Long Beach with Medina and now works alongside him in the gang unit in the LAPDs Harbor Division.

Blood transfusions can sustain Medina for now, but the only possible cure for aplastic anemia is a transplant, said Dr. Len Farol, a bone marrow transplant specialist at City of Hope National Medical Center and one of Medinas physicians.

Medina is quarantined at his home in Bellflower, where he lives with his wife and two young daughters. But he needs a transplant soon because his immune system is so weakened from his disease that exposure to a common virus could kill him, Farol said.

Doctors checked to see if Medinas sister could be a match, but she wasnt siblings provide a match only about 25% of the time. They started combing through the registry, but trying to find a donor there can be like finding a needle in a haystack, Farol said.

Doctors look to see if the patient and potential donor share eight cell markers called human leukocyte antigens, or HLA. All eight have to match, but thats rare because there are thousands of possibilities for each marker, experts say.

There could be billions of combinations, said Stephen Spellman, director of immunobiology and observational research for the Center for International Blood and Marrow Transplant Research. Within any group, finding a match for HLA is difficult.

Spellman said that people whose ancestors are from the same place tend to have the same markers because they evolved over time in response to different pathogens and diseases that were present in their environment.

According to a 2014 report in the New England Journal of Medicine, a person of white European descent has the highest chance of finding a perfect match eight out of eight HLA markers in the national registry of any ethnic group.

What's your chance of finding a perfect match? If you're...

Source: HLA Match Likelihoods for Hematopoietic Stem-Cell Grafts in the U.S. Registry, New England Journal of Medicine, 2014

Pagulayan, who is also Filipino, said neither he nor Medina knew ethnicity would affect his chances of being cured. Finding out that less than 1% of people in the registry were Filipino was very disheartening, he said.

There are international registries, but the vast majority of people worldwide whove signed up to donate bone marrow are from the U.S and Europe.

Plus, nonwhite populations in general tend to have more genetic diversity. African Americans, for example, have highly diverse genetics because of mixing with other groups since arriving in the United States, experts say. Filipinos are also very diverse because of the countrys long history of colonization.

Still, experts say that everyone who wants to help Medina should sign up for the registry, regardless of ethnicity.

Matches often break down along ethnic lines, but not always. Sometimes markers in one population also appear in another, or people dont know their lineage.

Maya Chamberlin, who is half Indian and half white, had two bone marrow transplants after she was diagnosed with a rare blood disease called HLH in 2009 when she was 4.

Mayas first donor was half Japanese and half Latino, and her second was half Japanese and half Filipino.

So you never know how this works until you get on the registry, said her mother, Mina Chamberlin, who lived in Torrance when Maya was diagnosed but has since relocated to Cincinnati to be closer to physicians who specialize in her daughters disease. You just never know.

Angelee Medina canceled her familys vacation to Mexico scheduled for this summer. Shed been commuting to a job as a graphic designer 20 miles from home when Matt was diagnosed, but found a closer place to work so she could take care of the kids and be near her husband.

It was very, very overwhelming in the beginning, she said. With all the support were getting from everyone around us, it feels hopeful.

More than 1,000 people have signed up to donate bone marrow over the past few months through dozens of drives for Medina, said Chris Chen, a recruitment coordinator for Little Tokyo-based nonprofit A3M, which focuses on getting more Asians to sign up for the Be the Match registry to donate bone marrow.

Potential donors submit cell samples by having the inside of their cheek swabbed. The cells are then analyzed to determine their HLA markers.

About 70% of transplants employ a process called peripheral blood stem cell donation, which is similar to a blood donation but can take several hours. In the other 30% of cases, donors are admitted to the hospital and anesthetized so doctors can remove marrow from their pelvic bone with a needle.

Ayumi Nagata, recruitment manager for A3M, knows that asking people to volunteer for a medical procedure they dont need themselves can be a hard sell. But she tries to impress upon them how they could be the cure for someones cancer or other disease and save their life.

How often do we have that kind of opportunity? Nagata said.

The Medinas 8-year-old daughter, Cassiah, made a sticker thats distributed at donor drives that says, Keep calm and help our daddy fight! When Angelee picked up Cassiah from day care recently, she found out that her daughter had been asking the other kids parents: Did you get swabbed? Have you gotten swabbed yet?

Doctors are testing ways to perform transplants on patients who cant find a bone marrow match. Some are using umbilical cord blood, donated by mothers whove just given birth, which scientists say has a lower chance of rejection even if its not a complete match.

Haploidentical transplants, in which the donor and patient share only half of the eight markers, have also been successful in clinical trials, Spellman said.

Medinas doctors think his best shot is still a perfect match for a bone marrow transplant, his wife said.

Thats just what were waiting for, she said. I remind him one day soon, hopefully everything will be better.

What to know about joining the bone marrow registry

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An LAPD officer needs a bone marrow transplant. His ethnicity limits his chances of getting one - Los Angeles Times

Bone Marrow Stem Cells Comments Off on An LAPD officer needs a bone marrow transplant. His ethnicity limits his chances of getting one – Los Angeles Times | June 22nd, 2017

When Will We Clone a Human?

