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Want to live longer? Forever Labs wants to help, using your stem cells Digital Trends Using a patented device, Forever Labs collects stem cells from your blood marrow, which the team calls a wellspring for stem cells that replenish your blood, bone, immune system, and other vital tissues. The whole process is said to take around 15 ...

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Want to live longer? Forever Labs wants to help, using your stem cells - Digital Trends

The study suggests it may encourage blood cancer stem cells to die.

Researchers say Vitamin C may "tell" faulty stem cells in the bone marrow to mature and die normally, instead of multiplying to cause blood cancers.

They explained that certain genetic changes are known to reduce the ability of an enzyme called TET2 to encourage stem cells to become mature blood cells, which eventually die, in many patients with certain kinds of leukaemia.

The new study, published online by the journal Cell. found that vitamin C activated TET2 function in mice engineered to be deficient in the enzyme.

Study corresponding author Professor Benjamin Neel, of the Perlmutter Cancer Centre in the United States, said: "We're excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases caused by TET2-deficient leukemia stem cells, most likely in combination with other targeted therapies."

He said changes in the genetic code that reduce TET2 function are found in 10 per cent of patients with acute myeloid leukaemia (AML), 30 per cent of those with a form of pre-leukaemia called myelodysplastic syndrome, and in nearly 50 per cent of patients with chronic myelomonocytic leukaemia.

Such cancers cause anaemia, infection risk, and bleeding as abnormal stem cells multiply in the bone marrow until they interfere with blood cell production, with the number of cases increasing as the population ages.

Prof Neel said the study results revolve around the relationship between TET2 and cytosine, one of the four nucleic acid "letters" that comprise the DNA code in genes.

To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the researchers genetically engineered mice such that the scientists could switch the TET2 gene on or off.

Similar to the naturally occurring effects of TET2 mutations in mice or humans, using molecular biology techniques to turn off TET2 in mice caused abnormal stem cell behaviour.

Prof Neel said, remarkably, the changes were reversed when TET2 expression was restored by a genetic trick.

Previous work had shown that vitamin C could stimulate the activity of TET2 and its relatives TET1 and TET3.

Because only one of the two copies of the TET2 gene in each stem cell is usually affected in TET2-mutant blood diseases, the researchers hypothesised that high doses of vitamin C, which can only be given intravenously, might reverse the effects of TET2 deficiency by turning up the action of the remaining functional gene.

They found that vitamin C did the same thing as restoring TET2 function genetically.

By promoting DNA demethylation, high-dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukaemia cancer stem cells from human patients implanted in mice.

Study first author Doctor Luisa Cimmino, of New York University Langone Health, said: "Interestingly, we also found that vitamin C treatment had an effect on leukaemic stem cells that resembled damage to their DNA.

"For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer."

The researchers found that the combination had an enhanced effect on leukaemia stem cells, further shifting them from self-renewal back toward maturity and cell death.

Dr Cimmino said the results also suggest that vitamin C might drive leukaemic stem cells without TET2 mutations toward death, given that it turns up any TET2 activity normally in place.

Corresponding author Professor Iannis Aifantis, also of NYU Langone Health, added: "Our team is working to systematically identify genetic changes that contribute to risk for leukaemia in significant groups of patients.

"This study adds the targeting of abnormal TET2-driven DNA demethylation to our list of potential new treatment approaches."

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Blood cancer: High doses of vitamin C could encourage stem cells ... - Express.co.uk

WASHINGTON D.C: Good news! A study has recently revealed that vitamin C may tell faulty stem cells in the bone marrow to mature and die normally, instead of multiplying to cause blood cancers.

According to researchers, certain genetic changes are known to reduce the ability of an enzyme called TET2 to encourage stem cells to become mature blood cells, which eventually die, in many patients with certain kinds of leukemia.

The new study found that vitamin C activated TET2 function in mice engineered to be deficient in the enzyme.

Corresponding study author Benjamin G. Neel said, "We're excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases caused by TET2-deficient leukemia stem cells, most likely in combination with other targeted therapies."

The results suggested that changes in the genetic code (mutations) that reduce TET2 function are found in 10 percent of patients with acute myeloid leukemia (AML), 30 percent of those with a form of pre-leukemia called myelodysplastic syndrome, and in nearly 50 percent of patients with chronic myelomonocytic leukemia.

The study results revolve around the relationship between TET2 and cytosine, one of the four nucleic acid "letters" that comprise the DNA code in genes.

To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the team genetically engineered mice such that the scientists could switch the TET2 gene on or off.

The findings indicated that vitamin C did the same thing as restoring TET2 function genetically. By promoting DNA demethylation, high-dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukemia cancer stem cells from human patients implanted in mice.

"Interestingly, we also found that vitamin C treatment had an effect on leukemic stem cells that resembled damage to their DNA," said first study author Luisa Cimmino.

"For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer," Cimmino added.

The findings appear in journal Cell.

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Vitamin C could help genes kill blood cancer stem cells - Economic Times

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Bone Marrow Transplant gives local cancer patient more time with his family - KTBS

Scientists recently used a gene-editing tool to fix a mutation in a human embryo. Around the world, researchers are chasing cures for other genetic diseases.

Now that the gene-editing genie is out of the bottle, what would you wish for first?

Babies with perfect eyes, over-the-top intelligence, and a touch of movie star charisma?

Or a world free of disease not just for your family, but for every family in the world?

Based on recent events, many scientists are working toward the latter.

Earlier this month, scientists from the Oregon Health & Science University used a gene editing tool to correct a disease-causing mutation in an embryo.

The technique, known as CRISPR-Cas9, fixed the mutation in the embryos nuclear DNA that causes hypertrophic cardiomyopathy, a common heart condition that can lead to heart failure or cardiac death.

This is the first time that this gene-editing tool has been tested on clinical-quality human eggs.

Had one of these embryos been implanted into a womans uterus and allowed to fully develop, the baby would have been free of the disease-causing variation of the gene.

This type of beneficial change would also have been passed down to future generations.

None of the embryos in this study were implanted or allowed to develop. But the success of the experiment offers a glimpse at the potential of CRISPR-Cas9.

Still, will we ever be able to gene-edit our world free of disease?

According to the Genetic Disease Foundation, there are more than 6,000 human genetic disorders.

Scientists could theoretically use CRISPR-Cas9 to correct any of these diseases in an embryo.

To do this, they would need an appropriate piece of RNA to target corresponding stretches of genetic material.

The Cas9 enzyme cuts DNA at that spot, which allows scientists to delete, repair, or replace a specific gene.

Some genetic diseases, though, may be easier to treat with this method than others.

Most people are focusing, at least initially, on diseases where there really is only one gene involved or a limited number of genes and theyre really well understood, Megan Hochstrasser, PhD, science communications manager at the Innovative Genomics Institute in California, told Healthline.

Diseases caused by a mutation in a single gene include sickle cell disease, cystic fibrosis, and Tay-Sachs disease. These affect millions of people worldwide.

These types of diseases, though, are far outnumbered by diseases like cardiovascular disease, diabetes, and cancer, which kill millions of people across the globe each year.

Genetics along with environmental factors also contribute to obesity, mental illness, and Alzheimers disease, although scientists are still working on understanding exactly how.

Right now, most CRISPR-Cas9 research focuses on simpler diseases.

There are a lot of things that have to be worked out with the technology for it to get to the place where we could ever apply it to one of those polygenic diseases, where multiple genes contribute or one gene has multiple effects, said Hochstrasser.

Although designer babies gain a lot of media attention, much CRISPR-Cas9 research is focused elsewhere.

