CONTEXT: B vitamins and factors related to 1-carbon metabolism help to maintain DNA integrity and regulate gene expression and may affect cancer risk. OBJECTIVE: To investigate if 1-carbon metabolism factors are associated with onset of lung cancer. DESIGN, SETTING, AND PARTICIPANTS: The European Prospective Investigation into Cancer and Nutrition (EPIC) recruited 519,978 participants from 10 countries between 1992 and 2000, of whom 385,747 donated blood. By 2006, 899 lung cancer cases were identified and 1770 control participants were individually matched by country, sex, date of birth, and date of blood collection. Serum levels were measured for 6 factors of 1-carbon metabolism and cotinine. MAIN OUTCOME MEASURE: Odds ratios (ORs) of lung cancer by serum levels of 4 B vitamins (B(2), B(6), folate [B(9)], and B(12)), methionine, and homocysteine. RESULTS: Within the entire EPIC cohort, the age-standardized incidence rates of lung cancer (standardized to the world population, aged 35-79 years) were 6.6, 44.9, and 156.1 per 100,000 person-years among never, former, and current smokers for men, respectively.

Earlier studies have shown that resveratrol could induce death in several human
cancer cell lines in culture. Here we report our observation that resveratrol
can also promote the growth of certain human cancer cells when they are grown
either in culture or in athymic nude mice as xenografts. At relatively low
concentrations (</=5 microM), resveratrol exerted a significant
growth-stimulatory effect in the MDA-MB-435s human cancer cells, but this effect
was not observed in several other human cell lines tested. Analysis of cell
signaling molecules showed that resveratrol induced the activation of JNK, p38,
Akt, and NF-kappaB signaling pathways in these cells. Further analysis using
pharmacological inhibitors showed that only the NF-kappaB inhibitor (BAY11-7082)
abrogated the growth-stimulatory effect of resveratrol in cultured cells. In
athymic nude mice, resveratrol at 16.5 mg/kg body weight enhanced the growth of
MDA-MB-435s xenografts compared to the control group, while resveratrol at the
33 mg/kg body weight dose did not have a similar effect. Additional analyses
confirmed that resveratrol stimulated cancer cell growth in vivo through

Biologist Doug Inkley – BP Oil Ashore ‘just the tip of the iceberg’

How can benzene affect my health?

Breathing very high levels of benzene can result in death, while high
levels can cause drowsiness, dizziness, rapid heart rate, headaches,
tremors, confusion, and unconsciousness. Eating or drinking foods
containing high levels of benzene can cause vomiting, irritation of the
stomach, dizziness, sleepiness, convulsions, rapid heart rate, and
death.

The major effect of benzene from long-term exposure is on the blood.
Benzene causes harmful effects on the bone marrow and can cause a
decrease in red blood cells leading to anemia. It can also cause
excessive bleeding and can affect the immune system, increasing the
chance for infection.

Some women who breathed high levels of benzene for many months had
irregular menstrual periods and a decrease in the size of their ovaries,
but we do not know for certain that benzene caused the effects. It is
not known whether benzene will affect fertility in men

Read more at : http://bpoilleak.org/

I was just asked by PM about the latest, rather strong confirmation of an elevated risk of cancer in users of folic acid supplements. The person noted that the mechanism is probably because of increased folic acid availability for nucleotide synthesis, for which many cancers have an unusually-high demand, so that the risk would be to people who already have a cancer in their body, whereas "the rest of us" wouldn't be providing 'permission' for growth to nonexistant cancers.

Thiamine deficiency frequently occurs in patients with advanced cancer and therefore thiamine supplementation is used as nutritional support. Thiamine (vitamin B1) is metabolized to thiamine pyrophosphate, the cofactor of transketolase, which is involved in ribose synthesis, necessary for cell replication. Thus, it is important to determine whether the benefits of thiamine supplementation outweigh the risks of tumor proliferation. Using oxythiamine (an irreversible inhibitor of transketolase) and metabolic control analysis (MCA) methods, we measured an in vivo tumour growth control coefficient of 0.9 for the thiamine-transketolase complex in mice with Ehrlich's ascites tumour. Thus, transketolase enzyme and thiamine clearly determine cell proliferation in the Ehrlich's ascites tumour model. This high control coefficient allows us to predict that in advanced tumours, which are commonly thiamine deficient, supplementation of thiamine could significantly increase tumour growth through transketolase activation.

Patients with heart disease in Norway, a country with no fortification of foods with folic acid, had an associated increased risk of cancer and death from any cause if they had received treatment with folic acid and vitamin B12, according to a study in the November 18 issue of JAMA.

Most epidemiological studies have found inverse associations between folate (a B vitamin) intake and risk of colorectal cancer, although such associations have been inconsistent or absent for other cancers, according to background information in the article. "Experimental evidence suggests that folate deficiency may promote initial stages of carcinogenesis, whereas high doses of folic acid may enhance growth of cancer cells. Since 1998, many countries, including the United States, have implemented mandatory folic acid fortification of flour and grain products to reduce the risk of neural-tube birth defects," the authors write. "Recently, concerns have emerged about the safety of folic acid, in particular with respect to cancer risk."