Human cloning may endure as one of the go-to science fiction tropes, but in reality we may be much closer to achieving it than our fictional heroes might imply. At least in terms of the science required. On of the most prominent hurdles facing us may have less to do with the process and more to do with its potential consequences, and our collective struggle to reconcile the ethics involved.That being said, while science has come a long way in the last century when it comes to cloning a menagerie of animals, cloning humans and other primates has actually proven to be incredibly difficult. While we might not be on the brink ofcloning entire human beings, were already capable of cloning human cells the question is,should we be?Click to View Full Infographic

The astoundingly complex concept of cloning boils down to a fairly simple (in theory, at least) practice:you need two cells from the same animal one of which is an egg cell from which youve removed the DNA. You take the DNA from the othersomatic cell and put it inside the devoid-of-DNA egg cell. Whatever that egg cell goes on to produce for offspring will be genetically identical to the parent cell.While human reproduction is the result of the joining of two cells (one from each parent, each with their own DNA) the cellular photocopy technique does occur in nature.Bacteria reproduce through binary fission: each time it divides, its DNA is divided too so that each new bacterium is genetically identical to its predecessor. Except sometimes mutations occur in this process and in fact, that can be by design and function as a survival mechanism. Such mutations allow bacteria to, for example, become resistant to antibiotics bent on destroying them. On the other hand,some mutations are fatal to an organism or preclude them coming into existence at all. And while it might seem like the picking-and-choosing thats inherent to cloning could sidestep these potential genetic hiccups, scientists have found thats not necessarily the case.

Image Credit: Pixabay

While Dolly the sheep might be the most famous mammal science has ever cloned, shes by no means the only one: scientists have cloned mice, cats, and several types of livestock in addition to sheep. The cloning of cows has, in recent years, provided a great deal of knowledge to scientists about why the processdoesnt work: everything from implantation failure to those aforementioned mutations that render offspring unable to survive.Harris Lewin, professor in the UC Davis Department of Evolution and Ecology, and his team published their findings on the impact cloning has ongene expression in the journalProceedings of the National Academy of Sciencesback in 2016. In the studys press release Lewin noted that the findings were certainly invaluable to refining cloning techniques in mammals, but that their discoveries also reinforce the need for a strict ban on human cloning for any purposes.

The creation ofentiremammals via reproductive cloning has proven a difficult process both practically and ethnically, as legal scholar and ethicist Hank Greely of Stanford University explained toBusiness Insiderin 2016:

The cloning of human cells,however, may be a far more immediate application for humans.Researchers call it therapeutic cloning, and differentiate it from traditional cloning that has reproductive intent. In 2014, researchers created human stem cells through the same cloning technique that generated Dolly the sheep. Because stem cells can differentiate to become any kind of cell in the body, they could be utilized for a wide variety of purposes when it comes to treating diseases particularly genetic diseases, or diseases where a patient would require a transplant from an often elusive perfect match donor.This potential application is already well underway: earlier this year a woman in Japansuffering from age-related macular degeneration was treated with induced pluripotent stem (iPS) cells created from her own skin cells, which were then implanted into her retinas andstopped her vision from degenerating further.

We asked the Futurism community to predict when they think well be able to successfully clone a full human, and the majority of those who responded agree that it feels like were getting close: nearly 30 percent predicted well clone our first human by the 2020s. We have replaced, and replicated almost every biology on earth, said reader Alicja Laskowska, [the] next step is for cures and to do that you need clean DNA, and theres your start.

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How Close Are We to Successfully Cloning the First Human? - Futurism

Skin Stem Cells Comments Off on How Close Are We to Successfully Cloning the First Human? – Futurism | June 22nd, 2017

Founded in 2004, LifeCcell has technological collaboration with the US-based Cryo-Cell Internationalthe worlds first private stem cell bank with over 25 years of experience. (PTI)

Chennai-based LifeCell, the provider of preventive healthcare services for family wellness, is the worlds second-largest provider of umbilical cord stem cells. Founded in 2004, the company has technological collaboration with the US-based Cryo-Cell Internationalthe worlds first private stem cell bank with over 25 years of experience. As many as 2 lakh Indian parents have chosen to trust their newborns umbilical cords to LifeCell through its umbilical cord banking service BabyCord. The company has a 60% share in the Indian market.Stem cells are mother cells that have the potential to become any type of cell in the body. One of the main characteristics of stem cells is their ability to self-renew or multiply, while maintaining the potential to develop into other types of cells. These cells can repair and rebuild damaged tissue. The uses of stem cells are still being researched. In fact, stem cell tissues have proved effective in cancer treatment too. The applications have been steadily increasing in the last few years. They have been used for treating wound healing, including diabetic foot ulcers. In a country where concepts like bone marrow donations and stem cell banking are still not widely known, Mayur Abhaya, the CEO and managing director of the company, is betting on these treatments of the future.