Most people who are working on this are not working in human embryos, said Hochstrasser. Theyre trying to figure out how we can develop treatments for people that already have diseases.

These types of treatments would benefit children and adults who are already living with a genetic disease, as well as people who develop cancer.

This approach may also help the 25 million to 30 million Americans who have one of the more than 6,800 rare diseases.

Gene editing is a really powerful option for people with rare disease, said Hochstrasser. You could theoretically do a phase I clinical trial with all the people in the world that have a certain [rare] condition and cure them all if it worked.

Rare diseases affect fewer than 200,000 people in the United States at any given time, which means there is less incentive for pharmaceutical companies to develop treatments.

These less-common diseases include cystic fibrosis, Huntingtons disease, muscular dystrophies, and certain types of cancer.

Last year researchers at the University of California Berkeley made progress in developing an ex vivo therapy where you take cells out of a person, modify them, and put them back into the body.

This treatment was for sickle cell disease. In this condition, a genetic mutation causes hemoglobin molecules to stick together, which deforms red blood cells. This can lead to blockages in the blood vessels, anemia, pain, and organ failure.

Researchers used CRISPR-Cas9 to genetically engineer stem cells to fix the sickle cell disease mutation. They then injected these cells into mice.

The stem cells migrated to the bone marrow and developed into healthy red blood cells. Four months later, these cells could still be found in the mices blood.

This is not a cure for the disease, because the body would continue to make red blood cells that have the sickle cell disease mutation.

But researchers think that if enough healthy stem cells take root in the bone marrow, it could reduce the severity of disease symptoms.

More work is needed before researchers can test this treatment in people.

A group of Chinese researchers used a similar technique last year to treat people with an aggressive form of lung cancer the first clinical trial of its kind.

In this trial, researchers modified patients immune cells to disable a gene that is involved in stopping the cells immune response.

Researchers hope that, once injected into the body, the genetically edited immune cells will mount a stronger attack against the cancer cells.

These types of therapies might also work for other blood diseases, cancers, or immune problems.

But certain diseases will be more challenging to treat this way.

If you have a disorder of the brain, for example, you cant remove someones brain, do gene editing and then put it back in, said Hochstrasser. So we have to figure out how to get these reagents to the places they need to be in the body.

Not every human disease is caused by mutations in our genome.

Vector-borne diseases like malaria, yellow fever, dengue fever, and sleeping sickness kill more than 1 million people worldwide each year.

Many of these diseases are transmitted by mosquitoes, but also by ticks, flies, fleas, and freshwater snails.

Scientists are working on ways to use gene editing to reduce the toll of these diseases on the health of people around the world.

We could potentially get rid of malaria by engineering mosquitoes that cant transmit the parasite that causes malaria, said Hochstrasser. We could do this using the CRISPR-Cas9 technique to push this trait through the entire mosquito population very quickly.

Researchers are also using CRISPR-Cas9 to create designer foods.

DuPont recently used gene editing to produce a new variety of waxy corn that contains higher amounts of starch, which has uses in food and industry.

Modified crops may also help reduce deaths due to malnutrition, which is responsible for nearly half of all deaths worldwide in children under 5.

Scientists could potentially use CRISPR-Cas9 to create new varieties of food that are pest-resistant, drought-resistant, or contain more micronutrients.

One benefit of CRISPR-Cas9, compared to traditional plant breeding methods, is that it allows scientists to insert a single gene from a related wild plant into a domesticated variety, without other unwanted traits.

Gene editing in agriculture may also move more quickly than research in people because there is no need for years of lab, animal, and human clinical trials.

Even though plants grow pretty slowly, said Hochstrasser, it really is quicker to get [genetically engineered plants] out into the world than doing a clinical trial in people.

Safety and ethical concerns

CRISPR-Cas9 is a powerful tool, but it also raises several concerns.

Theres a lot of discussion right now about how best to detect so-called off-target effects, said Hochstrasser. This is what happens when the [Cas9] protein cuts somewhere similar to where you want it to cut.

Off-target cuts could lead to unexpected genetic problems that cause an embryo to die. An edit in the wrong gene could also create an entirely new genetic disease that would be passed onto future generations.

Even using CRISPR-Cas9 to modify mosquitoes and other insects raises safety concerns like what happens when you make large-scale changes to an ecosystem or a trait in a population that gets out of control.

There are also many ethical issues that come with modifying human embryos.

So will CRISPR-Cas9 help rid the world of disease?

Theres no doubt that it will make a sizeable dent in many diseases, but its unlikely to cure all of them any time soon.

We already have tools for avoiding genetic diseases like early genetic screening of fetuses and embryos but these are not universally used.

We still dont avoid tons of genetic diseases, because a lot of people dont know that they harbor mutations that can be inherited, said Hochstrasser.

Some genetic mutations also happen spontaneously. This is the case with many cancers that result from environmental factors such as UV rays, tobacco smoke, and certain chemicals.

People also make choices that increase their risk of heart disease, stroke, obesity, and diabetes.

So unless scientists can use CRISPR-Cas9 to find treatments for these lifestyle diseases or genetically engineer people to stop smoking and start biking to work these diseases will linger in human society.

Things like that are always going to need to be treated, said Hochstrasser. I dont think its realistic to think we would ever prevent every disease from happening in a human.

Continue reading here:
Will Gene Editing Allow Us to Rid the World of Diseases? - Healthline

Forever Labs, a startup in Y Combinators latest batch, is preserving adult stem cells with the aim to help you live longer and healthier.

Stem cells have the potential to become any type of cell needed in the body. Its very helpful to have younger stem cells from your own body on hand should you ever need some type of medical intervention, like a bone marrow transplant as the risk of rejection is greatly reduced when the cells are yours.

Mark Katakowski spent the last 15 years studying stem cells. What he found is that not only do we have less of them the older we get, but they also lose their function as we age.So, he and his co-founders Edward Cibor and Steve Clausnitzer started looking at how to bank them while they were young.

Clausnitzer banked his cells two years ago at the age of 38. So, while he is biologically now age 40, his cells remain the age in which they were harvested or as he calls it, stem cell time travel.

Steven Clausnitzer with his 38-year-old banked stem cells.

There are places offering stem cell therapy and Botox, he said.

Forever Labs is backed by a team of Ivy League-trained scientists with decades of experience between them. Jason Camm, chief medical officer for Thiel Capital, is also one of the companys medical advisors however, the startup is quick to point out it is not associated with Thiel Capital.

The process involves using a patented device to collect the cells. Forever Labs can then grow and bank your cells for $2,500, plus another $250 for storage per year (or a flat fee of $7,000 for life).

The startup is FDA-approved to bank these cells and is offering the service in seven states. What it does not have FDA approval for is the modification of those cells for rejuvenation therapy.

Katakowski refers to what the company is doing as longevity as a service, with the goal being to eventually take your banked cells and modify them to reverse the biological clock.

But that may take a few years. There are hundreds of clinical trials looking at stem cell uses right now. Forever Labs has also proposed its own clinical trial to take your stem cells and give them to your older cells.

Youll essentially young-blood effect yourself, Katakowski joked of course, in this case, youd be using your own blood made from your own stem cells, not the blood of random teens.

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Forever Labs preserves young stem cells to prevent your older self from aging - TechCrunch

Ball-and-stick model of the L-ascorbic acid (vitamin C) molecule, C6H8O6, as found in the crystal structure. Credit: public domain

Vitamin C may "tell" faulty stem cells in the bone marrow to mature and die normally, instead of multiplying to cause blood cancers. This is the finding of a study led by researchers from Perlmutter Cancer Center at NYU Langone Health, and published online August 17 in the journal Cell.

