In the past researchers have observed an association between poor mitochondrial function and Parkinson's disease, a neurodegenerative disorder of the central nervous system that impairs speech and motor functions and affects five million people worldwide. A new meta-analysis suggests that low expression levels of 10 related gene sets responsible for mitochondrial machinery play an important role in this disorder--all previously unlinked to Parkinson's. The study, published online today in Science Translational Medicine , further points to a master switch for these gene sets as a potential target of future therapies. [More]

Editor's Note: This is an expanded version of the Q&A that will appear in the November 2010 issue of Scientific American.

Name: Greg Graffin [More]

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Realistic stem cell therapies to replace diseased or damaged tissue may still be years away, but researchers have uncovered a promising new use for these undifferentiated cells: they can be programmed to become patient-specific laboratory models of inherited liver disease. These new tools could be useful for teasing out disease mechanisms and testing new drug therapies.

Scientists from the University of Cambridge's Institute for Medical Research obtained skin cells from 10 patients--seven who had various forms of inherited liver disease, and three healthy controls. They reprogrammed the skin cells, rejuvenating them into an embryolike state (using the four-gene approach described in 2007). The researchers then cultured these so-called induced pluripotent stem cells (iPS cells) in a mixture of chemical factors that triggered their conversion into liver cells, which had the appearance and functional properties of native liver cells.

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Stem cell - Cambridge University - Liver - Medical Research - Disease

Product marketing teams look at the software buying cycle as a consistent series of steps: awareness, consideration, trial, purchase, implementation and renewal.   For years, these steps have been manipulated through solution selling  where the key to success is control.  By knowing the buyer, the steps and the product, a skilled selling team is able to control the process and predict favorable outcomes on a consistent basis.  Oracle, SAP and Mic … Read More

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GE Healthcare announced that the Smart Patient Room pilot at Bassett Medical Center has been approved by the site’s Institutional Review Board to begin data collection. The innovative technology solution was installed as part of GE’s healthymagination initiative with the goal of helping healthcare providers to reduce patient safety risks and improve patient outcomes.

“GE is developing a unique solution for the healthcare industry that helps hospitals and staff identify and mitigate patient safety risks while offering meaningful solutions to improve patient outcomes,” said Jan De Witte, President & CEO, GE Healthcare Performance Solutions. “GE’s real-time, adaptable solution will provide actionable data to healthcare providers regarding patient safety and potential medical errors which in turn will affect the necessary behavioral changes to avoid preventable errors.”

The Smart Patient Room can collect real-time information from the system to generate actionable data to manage clinical workflow, and uncover opportunities for influencing process and behavioral changes to create a safer patient environment.

developers at Mount Sinai develop a New database and software, called ChEA which can speed up drug discovery at Mount Sinai develop a New database and software, called ChEA which can speed up drug discovery

The ChEA software and ChIP-X database is freely available online at:http://amp.pharm.mssm.edu/lib/chea.jsp.

until ChEA was developed, no centralized database integrated results from, for instance, ChIP-seq and ChIP-chip experiments (these are used to identify how “transcription factor” proteins might regulate all genes in humans and mice). Now this new computational method should help streamline how scientists analyze these gene expression experiments

Do we have to kill the last CML cell? DM Ross, TP Hughes and JV Melo, Leukemia 2010(Sep 16) [Epub ahead of print][FriendFeed entry][PubMed citation][Full text]. The abstract of this OA review:

Previous experience in the treatment of chronic myeloid leukaemic (CML) has shown that the achievement of clinical, morphological and cytogenetic remission does not indicate eradication of the disease. A complete molecular response (CMR; no detectable BCR-ABL mRNA) represents a deeper level of response, but even CMR is not a guarantee of elimination of the leukaemic, because the significance of CMR is determined by the detection limit of the assay that is used. Two studies of imatinib cessation in CMR are underway, cumulatively involving over 100 patients. The current estimated rate of stable CMR after stopping imatinib is approximately 40%, but the duration of follow-up is relatively short. The factors that determine relapse risk are yet to be identified. The intrinsic capacity of any residual leukaemic cells to proliferate following the withdrawal of treatment may be important, but there may also be a role for immunological suppression of the leukaemic clone. No currently available test can formally prove that the leukaemic clone is eradicated. Here we discuss the sensitive measurement of minimal residual disease, and speculate on the biology of BCR-ABL-positive cells that may persist after effective therapy of CML.