The company is the most accredited stem cell bank in the country, with certifications from national and international organisations for standards. It is also the only player in the industry providing comprehensive stem cell solutions, including menstrual stem cell banking, R&D and point-of-care stem cell therapy for orthopaedic and vascular specialities.Mayur has been heading LifeCell since 2008. He comes from the family that set up Shasun Group of companiesthe provider of contract pharmaceutical manufacturing services for global companies. Mayur studied biotechnology in India and the US, and then worked in the US for a year. Before moving to LifeCell, he worked for many years at Shasun Pharmaceuticals, where he led their new product development, intellectual property and licensing initiatives. In 2013, LifeCell International got an investment of Rs35 crore from Helion Venture Partners, an India-focused venture fund, to support its plans of increasing market penetration of stem cell banking in India and enabling the development of novel cell-based therapies.

Also Watch: Mayur says LifeCell currently operates in 150 cities, employing more than 1,500 people. We have given an opportunity to our sales people to become their own bosses. They remain on company rolls and get to enjoy all the company benefit plans, such as insurance and welfare schemes. They grow with the company and also have the opportunity to explore and add non-conflicting products or services to their distribution network and enhance their earnings. These internal franchisees bring 50% of our revenue and it is growing. More than 50 such entrepreneurs have been created.LifeCell recently bought over the stake held by Helion Ventures with borrowings from family-owned firms. Three months ago, it changed its business model. We are introducing an on-demand model for sharing cord blood cells, Mayur says. Parents can let the company know if their babies cord blood cells can be used for other needy patients. Cancer patients cannot be treated with their own stem cells. Patients usually do not have much time. Cord cells can be used even if all the six parameters that are required to transplant tissues do not match. By letting their stem cells be used by others, parents and their children get access to cord blood cellsof the entire cord blood cell bankwhen they are in need. So far, stem cells were banked only for the baby from whom these were removed.

Our inventory will come to the aid of people who do not have babies. We will refund the amount paid for having their babys stem cell stored. The processing fee is Rs17,000 and the storage fee each year is Rs4,000. Mayur says that the worlds largest birthing country has a long way to go to create a viable stem cell bank. We are going to follow the blood bank model and hope to bank 2,50,000 cords, which is the critical amount, he adds. We hope to contribute significantly to the ever-developing scope of transplant medicine. Currently, India is importing cord cells, which are prohibitively expensive. With scale, prices will come down in the country. Parents in India will have higher future access to stem cells than even those enjoyed by patients in advanced countries such as the US. We will have a linkage with global inventory. Earlier this month, LifeCell was invited by AABB (formerly American Association of Blood Banks) to present the concept of Community Stem Cell Banking at the 15th International Cord Blood Symposium held in San Diego, US. In 15 years, it is the only second stem cell bank to present its innovation at such a prestigious global platform.

With a turnover of Rs126 crore, LifeCell is operationally profitable. It has enough cash to run its business, but is yet to make net profits. However, Mayur believes very soon LifeCell will turn profitable, and that this year the number of stem cells brought into the labs will be higher by at least 30%. Mayur has extended LifeCells services to introduce and popularise the concept of essential preventive diagnostics for mothers and babies. BabyShield has been introduced to bring down infant mortality ratio. Addressing gaps in marketplace and with innovative business models, it has established market leadership in newborn screening. It has also acquired a prenatal screening service provider. In India, only 2% babies go through prenatal and newborn screening. Nobody has focused on this. We will also be providing diagnostic medication. Doing this can prevent so many false positives. We are building all this together as a package and are offering it at an affordable price, he says.

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How LifeCell became the most accredited stem cell bank in India - Financial Express

Bone Marrow Stem Cells Comments Off on How LifeCell became the most accredited stem cell bank in India – Financial Express | June 21st, 2017

Start eating grapes daily, as a research has revealed that the compounds, found in the skin and seeds of grapes, may help in killing colon cancer stem cells. The compounds, resveratrol, which are found in grape skins and seeds, could also eventually lead to treatments to help prevent colon cancer, said Jairam K.P. Vanamala from Penn State Hershey Cancer Institute.

The combination of resveratrol and grape seed extract is very effective at killing colon cancer cells, Vanamala added. The researchers suggest that the findings could pave the way for clinical testing of the compounds on human colon cancer, which is the second most common cancer in women and the third in men.

If successful, the compounds could then be used in a pill to help prevent colon cancer and lessen the recurrence of the disease in colon cancer survivors.

Vanamala noted that according to cancer stem-cell theory, cancerous tumors are driven by cancer stem cells. Cancer stem cells are capable of self-renewal, cellular differentiation and maintain their stem cell-like characteristics even after invasion and metastasis.

When taken separately in low doses, resveratrol and grape seed extract are not as effective against cancer stem-cell suppression as when they are combined together, according to the researchers.

Grape compounds could now be used in a pill to help prevent colon cancer and lessen the recurrence of the disease in survivors. (HTFile photo )

This also connects well with a plant-based diet that is structured so that the person is getting a little bit of different types of plants, of different parts of the plant and different colors of the plant, said Vanamala.

For the animal study, they separated 52 mice with colon cancer tumors into three groups, including a control group and groups that were fed either the grape compounds or sulindac, an anti-inflammatory drug, which was chosen because a previous study showed it significantly reduced the number of tumors in humans.