Certain genetic changes are known to reduce the ability of an enzyme called TET2 to encourage stem cells to become mature blood cells, which eventually die, in many patients with certain kinds of leukemia, say the authors. The new study found that vitamin C activated TET2 function in mice engineered to be deficient in the enzyme.

"We're excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases caused by TET2-deficient leukemia stem cells, most likely in combination with other targeted therapies," says corresponding study author Benjamin G. Neel, MD, PhD, professor in the Department of Medicine and director of the Perlmutter Cancer Center.

Changes in the genetic code (mutations) that reduce TET2 function are found in 10 percent of patients with acute myeloid leukemia (AML), 30 percent of those with a form of pre-leukemia called myelodysplastic syndrome, and in nearly 50 percent of patients with chronic myelomonocytic leukemia. Such cancers cause anemia, infection risk, and bleeding as abnormal stem cells multiply in the bone marrow until they interfere with blood cell production, with the number of cases increasing as the population ages.

Along with these diseases, new tests suggest that about 2.5 percent of all U.S. cancer patients - or about 42,500 new patients each year - may develop TET2 mutations, including some with lymphomas and solid tumors, say the authors.

Cell Death Switch

The study results revolve around the relationship between TET2 and cytosine, one of the four nucleic acid "letters" that comprise the DNA code in genes. Every cell type has the same genes, but each gets different instructions to turn on only those needed in a given cellular context.

These "epigenetic" regulatory mechanisms include DNA methylation, the attachment of a small molecule termed a methyl group to cytosine bases that shuts down the action of a gene containing them.

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The back- and-forth attachment and removal of methyl groups also fine-tunes gene expression in stem cells, which can mature, specialize and multiply to become muscle, bone, nerve, or other cell types. This happens as the body first forms, but the bone marrow also keeps pools of stem cells on hand into adulthood, ready to become replacement cells as needed. In leukemia, signals that normally tell a blood stem cell to mature malfunction, leaving it to endlessly multiply and "self-renew" instead of producing normal white blood cells needed to fight infection.

The enzyme studied in this report, Tet methylcytosine dioxygenase 2 (TET2), enables a change in the molecular structure (oxidation) of methyl groups that is needed for them to be removed from cytosines. This "demethylation" turns on genes that direct stem cells to mature, and to start a count-down toward self-destruction as part of normal turnover. This serves as an anti-cancer safety mechanism, one that is disrupted in blood cancer patients with TET2 mutations, says Neel.

To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the research team genetically engineered mice such that the scientists could switch the TET2 gene on or off.

Similar to the naturally occurring effects of TET2 mutations in mice or humans, using molecular biology techniques to turn off TET2 in mice caused abnormal stem cell behavior. Remarkably, these changes were reversed when TET2 expression was restored by a genetic trick. Previous work had shown that vitamin C could stimulate the activity of TET2 and its relatives TET1 and TET3. Because only one of the two copies of the TET2 gene in each stem cell is usually affected in TET2-mutant blood diseases, the authors hypothesized that high doses of vitamin C, which can only be given intravenously, might reverse the effects of TET2 deficiency by turning up the action of the remaining functional gene.

Indeed, they found that vitamin C did the same thing as restoring TET2 function genetically. By promoting DNA demethylation, high-dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukemia cancer stem cells from human patients implanted in mice.

"Interestingly, we also found that vitamin C treatment had an effect on leukemic stem cells that resembled damage to their DNA," says first study author Luisa Cimmino, PhD, an assistant professor in the Department of Pathology at NYU Langone Health. "For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer."

Researchers found that the combination had an enhanced effect on leukemia stem cells, further shifting them from self-renewal back toward maturity and cell death. The results also suggest that vitamin C might drive leukemic stem cells without TET2 mutations toward death, says Cimmino, given that it turns up any TET2 activity normally in place.

"Our team is working to systematically identify genetic changes that contribute to risk for leukemia in significant groups of patients," says corresponding author Iannis Aifantis, PhD, professor and chair of the Department of Pathology at NYU Langone Health. "This study adds the targeting of abnormal TET2-driven DNA demethylation to our list of potential new treatment approaches."

Explore further: A tumor-suppressing gene can be harmful in some cancers

Journal reference: Cell

Provided by: NYU Langone Health / NYU School of Medicine

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Vitamin C may encourage blood cancer stem cells to die - Medical Xpress

HELENA ExplorationWorks is hosting the Be The Match bone marrow donor drive this week at the Great Northern Town Center.

The drive is intended to support those in need of bone marrow or blood stem cell transplants around the world. Its being held in conjunction with ExplorationWorks Kids Kicking Cancer Camp.

The camp is open to children who are directly affected by cancer in their lives. Campers had the opportunity to make a card for Be the Match child who is currently undergoing or awaiting treatment.

Our hope is that the kids attending our camp will be able to connect with the Be The Match kids on a level most other children wouldnt understand. Knowing someone else is fighting the same fight will hopefully be a healing activity for all of the kids involved, said ExplorationWorks Education Director Lauren Rivers.

John Philpott of Be the Match said that sadly, some of the Be The Match kids children are still waiting to be matched with a donor.

There are still thousands of patients every year who have to hear their doctor say theres no match for you, said Phillpott, One Montanan [donation] can mean the difference for one patient.

According to Be the Match, someone is diagnosed with blood cancer every three minutes and every 10 minutes someone dies from not receiving a transplant.

The Marrow Donor Registry Drive will continue at ExplorationWorks from 10 a.m. to 5 p.m. Friday and from 12:30 to 3 p.m. on Saturday.

Registration takes around 10 minutes to complete and only involves some paper work and a few cheek swabs. You must be between the ages of 18 and 44 in order to register.

For more information about bone marrow donation and how to register click here.

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Bone marrow drive held at ExplorationWorks - KTVH

US researchers found high doses of vitamin C found in fruits such as oranges and green leafy vegetables such as kale and broccoli may be a new weapon against the disease.

The study suggests that vitamin C may tell faulty stem cells in our bone marrow to mature and die.

That means the traditional blood cancer danger cells would naturally disappear instead of multiplying to cause leukaemia.

The findings were uncovered by researchers from Perlmutter Cancer Center in New York and published in the cancer journal Cell. Perlmutter director Professor Benjamin G. Neel said: Were excited by the prospect that highdose vitamin C might become a safe treatment for blood diseases caused by leukaemia stem cells, most likely in combination with other targeted therapies.

Vitamin C is an antioxidant and several previous studies had hinted that high levels could affect cancer cells. High vitamin C fruit and vegetables include bell peppers, dark leafy greens, kiwifruit, broccoli, berries, oranges, tomatoes, green peas, and papayas.

The current recommended daily value for vitamin C is 60mg taken from either fruit and vegetables or tablet supplements.

The New York study explored the link between vitamin C and a tumour suppressor protein enzyme in the human body called TET2.

The enzyme helps to guard against blood cancers such as leukaemia and is believed also to protect against heart disease.

But mutations in the gene affect about one per cent of the over-65s, making them extremely susceptible to blood cancer.

Although TET2 loss does not create cancer, it helps to create the conditions for blood cancers to thrive.

Scientists in the New York study found that, in mice engineered to have just small amounts of TET2, high doses of vitamin C given intravenously dramatically activated the enzyme.

The study found changes in the genetic code that reduces TET2 function are found in 10 per cent of patients with acute myeloid leukaemia (AML).

The scientists also claim that, when they implanted leukaemia cancer stem cells from human patients into mice, high doses of vitamin C suppressed the cells growth.

Anna Perman, Cancer Research UKs senior science information manager, said: Some doctors think that antioxidants like vitamin C might interfere with chemotherapy which, we know can be effective treatment.

