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ScienceDaily (June 11, 2009) - University of Florida researchers have come up with a new gene therapy method to disrupt cancer growth by using a synthetic protein to induce blood clotting that cuts off a tumor's blood and nutrient supply. In mice implanted with human colorectal cancer cells, tumor volume decreased 53 percent and cancer cell growth slowed by 49 percent in those treated with a gene that encodes for the artificial protein, compared with those that were untreated.

A ground-breaking Canada-wide clinical trial led by Dr. Katherine Borden, at the Institute for Research in Immunology and Cancer (IRIC) of the Universit de Montral, has shown that a common anti-viral drug, ribavirin, can be beneficial in the treatment of cancer patients. Published in the journal Blood (First Edition), the study demonstrates that ribavirin suppresses the activities of the eIF4E gene in patients. This gene is dysregulated in 30 percent of cancers including breast, prostate, head and neck, colon and stomach cancer.

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

The relevance of vitamin D receptor (VDR) gene polymorphisms for cancer: a review of the literature. Köstner K, Denzer N, Müller CS, Klein R, Tilgen W, Reichrath J. Anticancer Res. 2009 Sep;29(9):3511-36. Review. PMID: 19667145 CONCLUSION: Significant associations with VDR polymorphisms have been reported in cancer of the breast (Fok1, Bsm1, Taq1, Apa1, poly (A)), prostate (Fok1, Bsm1, Taq1, poly (A)), skin (Fok1, Bsm1, A-1210), colorectum (Fok1, Bsm1), ovary (Fok1, Apa1) and bladder (Fok1), and in renal cell carcinoma (Taq1, Apa1). However, conflicting data have been reported for most malignancies. After careful evaluation of the actual literature, it can be summarized that data indicating an association of VDR polymorphisms and cancer risk are strongest for breast cancer (Bsm1, Fok1), prostate cancer (Fok1) and malignant melanoma (MM) (Fok1). Data indicating an association of VDR polymorphisms and cancer prognosis are strongest for prostate cancer (Fok1), breast cancer (Bsm1, Taq1), MM (Bsm1) and renal cell carcinoma (Taq1).

Creative Bioarray provides different types of Custom gene specific FISH probes for rapid determination of gene copy number. Contact us for more information from our website.

Fish oil and treatment of cancer cachexia. Giacosa A, Rondanelli M. Genes Nutr. 2008 Apr;3(1):25-8. PMID: 18850196

n international consortium led by Baylor College of Medicine and The University of Texas M.D. Anderson Cancer Center has narrowed the search for the gene or genes associated with inherited susceptibility to glioma, a deadly form of brain Cancer, to a region on chromosome 17.

Blueberry Punch is an Australian product but is available for sale on the internet at £16 a bottle.\n\nIt also includes a host of other natural ingredients thought to boost health, including green tea, olive leaves, the herb tarragon and the spices turmeric and ginger.\n\nIt is thought the ingredients act together to cut inflammation and block a cancer gene.\n\nDr Jas Singh, who conducted the research on mice at Sydney University, said: "We have undertaken efficacy studies on individual components of Blueberry Punch in the same laboratory setting and found these effective in suppressing cell growth in culture.\n\n"We reasoned that synergistic or additive effects are likely to be achieved when they are combined."\n\nThe researchers looked at the effect of Blueberry Punch on both cancer cell cultures in the laboratory and genetically engineered mice with human prostate tumours. After only two weeks of having the syrupy solution added to their drinking water, their tumours had shrunk by

ScienceDaily (Feb. 22, 2009) - Cancer cells need a lot of nutrients to multiply and survive. While much is understood about how cancer cells use blood sugar to make energy, not much is known about how they get other nutrients. Now, researchers at the Johns Hopkins University School of Medicine have discovered how the Myc cancer-promoting gene uses microRNAs to control the use of glutamine, a major energy source. The results, which shed light on a new angle of cancer that might help scientists figure out a way to stop the disease, appear Feb. 15 online at Nature

Targeted cancer therapy and gene therapy have been mentioned in the blue before, but oncolytic viruses are the hot young thing. For consideration in cancer treatment, an virus must replicate in and kill a high number of exclusively cancer cells, while sparing healthy tissue. A Philadelphia-based company called Neotropix has won awards for its research into a prime contender - the Seneca Valley Virus. It has been the subject of Phase I adult clinical trials, with Phase II adult and Phase I pediatric clinical trials to start this year. SVV has advantages over some other contenders in that it is a naturally occurring (lest we create a race of mutant zombies) organism and studies so far suggest it is not harmful to healthy human cells. While a number of other oncolytic viruses are being examined, NTX-010 seems able to treat a very wide range of common and rare forms of cancer, some of which are now considered uniformly fatal. In addition, unlike some other tested viruses, it can travel through the bloodstream to treat metastatic and not just local disease. Compared to the side-effects and late effects of chemotherapy and radiation treatment, and because many of the cancers ideal for treatment with an oncolytic virus have no surgical options, this may be the next big breakthrough.

Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. Berquin IM, Min Y, Wu R, Wu J, Perry D, Cline JM, Thomas MJ, Thornburg T, Kulik G, Smith A, Edwards IJ, D'Agostino R, Zhang H, Wu H, Kang JX, Chen YQ. J Clin Invest. 2007 Jul;117(7):1866-75. PMID: 17607361 Our data suggest that modulation of prostate cancer development by polyunsaturated fatty acids is mediated in part through Bad-dependent apoptosis. This study highlights the importance of gene-diet interactions in prostate cancer.

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro

Creative Bioarray has developed cell immortalization service with a year of research and experience. We successfully immortalize cells of human, mouse and other animals using genes.

Nowadays, mutagenesis has become a widely used approach in DNA functional research and testing. Biologists in this field are devoting themselves to study and create new mutant genes that are beneficial to human development. The problems, however, still remain to be solved.

White button mushroom (Agaricus bisporus) exhibits antiproliferative and proapoptotic properties and inhibits prostate tumor growth in athymic mice. Adams LS, Phung S, Wu X, Ki L, Chen S. Nutr Cancer. 2008;60(6):744-56. PMID: 19005974

new (March 24th) report in Clinical Cancer Research, a journal of the American Association for Cancer Research, shows that Omega-3 fatty acids appear protective against advanced prostate cancer. Dr. John S. Witte, Ph.D., professor of epidemiology and biostatistics at the University of California San Francisco, says that previous research has shown protection against prostate cancer, but that this is one of the first studies to show protection against advanced prostate cancer.