The incidence of tumors was suppressed in the mice consuming the grape compounds alone by 50 percent, similar to the rate in the group consuming the diet with sulindac.

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Grape skin and seeds may help fight against colon cancer, says study - Hindustan Times

Skin Stem Cells Comments Off on Grape skin and seeds may help fight against colon cancer, says study – Hindustan Times | June 21st, 2017

Contemporary Examples

Infections can strike joints, airways, the lungs, the brain and the tissues lining the spinal cord, or the bloodstream.

Other spinal cord regeneration efforts involve using stem cells to regrow damaged or lost neurons.

As a result, Smith lost his right arm underneath the elbow and parts of his leg, hip and spinal cord.

Generally, a human will only be infected if they eat the nerve tissuebrains or spinal cordof an infected animal.

The bulleta live fire bulletexited through his back but not before severing his spinal cord.

British Dictionary definitions for spinal cord Expand

the thick cord of nerve tissue within the spinal canal, which in man gives rise to 31 pairs of spinal nerves, and together with the brain forms the central nervous system

spinal cord in Medicine Expand

spinal cord n. The thick, whitish cord of nerve tissue that extends from the medulla oblongata down through the spinal column and from which the spinal nerves branch off to various parts of the body. Also called spinal marrow.

spinal cord in Science Expand

The long, cordlike part of the central nervous system that is enclosed within the vertebral column (spine) and descends from the base of the brain, with which it is continuous. The spinal cord branches to form the nerves that convey motor and sensory impulses to and from the tissues of the body.

spinal cord in Culture Expand

The thick column of nerve tissue that extends from the base of the brain about two thirds of the way down the backbone. As part of the central nervous system, the spinal cord carries impulses back and forth between the brain and other parts of the body through a network of nerves that extend out from it like branches.

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Spinal cord | Define Spinal cord at Dictionary.com

Spinal Cord Stem Cells Comments Off on Spinal cord | Define Spinal cord at Dictionary.com | June 19th, 2017

17 Jun 2017

Animal models and engineered cells have contributed their fair share of insight into the pathogenesis of amyotrophic lateral sclerosis (ALS), but researchers do not often have the opportunity to peer into afflicted human neurons. In a study published May 30 in Cell Reports, researchers led by Rickie Patani and Sonia Gandhi at University College London offer a new model for human disease by using motoneurons and astrocytes derived from amyotrophic lateral sclerosis (ALS) patient stemcells.

The researchers generated spinal motoneurons and astrocytes from induced pluripotent stem cells (iPSCs) of ALS patients carrying mutations in the valosin-containing protein (VCP) gene. VCP mutations account for 2 percent of familial ALS cases and have been linked to other disorders as well, including hereditary inclusion body myopathy with Paget disease of bone and frontotemporal dementia (IBMPFD), jointly termed multisystemproteinopathy.

Previously, researchers reported that VCP mutations promoted the formation of cytoplasmic aggregates of TDP-43,one of the hallmarks of motoneuron disease, and that these aggregates were at least partially responsible for the VCP-induced neurodegeneration seen in a fly model (Neumann et al., 2007; Ritson et al., 2010).

Few studies have tested what VCP mutations do to human neurons, however. Using an iPSC-derived neuronal model, Virginia Kimonis at the University of California, Irvine, found that the VCP R155H mutation boosted cells levels of TDP-43 and several proteins involved in protein disposal (Dec et al., 2014).

In search of a more complete view of how VCPs effects unfold over time, first co-authors Claire Hall, Zhi Yao, Minee Choi, and Giulia Tyzach used iPSC-derived populations of spinal cord motoneurons and astrocytes to track several cellular functions. The cells originated from two patients (four clones) with VCP mutations and three healthycontrols.

TDP-43 (red) stays in the nucleus (blue) in control motoneurons (left) but leaks into the cytoplasm in three-day old VCP-mutant motoneurons (right). [Cell Reports, Hall et al.,2017.]

More VCP-mutant motoneurons than controls died; they also made fewer synapses with their neighbors, and had less intense and fewer coordinated bursts of firing than controls. Monitoring the whereabouts of TDP-43, the authors found no difference between mutant and normal cells when the cells were at an early stage of differentiation, as neural precursor cells. But by the third day after becoming motoneuron-like, the mutant cells were leaking TDP-43 from their nuclei into the cytoplasm (see image above). At the same time, they had increased levels of markers of endoplasmic reticulum (ER) stress, became less able than controls to survive an ER stress assay, and began producing reactive oxygen species (ROS) at a higherrate.

By day 17, the mutant motoneurons had sickly ER tubules. Some were swollen, others cozied up to mitochondria, both signs of continued ER stress. The neurons also had low mitochondrial membrane potential and low glutathione levels, indicating mitochondrial dysfunction and oxidative stress,respectively.

Putting these findings together, Patani and Gandhi suggested that cyotosolic TDP-43 generates ER stress, which next triggers increased tethering of the ER to mitochondria. This could depolarize mitochondria, which could impair mitochondrial function and ultimately lead to high levels of free radical production and oxidative stress.The findings support a role for TDP-43 wreaking havoc in the cytoplasm, saidPatani.