The important thing for cancer patients to remember is that this study is looking at the action of vitamin C in the laboratory, not the effect of eating foods or supplements that contain vitamin C.

This should not prompt anyone receiving treatment for cancer to change their diet or treatment plan.

The rest is here:
Vitamin C could help to fight cancer, a study claims - Express.co.uk

Fertile sperm are rare in men with an extra sex chromosome

Dennis Kunkle Microscopy/SPL

By Andy Coghlan

Turning skin cells into sperm may one day help some infertile men have babies. Research in mice has found a way to make fertile sperm from animals born with too many sex chromosomes.

Most men have two sex chromosomes one X and one Y but some have three, which makes it difficult to produce fertile sperm. Around 1 in 500 men are born with Klinefelter syndrome, caused by having an extra X chromosome, while roughly 1 in 1000 have Double Y syndrome.

James Turner of the Francis Crick Institute in London and his team have found a way to get around the infertility caused by these extra chromosomes. First, they bred mice that each had an extra X or Y chromosome. They then tried to reprogram skin cells from the animals, turning them into induced pluripotent stem cells (iPS), which are capable of forming other types of cell.

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To their surprise, this was enough to make around a third of the skin cells jettison their extra chromosome. When these cells were then coaxed into forming sperm cells and used to fertilise eggs, 50 to 60 per cent of the resulting pregnancies led to live births.

This suggests that a similar technique might enable men with Klinefelter or Double Y-related infertility to conceive. But there is a significant catch.

We dont yet know how to fully turn stem cells into sperm, so the team got around this by injecting the cells into mouse testes for the last stages of development. While this led to fertile sperm, it also caused tumours to form in between 29 and 50 per cent of mice.

What we really need to make this work is being able to go from iPS cells to sperm in a dish, says Turner.

It has to be done all in vitro, so only normal sperm cells would be used to fertilise eggs, says Zev Rosenwaks of the Weill Cornell Medical College in New York. The danger with all iPS cell technology is cancer.

Journal reference: Science, DOI: 10.1126/science.aam9046

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Stem cell technique could reverse a major type of infertility - New Scientist

Blumen has been diagnosed with Chronic Myeloid Leukemia and is awaiting a donor stem cell that matches his DNA

Running a difficult race isn't something that's new to Chennai-based BlumenRajan Sathya. An exceptionally gifted track athlete, a state record holder, a University gold medalist and a national level silver medalist in the 400m sprint, Blumenhad always been one to push his physical limits.

But this time, he's facing the most difficult track of his life. In December 2014, there was a sudden drop in his blood count. He was soon diagnosed with Chronic Myeloid Leukemia, a type of cancer which starts in certain blood-forming cells of the bone marrow.

CML is a treatable condition, where the first level of treatment is oral chemotherapy, followed by the usual induction chemo. However, the most-effective proven treatment is stem cell transplant, which is basically where you transplant a stem cell from a donor whose DNA matches with you."We've been hunting for donors. The only problem is that the probability of finding a match is one in a lakh. We're looking at international registries as well. I had contacted a registry in Germany while I did my homework online. But, they replied saying that the patient couldn't contact them directly," says the 27-year-old.

A graduate in Social Work from Madras Christian College and currently working with a local church, he adds, "In another three or four days, we will go ahead with the closest match available. We will wait for a hundred per cent match, but we can't wait too long."

When asked what kept him going strong throughout his whole battle, he says it was his faith in God and the support of his local church. Friends, family, colleagues and college mates have spread the word on social media, hoping for a miracle. Blumennow wants to ensure that there is awareness created about stem cell donation. "Most people have no clue about it. Most of us have never registered anywhere. There should be more awareness camps in colleges. If more people register, it would be much easier to find the right match. There won't be any trouble of finding volunteers," he says.

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Chennai sprinter Blumen Rajan is in a race against time to beat cancer. Are you the stem cell donor who can help out ... - EdexLive (press release)...

New research funded by the National Institutes of Health used 3-D collections of brain tissue grown from human cells to study the brains star-shaped astrocytes. (Image credit: Sergiu Pasca, Stanford University)

BETHESDA, Md. (CN) Its been two years since Stanford neurobiologists published a method for converting adult skin cells into induced pluripotent stem cells that could then be grown into 3-D clusters of brain cells.

The National Institutes of Health reported Wednesday that another crop of scientists have been studying the growth of star-shaped brain cells known as human cortical spheroids (hCSs) in these cell clusters.

Their findings, published in Neuron, confirm that the maturation of lab-grown cells largely mimics that of cells taken directly from brain tissue during very early life, a critical time for brain growth.

Because of the critical role this process plays in normal brain development, further study of lab-grown hCSs could uncover the underlying developmental biology at the core of various neurological and mental health disorders, such as schizophrenia and autism.

The hCS system makes it possible to replay astrocyte development from any patient, said Ben Barres, a Stanford professor of neurobiology who co-led the 2015 study, as quoted the NIH in a Wednesday article.

Thats huge, Barres added. Theres no other way one could ever do that without this method.

Steven Sloan, a student in Stanfords MD/Ph.D. program, led the astrocyte-comparison study published in the latest issue of Neuron.

The team grew the hCSs for 20 months, one of the longest-ever studies of lab-grown human brain cells, according to the report by the NIH, which funded the research in part through its National Institute of Neurological Disorders and Stroke.

Jill Morris, who directs the NINDS, said the work by Sloans team addresses a significant gap in human brain research by providing an invaluable technique to investigate the role of astrocytes in both normal development and disease.

David Panchision, program director at the National Institute of Mental Health, which also helped fund the study, also spoke to the studys importance.

Since astrocytes make up a greater proportion of brain cells in humans than in other species, it may reflect a greater need for astrocytes in normal human brain function, with more significant consequences when they dont work correctly, Panchision added.

One point that the researchers emphasized, however, is that hCSs are only a model and lack many features of real brains.

Moreover, certain genes that are active in fully mature astrocytes never switched on in the hCS-grown astrocytes, which they could conceivably do if the cells had more time to develop, the NIH article says. To address this question, the researchers now hope to identify ways to produce mature brain cells more quickly. hCSs could also be used to scrutinize precisely what causes astrocytes to change over time and to screen drugs that might correct any differences that occur in brain disease.

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New Cell Study Pulls Curtain on Schizophrenia, Autism - Courthouse News Service

JENNIE McKEON @JennieMnwfdn

NICEVILLE Jack Massey is ready to go back to school.

Only this time, the University of Florida senior will head back to campus with his mom and a new outlook on life.

Massey suffered a spinal cord injury in a pool accident in March and is paralyzed from the chest down. After months of rehab, he's eager to get back into a familiar routine.

"It's definitely boring," the 21-year-old said at his parents' home in Niceville. "There's not a lot to do. I want to go back to school. I still have my brain. I still have everything I need to be successful."

After the accident March 17, Massey was treated at the University of Florida Shands Hospital and then was transferred to Shepherd Center, a spinal cord and brain injury rehab center in Atlanta. At Shepherd Center he met with a peer mentor, counselors and physical therapists to help him find a new normal.

Jack has remained positive throughout the past six months.

"Jack has been a fighter through all of this," said his mother, Julie. "I think he's done well. I only saw him break down once."

Before the accident, Jack was a well-rounded athlete who playing baseball and basketball and ran. He was a star on the track and field team at Niceville High School, with his 4 X 800 relay winning state his senior year.

He says the biggest challenge now is not being able to do the same things he could before.

"I can't get up and go," he said. "It didn't really start to set in until after I got out of rehab."

