Scientists Discover Gene Mutation Common in a Class of Ovarian Cancers

2010-09-08 10:48 (0 comments)

hhmi.org:

Discovery Provides Strong Link between Genetics and Epigenetics of Cancer

A study of aggressive ovarian tumors has revealed a new class of major cancer-driving mutations. Howard Hughes Medical Institute (HHMI) researchers found that most of the clear cell ovarian carcinoma samples they studied carried a gene mutation that alters the epigenetics of cells.

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Use the Common Cold Virus to Target and Disrupt Cancer Cells?

2010-08-26 15:01 (0 comments)

sciencedaily.com:

A novel mechanism used by adenovirus to sidestep the cell's suicide program, could go a long way to explain how tumor suppressor genes are silenced in tumor cells and pave the way for a new type of targeted cancer therapy, report researchers at the Salk Institute for Biological Studies in the Aug. 26, 2010 issue of Nature.

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Vitamin D Deficiency as a Risk Factor for Multiple Sclerosis

2010-06-15 11:52 (0 comments)

rndsystems.com:

Multiple sclerosis (MS) is an autoimmune neurological disorder that affects over 2 million people worldwide. Onset of the disease is thought to occur following exposure of genetically predisposed individuals to an unknown environmental trigger that activates myelin-specific T cells. These cells cross the blood-brain barrier to trigger an inflammatory attack that demyelinates axons in the central nervous system. Polymorphisms in the vitamin D receptor are among the genetic variations that increase the risk of MS. The incidence of MS is also elevated in northern climates, where vitamin D deficiency is common. Since exposure of the skin to ultraviolet light aids in the conversion of inactive vitamin D to the active form, the short days, low UV intensity, and lack of exposed skin common to winter months, decrease the amount of active VitD3 that can be produced. Although the correlation between VitD3 deficiency and MS is intriguing, we are only now beginning to understand the biology that may explain this connection. In both human MS and in experimental autoimmune encephalomyelitis (EAE), the mouse model of the disease, VitD3 can influence specialized populations of cells that may play a critical role in protection against the disease. VitD3 promotes the formation of tolerogenic or “semi-mature” dendritic cells (DCs). These DCs induce the development of CD25–FoxP3+/–IL-10++ Tr1 cells, a subset of regulatory T cells (Treg), and downregulate the production of Th1 inflammatory cells. A pair of interacting co-inhibitory proteins, B7-H1 (also known as PD-L1) and PD-1, appear to be critical molecules in this process.

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Bestätigung der Virushypothese und Immunschwäche als Krankmacher (PubMed, Raltegravir, XMRV)

2010-04-01 02:01 (0 comments)

PubMed:

Raltegravir is a potent inhibitor of XMRV, a virus implicated in prostate cancer and chronic fatigue syndrome

Abstract

BACKGROUND: Xenotropic murine leukemia-related retrovirus (XMRV) is a recently discovered retrovirus that has been linked to human prostate cancer and chronic fatigue syndrome (CFS). Both diseases affect a large fraction of the world population, with prostate cancer affecting one in six men, and CFS affecting an estimated 0.4 to 1% of the population.

PRINCIPAL FINDINGS: Forty-five compounds, including twenty-eight drugs approved for use in humans, were evaluated against XMRV replication in vitro. We found that the retroviral integrase inhibitor, raltegravir, was potent and selective against XMRV at submicromolar concentrations, in MCF-7 and LNCaP cells, a breast cancer and prostate cancer cell line, respectively. Another integrase inhibitor, L-000870812, and two nucleoside reverse transcriptase inhibitors, zidovudine (ZDV), and tenofovir disoproxil fumarate (TDF) also inhibited XMRV replication. When combined, these drugs displayed mostly synergistic effects against this virus, suggesting that combination therapy may delay or prevent the selection of resistant viruses.

CONCLUSIONS: If XMRV proves to be a causal factor in prostate cancer or CFS, these discoveries may allow for rational design of clinical trials.

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Vitamin C restores healthy aging in a mouse model for Werner syndrome

2010-01-09 16:26 (0 comments)

www.fasebj.org:

Werner syndrome (WS) is a premature aging disorder caused by mutations in a RecQ-like DNA helicase. Mice lacking the helicase domain of the WRN homologue exhibit many phenotypic features of WS, including a prooxidant status and a shorter mean life span compared to wild-type animals. Here, we show that Wrn mutant mice also develop premature liver sinusoidal endothelial defenestration along with inflammation and metabolic syndrome. Vitamin C supplementation rescued the shorter mean life span of Wrn mutant mice and reversed several age-related abnormalities in adipose tissues and liver endothelial defenestration, genomic integrity, and inflammatory status. At the molecular level, phosphorylation of age-related stress markers like Akt kinase-specific substrates and the transcription factor NF- ${kappa}$ B, as well as protein kinase C ${delta}$ and Hif-1 ${alpha}$ transcription factor levels, which are increased in the liver of Wrn mutants, were normalized by vitamin C. Vitamin C also increased the transcriptional regulator of lipid metabolism PPAR ${alpha}$ . Finally, microarray and gene set enrichment analyses on liver tissues revealed that vitamin C decreased genes normally up-regulated in human WS fibroblasts and cancers, and it increased genes involved in tissue injury response and adipocyte dedifferentiation in obese mice. Vitamin C did not have such effect on wild-type mice. These results indicate that vitamin C supplementation could be beneficial for patients with WS.

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Vitamin C Enhances the Generation of Mouse and Human Induced Pluripotent Stem Cells

2010-01-09 16:21 (0 comments)

www.cell.com/cell-stem-cell/:

Somatic cells can be reprogrammed into induced pluripotent stem cells (iPSCs) by defined factors. However, the low efficiency and slow kinetics of the reprogramming process have hampered progress with this technology. Here we report that a natural compound, vitamin C (Vc), enhances iPSC generation from both mouse and human somatic cells. Vc acts at least in part by alleviating cell senescence, a recently identified roadblock for reprogramming. In addition, Vc accelerates gene expression changes and promotes the transition of pre-iPSC colonies to a fully reprogrammed state. Our results therefore highlight a straightforward method for improving the speed and efficiency of iPSC generation and provide additional insights into the mechanistic basis of the reprogramming process.

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Could Anti-Inflammatory Drugs Block Early Progression of Alzheimer's?

2009-11-25 18:15 (0 comments)

lerner.ccf.org:

New research points to inflammation within the brain as a critical contributor to neuronal abnormalities leading to Alzheimer's disease (AD) and suggests that early and prolonged treatment with common nonsteroidal anti-inflammatory drugs (NSAIDs) could block this inflammation before the disease establishes itself.

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Arnold Hilgers Institute

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