The mechanism that links TDP-43 and ER stress remains uncertain, said Kimonis. Patani and Gandhi acknowledge the link is probably complex, noting that, in addition to cyotplasmic TDP-43 aggregates inducing ER stress, ER stress itself seems to drive TDP-43 leakage (Walker et al., 2013).

The researchers then probed how mutant VCP might affect astrocytes. Studies of astrocytes in other ALS models have yielded varying results depending on the mutation. Superoxide dismutase 1 (SOD1) mutations, for example, can turn astrocytes into motoneuron killers (see Oct 2011 news),but it is unclear if they endanger the survival of the astrocytes themselves. Conversely, mutations in TDP-43 seem to sicken astrocytes without making them toxic to neighboring neurons (Serio et al., 2013).

On the left, healthy astrocytes (red) protect VCP-mutant motoneurons (yellow) from death (green). VCP-mutant astrocytes are much less protective (right). [Courtesy of ZhiYao.]

Interestingly, Patani and Gandhi found that VCP mutations had both cell-autonomous and non-cell-autonomous effects. They increased astrocytes risk of death and rendered them less able to support the survival of both control and VCP-mutant motoneurons (see image at right). The authors also found that the cell-autonomous effects on astrocytes differed from those in motoneurons. VCP-mutant astrocytes seemed more resistant when challenged with an ER stressor and had only a transient drop in mitochondrial membrane potential and a transient increase in ROS, with no change in glutathionelevels.

The study is a validation of key prior findings using iPS-derived neurons and glia from patients, which is a nice advance, wrote Paul Taylor at St. Jude Childrens Research Hospital in Memphis, Tennessee. The characterization of the role of glia is also interesting and potentially important.

Looking ahead, Patani and Gandhi want to generate isogenic controls, that is, cells derived from the same patients but with repaired VCP mutations. They also want to create iPSC-derived upper motoneurons, and to better understand muscle pathology, Kimonis hopes to extend her investigation of iPSC-derived muscle cells (Llewellyn et al., 2017).

Other model systems will be of value, too. iPSC-derived models are not equivalent to the decades-old cells inhabiting an adult nervous system. A study of dopaminergic neurons, for example, revealed that gene expression and DNA methylation patterns differed between iPSC-derived neurons and their in vivo counterparts (Roessler et al., 2014).

In the long term, Patani hopes that shedding light on the sequence of events that marks motoneuron degeneration in human cells will enable researchers to more effectively search for ALS therapies.MarinaChicurel

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Familial ALS Linked to Both Neuron and Astrocyte Pathology - Alzforum

Spinal Cord Stem Cells Comments Off on Familial ALS Linked to Both Neuron and Astrocyte Pathology – Alzforum | June 18th, 2017

MUMBAI: Three-year-old Kinaya Shah was diagnosed with thalassemia at the tender age of three months and has been undergoing regular blood transfusions ever since. The only cure for thalassemia is a bone marrow transplant (BMT), a form of stem cell therapy. Typically, the donor of the stem cells would be a sibling of the patient such that the stem cells of the donor are a near perfect match to those of the patient. The only complication was that Kinaya was a lone child.

So, city doctors in a first used stem cells donated by Kinaya's father - who was only a half or haploidentical match - to cure the child of the blood disorder. "We went to Vellore, Bangalore and Pune but no one was willing to do the transplant without a full match donor," said Kinaya's parents, Aneri and Shripal Shah. They approached Dr Santanu Sen at the Kokilaben Dhirubhai Ambani Hospital, Andheri, in October of 2016, after reading about a similar surgery that he had performed.

While haploidentical bone marrow transplants are carried out to cure leukaemia, it has only been done about half a dozen times for thalassemia in a couple of Indian cities. ``Haploidentical transplants are gradually increasing because of better techniques,'' said Dr Sen.

Dr Sen has completed 36 BMTs in the last two years, of which 12 were haploidentical donors. ``But this is the first time that a haploidentical transplant has been done in western India to cure thalassemia,'' he said.

Chennai-based haematologist Dr Revathy Raja said that there is a 85% chance of cure in thalassemia with a fully matched donor. ``The success rate falls to 70% with a half-match or haploidentical donor. We have hence not started it at our Chennai centre. Hopefully, techniques will further improve in the coming years,'' she said.

In order to perform the surgery, Dr Sen conditioned Kinaya's immune system over three months, with slight chemotherapy, to increase the chances of her body accepting the graft. "We found that her father's stem cells were a 70% match through genetic tests and decided to use them for the transplant. In the case that the graft was rejected we froze a couple of Kinaya's stem cells as insurance. The positive is that children have lower rejection rates for foreign cells as they have barely developed any active immunity," said Dr Sen. "BMT is the most viable treatment to cure thalassemia, the only barrier thus far was the necessity of a full match donor," he added.

However, Vinay Shetty of NGO Think Foundation, which works for thalassemia patients, said that it would be prudent to wait for a statistically significant number of successful halploidentical transplants before recommending it to all patients.