Jack has had to find enjoyment in other things, like reading or playing with the dogs. His friends have learned to transfer him from his wheelchair to a car so they can take him to the movies or out to eat. When they recently took a trip to the beach, Julie said five of Jack's friends carried him out to the sand a lesson on how hard it is to navigate the world in a wheelchair.

Jack said he believes technology one day will advance enough that he won't be paralyzed forever. He also volunteered to do stem cell surgery to allow doctors to study the affects of stem cells on his spine for the next 15 years. Instead of wallowing in self pity, he's moving forward. But he'll need help.

"I'm appreciating everything in the now," he said.

Doctors have said Jack has adapted faster than expected, but there are still some everyday essential tasks that are out of his reach. He cannot write or cook. He can shower himself but can't dry himself or transfer himself in and out of his wheelchair. The Massey family hopes to secure a personal care attendant for Jack at school, but until then Julie will be in Gainesville to help him transition. An occupational therapy student from the university will also help Jack on a temporary basis.

Finding proper care for her son has proven to be a learning experience for Julie and her husband, Lance.

"I don't know how people do it," she said. "We have good health care, but then there's hidden costs. There's travel expenses. ... It's kind of humbling. Nobody should have to go to GoFundMe for medical help."

Jack wants to spend his final year as an undergrad as independent as possible. After months of helping him recover, Julie said it will be hard to let her son go. Jack is the oldest of three; his brother Lance is 19 and a student at UF and his sister Alina is 14 and attends Ruckel Middle School.

"It's like letting him go off to kindergarten again," she said.

As for life after college, Jack said he doesn't feel limited in career choices. One of his professors in the geology department encouraged him by saying that there were plenty of opportunities he could pursue in that field. Jack said he may also consider law school. One thing he's learned through this life-altering experience is that there are no limits to what he can achieve.

"I haven't done that much deep thinking. I just go with the flow," he said. "But I learned I have more perseverance. I'm more mentally tough than I thought I was. I'm appreciative for life in general. That's one of the big things."

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'I still have my brain' - The Northwest Florida Daily News

The old rats appeared newly invigorated after receiving their injections. As hoped, the cardiac stem cells improved heart function yet also provided additional benefits. The rats' fur fur, shaved for surgery, grew back more quickly than expected, and their chromosomal telomeres, which commonly shrink with age, lengthened.

The old rats receiving the cardiac stem cells also had increased stamina overall, exercising more than before the infusion.

"It's extremely exciting," said Dr. Eduardo Marbn, primary investigator on the research and director of the Cedars-Sinai Heart Institute. Witnessing "the systemic rejuvenating effects," he said, "it's kind of like an unexpected fountain of youth."

"We've been studying new forms of cell therapy for the heart for some 12 years now," Marbn said.

Some of this research has focused on cardiosphere-derived cells.

"They're progenitor cells from the heart itself," Marbn said. Progenitor cells are generated from stem cells and share some, but not all, of the same properties. For instance, they can differentiate into more than one kind of cell like stem cells, but unlike stem cells, progenitor cells cannot divide and reproduce indefinitely.

Since heart failure with preserved ejection fraction is similar to aging, Marbn decided to experiment on old rats, ones that suffered from a type of heart problem "that's very typical of what we find in older human beings: The heart's stiff, and it doesn't relax right, and it causes fluid to back up some," Marbn explained.

He and his team injected cardiosphere-derived cells from newborn rats into the hearts of 22-month-old rats -- that's elderly for a rat. Similar old rats received a placebo injection of saline solution. Then, Marbn and his team compared both groups to young rats that were 4 months old. After a month, they compared the rats again.

Even though the cells were injected into the heart, their effects were noticeable throughout the body, Marbn said

"The animals could exercise further than they could before by about 20%, and one of the most striking things, especially for me (because I'm kind of losing my hair) the animals ... regrew their fur a lot better after they'd gotten cells" compared with the placebo rats, Marbn said.

The rats that received cardiosphere-derived cells also experienced improved heart function and showed longer heart cell telomeres.

Why did it work?

The working hypothesis is that the cells secrete exosomes, tiny vesicles that "contain a lot of nucleic acids, things like RNA, that can change patterns of the way the tissue responds to injury and the way genes are expressed in the tissue," Marbn said.

It is the exosomes that act on the heart and make it better as well as mediating long-distance effects on exercise capacity and hair regrowth, he explained.

Looking to the future, Marbn said he's begun to explore delivering the cardiac stem cells intravenously in a simple infusion -- instead of injecting them directly into the heart, which would be a complex procedure for a human patient -- and seeing whether the same beneficial effects occur.

Dr. Gary Gerstenblith, a professor of medicine in the cardiology division of Johns Hopkins Medicine, said the new study is "very comprehensive."

"Striking benefits are demonstrated not only from a cardiac perspective but across multiple organ systems," said Gerstenblith, who did not contribute to the new research. "The results suggest that stem cell therapies should be studied as an additional therapeutic option in the treatment of cardiac and other diseases common in the elderly."

Todd Herron, director of the University of Michigan Frankel Cardiovascular Center's Cardiovascular Regeneration Core Laboratory, said Marbn, with his previous work with cardiac stem cells, has "led the field in this area."

"The novelty of this bit of work is, they started to look at more precise molecular mechanisms to explain the phenomenon they've seen in the past," said Herron, who played no role in the new research.

One strength of the approach here is that the researchers have taken cells "from the organ that they want to rejuvenate, so that makes it likely that the cells stay there in that tissue," Herron said.

He believes that more extensive study, beginning with larger animals and including long-term followup, is needed before this technique could be used in humans.

"We need to make sure there's no harm being done," Herron said, adding that extending the lifetime and improving quality of life amounts to "a tradeoff between the potential risk and the potential good that can be done."

Capicor hasn't announced any plans to do studies in aging, but the possibility exists.

After all, the cells have been proven "completely safe" in "over 100 human patients," so it would be possible to fast-track them into the clinic, Marbn explained: "I can't tell you that there are any plans to do that, but it could easily be done from a safety viewpoint."

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Cardiac stem cells rejuvenate rats' aging hearts, study says - CNN

The early heart tube of a chick embryo: cardiac and endothelial cells are made visible by specifically expressing fluorescent proteins under the control of the Nkx2.5 (green) and Isl1 (red) cardiovascular genes. Credit: Weizmann Institute of Science

One of the first organ systems to form and function in the embryo is the cardiovascular system: in fact, this developmental process starts so early that scientists still have many unresolved questions on the origin of the primitive heart and blood vessels. How do the first cells the progenitors that are destined to become part of this system participate in shaping the developed cardiovascular system?

Dr. Lyad Zamir, a former PhD student in the lab of Prof. Eldad Tzahor in the Weizmann Institute of Science's Department of Molecular Cell Biology, developed a method to image the earliest cardiovascular progenitors and track them and their descendants through the developing embryo in real time. His movies took place in fertilized chicken eggs, in which a complex network of blood vessels forms within the yolk sac to nourish the embryo. The findings of this research were recently published in eLife.

Working in collaboration with the lab of Prof. Richard Harvey of the Victor Chang Cardiac Research Institute and the University of New South Wales, both in Australia, Prof. Tzahor and Dr. Zamir focused on a gene called Nkx2-5. This gene encodes a transcription factor, which is a regulatory protein that controls the expression of other genes involved in the development of the heart. "The new study revealed that Nkx2-5, independently of its role in the development of the heart, plays a central role in the genesis of the very first blood vessels and indeed the formation of blood," says Prof. Tzahor.