Critical molecular pathways in cancer stem cells of chronic myeloid leukemia by Y Chen, C Peng, C Sullivan, D Li and S Li, Leukemia 2010(Sep); 24(9): 1545-54. Epub 2010 Jun 24. [Connotea bookmark][PubMed citation][Full text]. The abstract of this OA review:

Inhibition of BCR-ABL with kinase inhibitors in the treatment of Philadelphia-positive (Ph(+)) chronic myeloid leukemia (CML) is highly effective in controlling but not curing the disease. This is largely due to the inability of these kinase inhibitors to kill leukemia stem cells (LSCs) responsible for disease relapse. This stem cell resistance is not associated with the BCR-ABL kinase domain mutations resistant to kinase inhibitors. Development of curative therapies for CML requires the identification of crucial molecular pathways responsible for the survival and self-renewal of LSCs. In this review, we will discuss our current understanding of these crucial molecular pathways in LSCs and the available therapeutic strategies for targeting these stem cells in CML.

Insights into the stem cells of chronic myeloid leukemia by I Sloma, X Jiang, A C Eaves and C J Eaves, Leukemia 2010(Sep 23). [Epub ahead of print][PubMed citation]. Abstract:

Chronic myeloid leukemia (CML) has long served as a paradigm for generating new insights into the cellular origin, pathogenesis and improved approaches to treating many types of human cancer. Early studies of the cellular phenotypes and genotypes represented in leukemic populations obtained from CML patients established the concept of an evolving clonal disorder originating in and initially sustained by a rare, multipotent, self-maintaining hematopoietic stem cell (HSC). More recent investigations continue to support this model, while also revealing new insights into the cellular and molecular mechanisms that explain how knowledge of CML stem cells and their early differentiating progeny can predict the differing and variable features of chronic phase and blast crisis. In particular, these emphasize the need for new agents that effectively and specifically target CML stem cells to produce non-toxic, but curative therapies that do not require lifelong treatments.

Surprise breast cancer source by Jennifer Welsh,TheScientist.com, September 2, 2010. First paragraph:

Some breast cancer tumors may not originate from stem cells as previously believed, according to a study published in the September 3rd issue of Cell Stem Cell. The discovery is an important step in the development of treatments for these cancers.

This news story is based on the publication: BRCA1 Basal-like Breast Cancers Originate from Luminal Epithelial Progenitors and Not from Basal Stem Cells by Gemma Molyneux and 11 co-authors, including Matthew J Smalley, Cell Stem Cell 2010(Sep 3); 7(3): 403-417. OA article [Full text] [PubMed citation].

A commentary: Cancer Cell of Origin: Spotlight on Luminal Progenitors by Christine L Chaffer and Robert A Weinberg, Cell Stem Cell 2010(Sep 3); 7(3): 271-272. [PubMed citation].

Tumor-Initiating Cells Are Rare in Many Human Tumors by Kota Ishizawa and 16 co-authors, including Benjamin G Neel and William Matsui, Cell Stem Cell 2010(Sep 3); 7(3): 279-282. [FriendFeed entry][PubMed citation]. Abstract:

Tumor-initiating cells (TICs) are defined by their ability to form tumors after xenotransplantation in immunodeficient mice and appear to be relatively rare in most human cancers. Recent data in melanoma indicate that the frequency of TICs increases dramatically via more permissive xenotransplantation conditions, raising the possibility that the true frequency of TICs has been greatly underestimated in most human tumors. We compared the growth of human pancreatic, non-small cell lung, and head and neck carcinomas in NOD/SCID and NSG mice. Although TIC frequency was detected up to 10-fold higher in NSG mice, it remained low (<1 in 2500 cells) in all cases. Moreover, aldehyde dehydrogenase-positive (ALDH(+)) and CD44(+)CD24(+) cells, phenotypically distinct cells enriched in TICs, were equally tumorigenic in NOD/SCID and NSG mice. Our findings demonstrate that TICs are rare in these cancers and that the identification of TICs and their frequency in other human malignancies should be validated via primary tumors and highly permissive xenotransplantation conditions.