Post the three months of conditioning, stem cells were collected from her father's bone marrow and the transplant was performed on May 10, 2017. After several tests to confirm that the graft was accepted, Kinaya was finally discharged from the hospital on June 13.

"The future of thalassemia treatment probably lies in gene therapy, but at the moment, haploidentical transplants have made BMT much more accessible," said Dr Sen, adding that he has two more cases such as Kinaya lined up. Kinaya is expected to be completely independent of medication and any trace of thalassemia in the coming six months.

What is Thalassemia?

Thalassemia is a genetic blood disorder when the body produces abnormal hemoglobin. Patients require regular blood transplant and well as dietary control to ensure that blood irons level stay suppressed.

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In a first, Mumbai doctors use dad's cells to fight blood disorder - Times of India

Bone Marrow Stem Cells Comments Off on In a first, Mumbai doctors use dad’s cells to fight blood disorder – Times of India | June 17th, 2017

Scientists have used artificial skin grafts grown from induced pluripotent stem cells to cover the developing spines of rat fetuses while still in the womb.

Asian Scientist Newsroom | June 14, 2017 | In the Lab

AsianScientist (Jun. 14, 2017) - Researchers from Japan have developed a stem cell-based therapy to treat a severe congenital bone defect known as myelomeningocele. Their findings have been published in Stem Cell Reports.

Myelomeningocele is the most serious and common form of spina bifida, a condition in which the backbone and spinal canal do not close before birth, leaving parts of the spinal cord and nerves exposed.

A baby born with this disorder typically has an open area or a fluid-filled sac on the mid to lower back. Most children with this condition are at risk of brain damage because too much fluid builds up in their brains. They also often experience symptoms such as loss of bladder or bowel control, loss of feeling in the legs or feet, and paralysis of the legs.

To develop a minimally invasive treatment to cover large myelomeningocele defects earlier during pregnancy, the researchers first generated artificial skin from human induced pluripotent stem cells (iPSCs), and then successfully transplanted the skin grafts into rat fetuses with the condition.

We provide preclinical proof of concept for a fetal therapy that could improve outcomes and prevent lifelong complications associated with myelomeningoceleone of the most severe birth defects, said senior study author Professor Akihiro Umezawa of Japan's National Research Institute for Child Health and Development.

Since our fetal cell treatment is minimally invasive, it has the potential to become a much-needed novel treatment for myelomeningocele.

The human iPSCs were generated from fetal cells taken from amniotic fluid from two pregnancies with severe fetal disease (Down syndrome and twin-twin transfusion syndrome). The researchers then used a chemical cocktail in a novel protocol to turn the iPSCs into skin cells and treated these cells with additional compounds such as epidermal growth factor to promote their growth into multi-layered skin.

In total, it took approximately 14 weeks from amniotic fluid preparation to 3D skin generation, which would allow for transplantation to be performed in humans during the therapeutic window of 28-29 weeks of gestation.

Next, the researchers transplanted the 3D skin grafts into 20 rat fetuses through a small incision in the uterine wall. The artificial skin partially covered the myelomeningocele defects in eight of the newborn rats and completely covered the defects in four of the newborn rats, protecting the spinal cord from direct exposure to harmful chemicals in the external environment.

Moreover, the engrafted 3D skin regenerated with the growth of the fetus and accelerated skin coverage throughout the pregnancy period. Notably, the transplanted skin cells did not lead to tumor formation, but the treatment significantly decreased birth weight and body length.

We are encouraged by our results and believe that our fetal stem cell therapy has great potential to become a novel treatment for myelomeningocele, Umezawa said. However, additional studies in larger animals are needed to demonstrate that our fetal stem cell therapy safely promotes long-term skin regeneration and neurological improvement.

The article can be found at: Kajiwara et al. (2017) Fetal Therapy Model of Myelomeningocele with Three-dimensional Skin Using Amniotic Fluid Cell-derived Induced Pluripotent Stem Cells.

Source: Cell Press; Photo: Kazuhiro Kajiwara. Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

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3D Artificial Skin Used To Treat Spina Bifida In Rats - Asian Scientist Magazine

IPS Cell Therapy Comments Off on 3D Artificial Skin Used To Treat Spina Bifida In Rats – Asian Scientist Magazine | June 14th, 2017

Keith Roach, To Your Health 6:38 p.m. ET June 13, 2017

Dear Dr. Roach: I hope you can answer some questions about myelodysplastic syndrome. What does it do to your body? Is there a known cause or cure? What is the prognosis?

P.B.

Dear P.B.: The myelodysplastic syndromes are a group of similar diseases, specific types of blood cancers, that prevent your bone marrow from working properly. They also can transform into acute leukemia. These are uncommon cancers, with perhaps 30,000 cases per year in the U.S. The specific myelodysplastic syndromes are now categorized by appearance, genetic abnormalities of the cells, and condition of the bone marrow.

MDS may arise from damage to DNA, such as from radiation or other toxic exposures. However, many cases have no known cause, and its likely that these are spontaneous mutations in the bone marrow cells.