Looking at the onset of Nkx2-5 expression, the team revealed the existence of progenitor cells called hemangioblasts. These cells give rise to both the blood and vascular progenitor cells those that lead to the formation of blood vessels. These unique cells are created from the mesoderm the middle layer of cells that appears in the very early developing embryo. Researchers have been hotly debating the existence of hemangioblasts and, if they do exist, their possible function.

In the chick embryo films, the researchers could see the hemangioblasts moving to create "blood islands," which form within the primitive embryonic vessels. The researchers were surprised to observe that some of the hemangioblast cells were moving into the heart, where they formed blood stem cells. This helped make sense of other studies revealing that the early heart tube contains cells that appear to assist in generating blood cells. The researchers also identified specialized Nkx2-5-expressing cells within the lining of the newly formed aorta, where they appeared to "bud off" to produce new blood cells. Later on in development, these specialized cells move into the liver, where they give rise to the blood-forming stem cells in the fetus.

Prof. Tzahor: "Even 20 years after one of the 'master genes' for heart development was discovered, we have managed to write a new story about its action, showing that it works briefly at a very early stage in development in the formation of vessels and blood before the main action takes place in the heart. We have provided solid evidence for the existence of these very early cells and their contribution to heart and vascular development."

Because these findings reveal the early origins of at least some of the blood-forming stem cells in the embryo, they may be especially helpful in research into diseases affecting the cardiovascular system.

Explore further: Kidney research leads to surprising discovery about how the heart forms

More information: Lyad Zamir et al. Nkx2.5 marks angioblasts that contribute to hemogenic endothelium of the endocardium and dorsal aorta, eLife (2017). DOI: 10.7554/eLife.20994

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The unexpected role of a well-known gene in creating blood - Medical Xpress

August 15, 2017

What if one day, we could teach our bodies to self-heal like a lizards tail, and make severe injury or disease no more threatening than a paper cut?

Or heal tissues by coaxing cells to multiply, repair or replace damaged regions in loved ones whose lives have been ravaged by stroke, Alzheimers or Parkinsons disease?

Such is the vision, promise and excitement in the burgeoning field of regenerative medicine, now a major ASU initiative to boost 21st-century medical research discoveries.

ASU Biodesign Institute researcher Nick Stephanopoulos is one of several rising stars in regenerative medicine. In 2015, Stephanopoulos, along with Alex Green and Jeremy Mills, were recruited to the Biodesign Institutes Center for Molecular Design and Biomimetics (CMDB), directed by Hao Yan, a world-recognized leader in nanotechnology.

One of the things that that attracted me most to the ASU and the Biodesign CMDB was Haos vision to build a group of researchers that use biological molecules and design principles to make new materials that can mimic, and one day surpass, the most complex functions of biology, Stephanopoulos said.

I have always been fascinated by using biological building blocks like proteins, peptides and DNA to construct self-assembled structures, devices and materials, and the interdisciplinary and highly collaborative team in the CMDB is the ideal place to put this vision into practice.

Yans research center uses DNA and other basic building blocks to build their nanotechnology structures only at a scale 1,000 times smaller than the width of a human hair.

Theyve already used nanotechnology to build containers to specially deliver drugs to tissues, build robots to navigate a maze or nanowires for electronics.

To build a manufacturing industry at that tiny scale, their bricks and mortar use a colorful assortment of molecular Legos. Just combine the ingredients, and these building blocks can self-assemble in a seemingly infinite number of ways only limited by the laws of chemistry and physics and the creative imaginations of these budding nano-architects.

The goal of the Center for Molecular Design and Biomimetics is to usenatures design rulesas an inspiration in advancing biomedical, energy and electronics innovation throughself-assembling moleculesto create intelligent materials for better component control and for synthesis intohigher-order systems, said Yan, who also holds the Milton Glick Chair in Chemistry and Biochemistry.

Prior to joining ASU, Stephanopoulos trained with experts in biological nanomaterials, obtaining his doctorate with the University of California Berkeleys Matthew Francis, and completed postdoctoral studies with Samuel Stupp at Northwestern University. At Northwestern, he was part of a team that developed a new category of quilt-like, self-assembling peptide and peptide-DNA biomaterials for regenerative medicine, with an emphasis in neural tissue engineering.

Weve learned from nature many of the rules behind materials that can self-assemble. Some of the most elegant complex and adaptable examples of self-assembly are found in biological systems, Stephanopoulos said.

Because they are built from the ground-up using molecules found in nature, these materials are also biocompatible and biodegradable, opening up brand-new vistas for regenerative medicine.

Stephanopoulos tool kit includes using proteins, peptides, lipids and nucleic acids like DNA that have a rich biological lexicon of self-assembly.

DNA possesses great potential for the construction of self-assembled biomaterials due to its highly programmable nature; any two strands of DNA can be coaxed to assemble to make nanoscale constructs and devices with exquisite precision and complexity, Stephanopoulos said.

During his time at Northwestern, Stephanopoulos worked on a number of projects and developed proof-of-concept technologies for spinal cord injury, bone regeneration and nanomaterials to guide stem cell differentiation.

Now, more recently, in a new studyin Nature Communications, Stephanopoulos and his colleague Ronit Freeman in the Stupp laboratory successfully demonstrated the ability to dynamically control the environment around stem cells, to guide their behavior in new and powerful ways.

In the new technology, materials are first chemically decorated with different strands of DNA, each with a unique code for a different signal to cells.

To activate signals within the cells, soluble molecules containing complementary DNA strands are coupled to short protein fragments, called peptides, and added to the material to create DNA double helices displaying the signal.

By adding a few drops of the DNA-peptide mixture, the material effectively gives a green light to stem cells to reproduce and generate more cells. In order to dynamically tune the signal presentation, the surface is exposed to a soluble single-stranded DNA molecule designed to grab the signal-containing strand of the duplex and form a new DNA double helix, displacing the old signal from the surface.

This new duplex can then be washed away, turning the signal off. To turn the signal back on, all that is needed is to now introduce a new copy of single-stranded DNA bearing a signal that will reattach to the materials surface.

One of the findings of this work is the possibility of using the synthetic material to signal neural stem cells to proliferate, then at a specific time selected by the scientist, trigger their differentiation into neurons for a while, before returning the stem cells to a proliferative state on demand.

One potential use of the new technology to manipulate cells could help cure a patient with neurodegenerative conditions like Parkinsons disease.

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Restoring loss: Bio-inspired materials give boost to regenerative medicine - Arizona State University

Newswise The University of New Mexico Comprehensive Cancer Center began helping New Mexicans with blood disorders a little more than one year ago. Since then, more than 30 New Mexicans have received treatment. Program Director Matthew Fero, MD, FACP, started the program after moving to New Mexico from the Fred Hutchinson Cancer Center in Seattle, Wash.

The UNM Comprehensive Cancer Center program is the states only bone marrow transplant program. It includes a nurse manager, nurse coordinator, a social worker, a pharmacist, infusion nurses, and an inpatient team. Bone marrow transplantation needs a multidisciplinary team because of the complexity in coordinating care, says Fero. The teams Nurse Manager, Maria Limanovich, says the team follows each person from the beginning of bone marrow transplant treatment through completion. According to Fero, the program is growing and is in the process of hiring two more doctors and an advanced practice provider.

The UNM Bone Marrow Transplant program offers treatment choices for people with lymphoma and myeloma and will expand to help people with other blood disorders. Almost 1,000 New Mexicans receive a blood cancer diagnosis each year, according to American Cancer Society estimates.

Fero and his team currently perform autologous transplants. Autologous bone marrow transplantation is the process of taking bone marrow stem cells out of a patient and then infusing them back in after the patient receives high dose therapy, says Fero. This allows us to use treatments that would otherwise harm the bone marrow.

