Group items matching

in title, tags, annotations or url

In situ hybridization (ISH) may not be a new phrase for today's Biological world. It has not been in this industry for long, but its promising future, without any doubt, is recognized by more biologists and institutions. In situ hybridization (ISH) is a technology being made up of combinations of molecular biology, histochemistry and cytology.

Vitamin D's days of obscurity seem pretty much over. Once just an afterthought to most people-relegated to the sides of milk cartons and the pages of medical texts-it's now on the cusp of becoming a full-fledged disease prevention star. Although vitamin D has long been known as an important factor in bone health, a quickly growing body of evidence now shows that it may also help lower the risk of cancer, heart disease, and even premature death.[1], [2] Not surprisingly, scientists and the public have started to take Note, particularly of vitamin D's potential to protect against cancer

The in vitro study, reported in the journal Carcinogenesis (Vol. 27, pp. 32-42), showed that vitamin D, in the form of the highly active 1alpha, 25-dihydroxyvitamin D3 (1,25-VD), inhibited the function of protease enzymes that are involved in tumour invasion. "We found that 1,25-VD decreased matric metalloproteinases (MMP-9) and cathepsins (CPs), while it [also] increased the activity of their counterparts, tissue inhibitors of metalloproteinase-1 (TIMP-1) and cathepsin inhibitors," wrote lead author Bo-Ying Bao from the University of Rochester and Taipei Medical University. "Mechanistic studies showed that 1,25-VD did not suppress MMP-9 expression at the transcriptional level, but reduced its mRNA stability," said Bao.

Vitamin D may not just be good for you, it may help save your life. Recent research from Johns Hopkins University suggests that higher amounts of vitamin D in your diet decreases your likelihood of dying. Studies found that a vitamin D deficiency increases your risk of death by 26 percent, and vitamin D decreases the mortality rate from almost every type of cancer including breast, colon and prostate. Research also suggests that vitamin D helps prevent diabetes, kidney disease and cardiovascular disease.

Complementary and alternative medicine (CAM) and complementary and integrative medicine (CIM) are therapies of proven or unproven efficacy that have been used to promote wellness, to manage symptoms associated with cancer and its treatment or to treat cancer. When properly combined with standard cancer treatments, some complementary therapies can enhance wellness and quality of life, but others may be harmful during or after treatment for cancer. Most, but not all, are natural products.

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

WARNING: This page was NOT created or approved by any doctor or medical researcher. The purpose of this page is to provide hard-to-find information on copper reduction cancer treatment, a new unapproved and experimental course of cancer treatment whose ef

CancerGuide is a cancer information page written by Steve Dunn, a fellow patient. I strongly believe, and indeed I know from personal experience, that information can save your life. This page is dedicated to helping cancer patients find the best treatment for their disease by finding, and understanding, the best and latest information on their disease. The focus here is on technical information. While this page does offer links to the best cancer information sources on the net, what makes this page special is no holds barred help and information about things on and off the net from someone who's been been where you are now. The information on this page is information with a point of view, not information sanitized by committee!

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. Michelakis ED, Webster L, Mackey JR. Br J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review. PMID: 18766181 doi:10.1038/sj.bjc.6604554 The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials More than 40 nonrandomised trials of DCA in small cohorts of patients have been reported, but the first two randomised control trials of chronic oral therapy with DCA in congenital mitochondrial diseases were reported in 2006. In the first, a blinded placebo-controlled study was performed with oral DCA administered at 25 mg kg-1 day-1 in 30 patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) (Kaufmann et al, 2006). Most patients enrolled in the DCA arm developed symptomatic peripheral neuropathy, compared with 4 out of 15 in the placebo arm, leading to the termination of the study. Seventeen out of 19 patients had at least partial resolution of peripheral neurological symptoms by 9 months after discontinuation of DCA. This neurotoxicity res

"Compounds similar to those found in cannabis have been shown to stop prostate cancer cells from multiplying. Two cannabinoid compounds, JWH-015 and MET, stopped prostate tumour growth in human prostate cells in Petri dishes and also in mice with the disease. They halted the cell-division cycle and killed the cancer cells, and had the greatest effect on aggressive prostate cancer cell types, which do not respond to hormone treatments. Some 192,000 men in the US alone are diagnosed with prostate cancer each year, and researchers Inés Díaz-Laviada Marturet at the University of Alcalá, Spain, and her colleagues say the results could offer hope to those affected. But before you go looking for a dealer, New Scientist answers a few questions"

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.

Actually there is no such medical condition called "throat cancer", although a number of sorts of cancer can arise in the throat and neck.

It is a cancer of the cells which form the structure of the stomach and intestine, not a cancer of the linings of the organ itself (that would be a carcinoma).

With out proper insurance, cancer sufferers can find themselves surrounded by piles and piles of medical bills and not sure what transfer to make next.

One prostate problem does not lead to another. For example, having prostatitis or an enlarged prostate does not increase the chance for prostate cancer.

T-helper/T-regulator lymphocyte ratio as a new immunobiological index to quantify the anticancer immune status in cancer patients. Brivio F, Fumagalli L, Parolini D, Messina G, Rovelli F, Rescaldani R, Vigore L, Vezzo R, Vaghi M, Di Bella S, Lissoni P. In Vivo. 2008 Sep-Oct;22(5):647-50. PMID: 18853761 RESULTS: The mean TH/TR ratio observed in patients with metasytases was significantly lower with respect to that found in both patients without metastases and controls. On the contrary, the absolute mean number of T-reg cells was higher in patients with metastases than in those without, but the difference was not statistically significant. CONCLUSION: The evaluation of T-reg cells in terms of their proportion with respect to T-helper cell total number seems to be more appropriate than the simple measurement of their absolute count, in order to quantify cancer-related immunosuppression. Thus, the TH/TR ratio could represent a useful biological marker to explore the immune status of cancer patients.

D structure of the virus, known as Seneca Valley Virus-001, reveals that it is unlike any other known member of the Picornaviridae viral family, and confirms its recent designation as a separate genus "Senecavirus." The new study reveals that the virus's outer protein shell looks like a craggy golf ball¬-one with uneven divets and raised spikes-and the RNA strand beneath it is arranged in a round mesh rather like a whiffleball. "It is not at all like other known picornaviruses that we are familiar with, including poliovirus and rhinoviruses, which cause the common cold," says the study's senior author, Associate Professor Vijay S. Reddy, Ph.D., of The Scripps Research Institute. "This crystal structure will now help us understand how Senecavirus works, and how we can take advantage of it." The Senecavirus is a "new" virus, discovered several years ago by Neotropix Inc., a biotech company in Malvern, Pennsylvania. It was at first thought to be a laboratory contaminant, but researchers found it was a pathogen, now believed to originate from cows or pigs. Further investigation found that the virus was harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer.

30 April,2007: Terminally ill patients with incurable cancers are increasingly using a compound via Internet trade that is not yet approved, reports Nature. The 'drug' in question -- dichloroacetate (DCA) - has been but found shrinking tumours in rats but yet to put on studies to ascertain its safety in human use.