Because MDS is a group of related diseases, the treatment and prognosis vary among the different subtypes. However, supporting the bone marrow with transfusions of red blood cells and platelets often is necessary. Medications to stimulate both red and white blood cell production can be used. A few people will be recommended for bone marrow (stem cell) transplant, but the decision to consider this treatment must be made cautiously, as many people who get MDS will not benefit from this treatment due to age or other medical conditions.

The prognosis depends on the age of the person affected and their specific MDS. A person younger than 60 with a low-risk MDS has a median survival (based on data published in 1997) of about 12 years. However, high-risk MDS has a much worse outcome: Half of people succumb within six months. Advances in treatment since these data were published have improved these results, but not as much as hoped.

Dear Dr. Roach: My 89-year-old mother suffers from fluttering in her heart. She saw an expert in cardiac arrhythmias, who diagnosed her with tachy-brady syndrome and sick sinus syndrome. A nurse also said she has PVCs. She is taking metoprolol, but still has episodes of fluttering.

What are these conditions? Are there other medications that she could take to correct this heart condition?

M.D.P.

Dear M.D.P.: Tachy-brady syndrome (from the Greek roots for fast and slow) and sick sinus syndrome are the same thing. The sinus in sick sinus syndrome refers to the sino-atrial node of the heart, which is the hearts natural pacemaker. It is where every beat normally starts. This part of the heart can become diseased, and the heart can beat too quickly (tachycardia) and, at other times, too slowly (bradycardia). Sick sinus syndrome can come from many different conditions and, rarely, from medications.

Medications are sometimes used for sick sinus syndrome. Beta blockers, like the metoprolol your mother is taking, are given to slow down the tachycardic component of sick sinus, but it can make the bradycardia worse. Most often, the treatment for sick sinus syndrome is a permanent pacemaker. Not everyone needs it, but Im sure your mothers cardiologist is monitoring her and will recommend a pacemaker if needed. If one is necessary, 89 years old is not too old to put in a pacemaker.

PVCs are very common and do not usually indicate disease in the heart, although they are more common in people with heart disease, especially poor blood flow to the heart. Premature ventricular contractions themselves seldom need treatment.

Email questions to ToYourGoodHealth@med.cornell.edu.

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Like I have consistently mentioned on many of my previous articles, the unlimited capacities of autologous stem cells and platelets never ceases to amaze me.

While at our StemCell Miami Institute (one of the few in the world) we specialize in treating orthopedic related illnesses like: osteoarthritis of the knee, hip, shoulder and issues related to the spine, there are times when we also try to help patients in need of treatments that are outside of the true realm of our medical specialty. Such is the case with Denisse, a close family friend and owner of a busy Nicaraguan restaurant in the city of Doral, where she unfortunately poured (by accident) a pot of hot oil all over the back of her legs, causing her a painful second degree type burn.

Two weeks ago, Denisse called us to see if we could do something to help her with her burn, since she had heard about the tremendous success of many of our stem cell procedures. While she was well aware that we specialized in orthopedic related problems, she hoped that we could help her to expedite the healing process, since the treatment that she initially received at the hospital emergency room (with sulfadiazine), had done little to improve her serious burn and she was also suffering from a severe pain in the affected area.

While this was theoretically in no way our specialty, we knew that cells have a great capacity to heal skin related issues. In addition, platelets have shown tremendous success in accelerating the scarring/curative process in healing wounds, ulcers and also burns. As a matter of fact, I treated a paralytic patient several years ago who was living in a nursing home in order to try and help with an ulcer she had developed in her leg and amazingly, her ulcer/wound completely healed in only one month after the treatment we conducted on her!

So after we discussed the recommended treatment with Denisse and she agreed to move forward with our procedure we created a gelatin like substance from her own plasma and combined it with growth factors (also from her same blood). We then covered the wounded skin area (about the size of a basketball behind her knees) and we initially planned to cover her wound with this gelatin substance every 72 hours.

On the second treatment, we were truly astonished on how well the wound/burn had healed (almost 50 percent improvement) and Denisse mentioned that ever since the first application her pain had subsided tremendously. By the third treatment, we were stunned by how her wound had healed almost 100 percent and we consequently decided to stop the treatment altogether, since her burn had basically already disappeared.

This is another classic example of the unlimited power of Regenerative Medicine. In this particular case, being successful at healing a severe second degree type burn by using the patients own PRP (Platelet Rich Plasma). Consequently, this type of treatment should be considered/implemented at hospital ERs and burn centers around the globe. Note that we would love the opportunity to teach doctors and nurses, hopefully in the future, this innovative treatment/technique, so they can in turn help other patients, just like we helped our friend Denisse. Furthermore, we are very happy to report that Denisse has been able to return to work at her busy restaurant and her burn has almost completely diminished!

So if you, a friend or any family members are interested in receiving one of these innovative stem cell or PRP procedures, please call us at 305-598-7777. For more information, please visit our website: http://www.stemcellmia.com(available in both English & Spanish) and you can also follow us on Facebook, Twitter and on our YouTube channel. Dr. Castellanos would be happy to address any of your specific questions or concerns via his email: stemdoc305@gmail.com.