Bone marrow, the soft reddish material that fills the inside of our bones, produces millions of new blood cells each second. These millions of cells come from a tiny number of bone marrow stem cells. These stem cells are special because they can mature into all of the different types of cells in the blood. These are the cells doctors collect for a transplant.

Because bone marrow is a liquid organ, Fero says, it can pass through an IV [intravenous] line. Doctors rarely need to take stem cells directly out of the bone, Fero explains. They use drugs to coax bone marrow stem cells into the bloodstream. From there, the blood travels through an IV line into an apheresis machine that sorts the stem cells out and returns the rest of the blood. The experience is like donating blood at a blood bank.

Once stem cells are safely stored out of the bloodstream, doctors use high-dose chemotherapy to eradicate the remaining cancer. When chemotherapy is out of their system, the patients stem cells are reinfused. The reinfusion process is similar to a blood transfusion. Once reinfused, stem cells find their way back to bone marrow where they begin to grow and make new blood cells.

Autologous bone marrow transplants are standard treatments for lymphoma and myeloma. This treatment works very well against aggressive lymphomas. In this case the goal is to cure the disease, says Fero. Autologous bone marrow transplants extend the lives of people with myeloma and gives them a better quality of life, too. Fero says, Were offering another option for their treatment.

Matthew Fero, MD, FACP, is a Professor in the Department of Internal Medicine, Division of Hematology/Oncology, at the UNM School of Medicine. He serves as Director of the Bone Marrow Stem Cell Program at the UNM Comprehensive Cancer Center. Dr. Fero received his medical degree from the University of California, Irvine, and completed his residency in Internal Medicine at the Mayo Graduate School of Medicine. He completed a medical fellowship in Medical Oncology at University of Washington and a research fellowship at Fred Hutchinson Cancer Research Center. He is a member of the American Society of Hematology and the American Society for Blood and Marrow Transplantation, and is a Fellow of the American College of Physicians. His research focuses on the molecular bases of cancer and translating new technologies into improved cancer diagnostics and novel therapies.

The University of New Mexico Comprehensive Cancer Center is the Official Cancer Center of New Mexico and the only National Cancer Institute-designated Cancer Center in a 500-mile radius. Its 125 board-certified oncology specialty physicians include cancer surgeons in every specialty (abdominal, thoracic, bone and soft tissue, neurosurgery, genitourinary, gynecology, and head and neck cancers), adult and pediatric hematologists/medical oncologists, gynecologic oncologists, and radiation oncologists. They, along with more than 500 other cancer healthcare professionals (nurses, pharmacists, nutritionists, navigators, psychologists and social workers), provided cancer care for nearly 60 percent of the adults and children in New Mexico affected by cancer. They treated 11,249 patients in 84,875 ambulatory clinic visits in addition to in-patient hospitalizations at UNM Hospital. These patients came from every county in the State. More than 12 percent of these patients participated in cancer clinical trials testing new cancer treatments and 35 percent of patients participated in other clinical research studies, including tests of novel cancer prevention strategies and cancer genome sequencing. The 130 cancer research scientists affiliated with the UNMCCC were awarded almost $60 million in federal and private grants and contracts for cancer research projects and published 301 high quality publications. Promoting economic development, they filed more than 30 new patents in FY16, and since 2010, have launched 11 new biotechnology start-up companies. Scientists associated with the UNMCCC Cancer Control & Disparities have conducted more than 60 statewide community-based cancer education, prevention, screening, and behavioral intervention studies involving more than 10,000 New Mexicans. Finally, the physicians, scientists and staff have provided education and training experiences to more than 230 high school, undergraduate, graduate, and postdoctoral fellowship students in cancer research and cancer health care delivery. Learn more at http://www.cancer.unm.edu.

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Stem Cell Transplant Program Celebrates First Year - Newswise (press release)

Q: I read that you can use your own stem cells to rejuvenate worn-out knees. Does this really work?

A: Worn out is a good way to term what happens to the knee joint with prolonged use. Lets look at how this happens, starting with cartilage.

The lower portion of the knee joint (at the tibia) contains shock absorbers called menisci made of cartilage. You have one on the inner portion and another on the outer portion of each knee. The upper portion of the knee joint (at the femur) is lined with cartilage as well. All of this cartilage helps protect the bones at the joint but it doesnt heal or regenerate well due to limited blood supply. When severe, worn cartilage leads to arthritis of the knee. In knee X-rays of people over age 60, 37 percent have shown evidence of arthritis of the knees.

The intriguing thing about stem cells is that they have the ability to become any type of cell that the body needs. The cells used for stem cell injections in the knees are called mesenchymal stem cells, and they can differentiate into bone, fat or cartilage cells. These stem cells can come from the fat cells of your body, from your bone marrow or from the inner lining of your knee joint; theyre then replicated in the laboratory and injected into the knee joint.

Heres what the research shows so far.

In a 2013 study, 32 patients with meniscal tears of the knee were injected with a combination of stem cells, platelet-rich plasma and hyaluronic acid. The study reported improved symptoms and even MRI evidence of meniscal cartilage regeneration.

In a 2014 study, 55 patients who had surgery for meniscal tears of the knees were separated into three groups, with two of the groups receiving stem cell injections. Researchers found that, after six weeks, pain had decreased substantially in the two groups that received stem cell injections and that the decrease was even greater at one and two years after the injection.

In a 2017 study in the British Journal of Sports Medicine, researchers analyzed six studies that used stem cells for osteoarthritis of the knees. In five of the studies, stem cells were given after surgery to the knee; in the other study, stem cells from a donor were administered without surgery. All the studies showed reduced pain and improved knee function. Further, in three of the four trials, MRIs corroborated the cartilage improvements.

There may be benefit to stem cell injections for cartilage loss of the knees, but more data are needed. Id also like to see more data on this type of therapy as a preventive measure for younger patients before their knees are worn out.

ASK THE DOCTORS is written by Robert Ashley, M.D., Eve Glazier, M.D., and Elizabeth Ko, M.D. Send questions to askthedoctors@

mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095.

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Stem cell therapy may help knees - Citizens Voice

New research analysis published in JCO definitively shows an overall survival benefit from ongoing treatment with lenalidomide for patients with multiple myeloma who have already received bone marrow transplant.

Buffalo, NY (PRWEB) August 15, 2017

The first study to report that overall survival was extended for patients receiving lenalidomide as maintenance treatment for multiple myeloma has been completed, with the team's findings now published online ahead of print in the Journal of Clinical Oncology, or JCO. Philip L. McCarthy, MD, Director of the Blood and Marrow Transplant Program at Roswell Park Cancer Institute, was principal investigator for one of the three clinical studies that are reported in this updated analysis, and is first author of the publication that compiles the international team's findings and analysis.

The new study is a "meta-analysis" reporting updated findings from three large randomized, controlled clinical trials conducted in the U.S., France and Italy by the Alliance for Clinical Trials in Oncology (formerly CALGB), Intergroupe Francophone du Mylome (IFM) and Gruppo Italiano Malattie Ematologiche dell'Adulto (GIMEMA), respectively. The research team compared outcomes for 605 patients with newly diagnosed multiple myeloma who were treated with continuous lenalidomide (brand name Revlimid) following autologous hematopoietic stem cell transplant, also known as bone marrow transplant, and 604 patients who received either a placebo or no maintenance at all.

The meta-analysis has allowed the team to evaluate for the first time, across all three studies, whether overall survival improved for patients receiving long-term treatment with oral lenalidomide following stem cell transplant.

At seven years of observation, the authors report, 62% of those treated with maintenance lenalidomide had survived, compared to 50% of those in the control group. "The use of lenalidomide maintenance for transplantation-eligible patients can be considered a standard of care," they write, noting recent refinements that have improved the efficacy of pre-transplant induction chemotherapy and autologous stem cell transplant.