OBJECTIVE: To examine whether antioxidant supplement use is associated with melanoma risk in light of recently published data from the Supplementation in Vitamins and Mineral Antioxidants (SUVIMAX) study, which reported a 4-fold higher melanoma risk in women randomized to receive a supplement with nutritionally appropriate doses of antioxidants. DESIGN: Population-based prospective study (Vitamins and Lifestyle [VITAL] cohort). SETTING: Western Washington State. PARTICIPANTS: A total of 69 671 men and women who self-reported (1) intake of multivitamins and supplemental antioxidants, including selenium and beta carotene, during the past 10 years and (2) melanoma risk factors on a baseline questionnaire. Main Outcome Measure Incident melanoma identified through linkage to the Surveillance, Epidemiology, and End Results (SEER) cancer registry. RESULTS: Cox proportional hazards regression models were used to estimate multivariable relative risks (RRs) and 95% confidence intervals (CIs) for multivitamin, supplemental selenium, and supplemental beta carotene use.

Prostate cancer (CaP) is a significant cause of death in American men. While men residing in Asia show a lower incidence of hormone-refractory prostate cancer (HRPC) compared to Caucasian males, Asian men who move to and live in the United States and adopt a western lifestyle have HRPC rates indistinguishable from Caucasian males. These findings suggest that Asian diets contain ingredients that might protect against the development of HRPC. The identity and mechanisms of such HRPC protective agents remain to be elucidated. An Asian diet may confer protection against HRPC owing to functional synergy between bioactive dietary agents, thus broadening the chemopreventive index, with increased distinct anticancer properties and decreased untoward effects. Here, whether or not a combination of epigallocatechin gallate (EGCG), genistein and quercetin, phytochemicals present in a traditional Asian diet, might exert synergy in controlling proliferation and gene expression was investigated in CWR22Rv1 CaP cells, an in vitro model mimicking CaP transition from AD (androgen dependence) to HRPC.

A research article to be published on September 28, 2009 in the World Journal of Gastroenterology addresses this question. The research team, led by Prof. Zong-fang Li from the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, investigated the effects of Chrysanthemum indicum extract (CIE) on inhibition of proliferation and on apoptosis, and the underlying mechanisms, in a human HCC MHCC97H cell line.

They examined viable rat hepatocytes and human endothelial ECV304 cells by trypan blue exclusion and MTT assay, respectively, as normal controls. The proliferation of MHCC97H cells was determined by MTT assay. The cellular morphology of MHCC97H cells was observed by phase contrast microscopy. Flow cytometry was performed to analyze cell apoptosis with annexin V/propidium iodide (PI), mitochondrial membrane potential with rhodamine 123 and cell cycle with PI in MHCC97H cells. Apoptotic proteins such as cytochrome C, caspase-9, caspase-3 and cell cycle proteins, including P21 and CDK4, were measured by Western blotting.

ABSTRACT: BACKGROUND: Blueberries may lower relative risk for cancers of the gastrointestinal tract. Previous work indicated an inhibitory effect of consumed blueberry (BB) on formation of aberrant crypt foci (ACF) in colons of male Fisher F344 rats (inbred strain). However, effects of Blueberry on colon tumors and in both genders are unknown.

The cancer stem cell hypothesis suggests that, unlike most cancer cells within a tumor, cancer stem cells resist chemotherapeutic drugs and can regenerate the various cell types in the tumor, thereby causing relapse of the disease. Thus, drugs that selectively target cancer stem cells offer great promise for cancer treatment, particularly in combination with chemotherapy. Here, we show that low doses of metformin, a standard drug for diabetes, inhibits cellular transformation and selectively kills cancer stem cells in four genetically different types of breast cancer. The combination of metformin and a well-defined chemotherapeutic agent, doxorubicin, kills both cancer stem cells and non–stem cancer cells in culture. Furthermore, this combinatorial therapy reduces tumor mass and prevents relapse much more effectively than either drug alone in a xenograft mouse model. Mice seem to remain tumor-free for at least 2 months after combinatorial therapy with metformin and doxorubicin is ended.

"We have found a compound selective for cancer stem cells," said senior author Kevin Struhl, the David Wesley Gaiser professor of biological chemistry and molecular pharmacology at HMS. "What's different is that ours is a first-line diabetes drug."

The findings add to a growing body of preliminary evidence in cells, mice, and people that metformin may improve breast cancer outcomes in people. In this study, the diabetes drug seemed to work independently of its ability to improve insulin sensitivity and lower blood sugar and insulin levels, all of which are also associated with better breast cancer outcomes.

The results fit within the cancer stem cell hypothesis, an intensely studied idea that a small subset of cancer cells has a special power to initiate tumors, fuel tumor growth, and promote recurrence of cancer. Cancer stem cells appear to resist conventional chemotherapies, which kill the bulk of the tumor.