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Using Stem Cells to Heal Burns - Miami's Community Newspapers

Skin Stem Cells Comments Off on Using Stem Cells to Heal Burns – Miami’s Community Newspapers | June 11th, 2017

Dr Su Metcalfe is sitting quietly reading through some documents in the lobby of the Judge Business School when I arrive for our interview. It would be easy to walk right past her and not know you were in the presence of a woman who could be on the verge of curing multiple sclerosis.

MS, an auto-immune condition which affects 2.3 million people around the world, attacks cells in the brain and the spinal cord, causing an array of physical and mental side effects including blindness and muscle weakness. At the moment theres no cure, but Su and her company, LIFNano, hope to change that.

Some people get progressive MS, so go straight to the severe form of the disease, but the majority have a relapsing or remitting version, she says.

It can start from the age of 30, and theres no cure, so all you can do is suppress the immune response, but the drugs that do that have side effects, and you cant repair the brain. The cost of those drugs is very high, and in the UK there are a lot of people who dont get treated at all.

But now a solution could be in sight thanks to Su, who has married one of the bodys cleverest functions with some cutting-edge technology. The natural side of the equation is provided by a stem cell particle called a LIF.

Su was working at the universitys department of surgery when she made her big breakthrough: I was looking to see what controls the immune response and stops it auto-attacking us, she explains.

I discovered a small binary switch, controlled by a LIF, which regulates inside the immune cell itself. LIF is able to control the cell to ensure it doesnt attack your own body but then releases the attack when needed.

That LIF, in addition to regulating and protecting us against attack, also plays a major role in keeping the brain and spinal cord healthy. In fact it plays a major role in tissue repair generally, turning on stem cells that are naturally occurring in the body, making it a natural regenerative medicine, but also plays a big part in repairing the brain when its been damaged.

So I thought, this is fantastic. We can treat auto-immune disease, and weve got something to treat MS, which attacks both the brain and the spinal cord. So you have a double whammy that can stop and reverse the auto-immunity, and also repair the damage caused in the brain.

Presumably Su, who has been in Cambridge since she was an undergraduate but retains a soft accent from her native Yorkshire, was dancing a jig of delight around her lab at this point, but she soon hit a snag; the LIF could only survive outside the cell for 20 minutes before being broken down by the body, meaning there was not enough time to deploy it in a therapy. And this is where the technology, in the form of nano-particles, comes in.

They are made from the same material as soluble stitches, so theyre compatible with the body and they slowly dissolve, says Su.

We load the cargo of the LIF into those particles, which become the delivery device that slowly dissolve and deliver the LIF over five days. The nano-particle itself is a protective environment, and the enzymes that break it down cant access it. You can also decorate the surface of the particles with antibodies, so it becomes a homing device that can target specific parts of the brain, for example. So you get the right dose, in the right place, and at the right time.

The particles themselves were developed at Yale University, which is listed as co-inventor with Su on the IP. But LIFNano has the worldwide licence to deploy them, and Su believes we are on the verge of a step-change in medicine.

She says: Nano-medicine is a new era, and big pharma has already entered this space to deliver drugs while trying to avoid the side effects. The quantum leap is to actually go into biologics and tap into the natural pathways of the body.

Were not using any drugs, were simply switching on the bodys own systems of self-tolerance and repair. There arent any side effects because all were doing is tipping the balance. Auto-immunity happens when that balance has gone awry slightly, and we simply reset that. Once youve done that, it becomes self-sustaining and you dont have to keep giving therapy, because the body has its balance back.

LIFNano has already attracted two major funding awards, from drug firm Merck and the Governments Innovate UK agency. Su herself is something of a novice when it comes to business, but has recruited cannily in the form of chairman Florian Kemmerich and ceo Oliver Jarry, both experienced operators in the pharma sector. With the support of the Judge, the company hopes to attract more investment, with the aim of starting clinical trials in 2020.

The 2020 date is ambitious, but with the funding weve got and the funding were hoping to raise, it should be possible, says Su.

Weve got everything we need in place to make the nano-particles in a clinically compliant manner, its just a case of flicking the switch when we have the money. Were looking at VCs and big pharma, because they have a strong interest in this area. Were doing all our pre-clinical work concurrently while bringing in the major funds the company needs to go forward in its own right.

Immune cells have been a big part of Sus career, and as we talk, her passion for her subject is obvious. I wanted to understand something that was so simple on one level but also so complex, she says.

The immune cell is the only single cell in the body that is its own unity, so it functions alone. Its probably one the most powerful cells in the body because it can kill you, and if you havent got it you die because you havent got it.

And MS may just be the start for LIFNano.

MS is our key driver at the moment, but its going to be leading through to other major auto-immune disease areas, Su adds.

Psoriasis is high up on our list, and diabetes is another. Downstream there are all the dementias, because a LIF is a major health factor for the brain. So if we can get it into the brain we can start protecting against dementia.

Now that would be something.

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Meet the Cambridge scientist on verge of curing Multiple Sclerosis - Cambridge News

Spinal Cord Stem Cells Comments Off on Meet the Cambridge scientist on verge of curing Multiple Sclerosis – Cambridge News | June 4th, 2017