"With this complete and mature data from three large multinational studies, we now have clear evidence that ongoing treatment with lenalidomide can prevent disease progression and extend survival in patients with multiple myeloma who've received a stem cell transplant," says Dr. McCarthy, Professor of Oncology at Roswell Park and also Professor of Internal Medicine at the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo. "All the investigators wish to express enormous gratitude to the patients who took part in these trials. Many others will benefit from their role in this research."

These study results were presented in abstract form at the 52nd annual meeting of the American Society of Clinical Oncology in Chicago and the 21st Congress of the European Hematology Association, Copenhagen, Denmark, both held in June 2016, and in March 2017 at the 16th International Myeloma Workshop in Delhi, India. Earlier this year, the U.S. Food and Drug Administration and its European counterpart, the European Medicines Agency, approved use of lenalidomide as maintenance therapy for multiple myeloma patients following transplant; this study was part of the regulatory submissions for those approvals.

The new publication, "Lenalidomide Maintenance After Autologous Stem-Cell Transplantation in Newly Diagnosed Multiple Myeloma: A Meta-Analysis," is available at ascopubs.org.

This press release is also available on the Roswell Park website: https://www.roswellpark.org/media/news/international-lenalidomide-trials-show-survival-benefit-maintenance-therapy-following

###

The mission of Roswell Park Cancer Institute (RPCI) is to understand, prevent and cure cancer. Founded in 1898, RPCI is one of the first cancer centers in the country to be named a National Cancer Institute-designated comprehensive cancer center and remains the only facility with this designation in Upstate New York. The Institute is a member of the prestigious National Comprehensive Cancer Network, an alliance of the nation's leading cancer centers; maintains affiliate sites; and is a partner in national and international collaborative programs. For more information, visit http://www.roswellpark.org, call 1-877-ASK-RPCI (1-877-275-7724) or email askrpci(at)roswellpark.org. Follow Roswell Park on Facebook and Twitter.

For the original version on PRWeb visit: http://www.prweb.com/releases/2017/08/prweb14605233.htm

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Roswell Park-Led Analysis Shows Survival Benefit of Lenalidomide Maintenance Therapy Following Transplant - Benzinga

Earlier had a guest on that protects it you might just that might we'll just talk music you know but yes I've done and yes. We have another and now I. You felt it just at the time we got her elbow and grad and out whose family owns the Portland sea dogs and I had to admit I'd bounce the first pitch up. Portland seed in their video of this hole and I thought I asked rotate another chance to sit. Her family owns the airport into dogs and there's been. Apparently I Wii I know exactly where to go to the video thank you very much day. Any back to Mary's here and and her doctor doctor Robert Zoellick for. And that any. It's 27 years old hat Milo this plastic syndrome which I have to admit. I've been sixteen of these things but that's a new one on me at I don't think effort that went before what what exactly did in tale. Yes so it's blood disorder again normally found it again. Older folks. So it was sort of rare for at 25. Year old to be diagnosed with that. But certainly shared today is a bone marrow transplant so. I mean was it meant it to Dana Farber once I found out hands. Did three rounds of chemo outpatient acting forever. An and accepting of both Americans and last June. It's as the impatient at the breakdown. That doctor cipher was my transplant doctor and tenth harbor. And doctor Roberts worked for is here and I heard you say yes when she talked about the rarity of the disease how rare is it. How he treated well itself. It's the disease that as Annie said he's much more common old people. People in the 60s80s. Very uncommon. Twenty's. He can be treated with support here medications and little dose chemotherapy when picked Poulter. When patients younger. We generally want to all Americans clause with out of bone marrow transplant mild to split will lead to keep. And it becomes very eager to treat so. Despite the rarity of the disease and he was that. Attracted the entire time she just made it head on. Did it too tough to what I have to do. I'll take the chemotherapy in the transplant her sister was her daughter which is remarkable story also that. She showed remarkable courage through the entire process in and it even knows something was wrong or you feel like how long that laughed. Tired. Too. Much. The bar. Like an appealing their I don't got a good story and that's what you're gonna carry you through the. I cannot relate to that I. But it hadn't had it takes I knew something really often action difficult. Week. So. It's late night after what happened to inch its way. Saturday Javed Ali counted that's very Massachusetts. My word and act out there. That come back. It's. It doctor Lieberman can tear your donor with your sister Molly. I assume that might have been a ten for ten match perhaps. Yes it was an exact match was awesome. Sister is a senior at the academy's actors like frank. Steamers that reflects well. Making sure to keep a schedule worked with the sisters schedule them. In between graduation. Widgets so. I was really fortunate to. Match. A week later after such a perfect. It worked out I was able to hurt at mission. And I. Speaking we transplant a year after the transplant something significant happened in your life tell us what that is and. Yes so I got engaged. Almost. Exactly here after the transplant which was pretty special. Dan my fiance was served with me through the whole ride. So it was awesome very exciting ends. Its focus on planning a wedding now wedges. And that. All of that in the past years. And he was right there was Hewitt said he knows the real deal yeah really just aren't as good as our guys. Yep it's sealed the deal. And had a question for your doctors is finding that match fortunately she had a sister without match there for the bone marrow transplant was once the match but for those who don't have sisters don't have a brother that able to do that how tricky can nappy. Will things really change over the past five to eight years the better. Twenty years ago we would only do bone marrow transplant on a patient who had eight siblings a brother or sister who matched. At about fifteen years ago we started to transplants from unrelated donors volunteers dealers. Who were able to actually provided the source of stem cells and actually good outcomes. More recently we've been able to even use half matches so even a win eight other sister does it. Match fully ten out of ten match dale said a week you actually get by with a five of ten match almost as well as we can't attempt. Our friend Tara who's going to be here tomorrow had her bone marrow transplant in November. And I know she was kind of isolated for about nine months I assume you've had a similar sort of regiment you had to go through. Yes of the first hundred days I was inside you know sort of contact them on in the outside world besides my family. So I was definitely tough and then. I work for an Austin Co. act Clijsters and so I was able to work from home through the spring. And they were awesome. Sort of helping me get through flu season because my immune system. Receivers susceptible to catching something. So yeah I was you know at home until April. Answered just get getting back in readjusted to you. I. It's a real family affair doc watched any buyers Oprah folks beyonc really all came together it. That'll give her support of actually help keep healthy. A community effort. When's the wedding I'd accept. If congratulations a couple of things that couples swapping one you do work out some companies how to increase in credit out of great Fredricka. And secondly in the scouting reports and future sea dogs that we should be looking out or. Bully doesn't devers Africans as loyal you know he's doing pretty well. Commandant and the obviously. I don't have a scouting report right now but I'm sure things. You're in the nickel you need a great little bull market. Yeah it's I'd love going up there and Ankara practice hitting get a chance to. Endeavour's much he was there are very now really kind of scooted through town and yes. Now he's here hitting home runs things like every every game every other game. We took into been intently from you two's yeah. Yeah I'm not a you've got your children to this point yes it's critical to see them say it. Progress. It's to fat cats watch. Well it's great to visit with both of you and MacNamara fallible Malone multi faceted. Can not just in case you didn't hear ripped up. And doctor Robert Lichter thanks you guys that are very much for coming in it's great people that it. Thanks for having classy guys into the past. Thank you thank you and good luck with a wedding thank you and I hear from September whenever that is good luck. Think it's.

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DHK - Annie McNamara, 27, myelodysplastic syndrome, Boston, with Dr. Robert Soiffer, chief, Hematologic ... - WEEI.com