Fasting Retards Tumor Growth

Fasting retards tumor growth

Fasting retards tumor growth

Friday, February 10, 2012. An article published on February 8, 2012 in Science Translational Medicine, one of the Science family of journals, reveals the discovery of a significant reduction in the growth of cancerous tumors subjected to short cycles of fasting. The regimen was found to improve the effect of chemotherapy but also worked well without drug treatment in cultured cancer cell lines and in mice.

"A limited time of exposure to a severely restricted diet (short-term starvation or fasting) can protect yeast, mammalian cells, mice, and possibly patients from the toxic effects of oxidative and chemotherapeutic agents without causing chronic weight loss," wrote University of Southern California professor of gerontology and biological sciences Valter D. Longo, PhD and his colleagues in their introduction to the article. "Fasting apparently protects normal cells by reallocating energy toward maintenance pathways from reproduction and growth processes when nutrients are scarce or absent. This switch to a protected mode occurs only in normal cells, not cancer cells, because oncogenes prevent the activation of stress resistance."

Dr Longo's team incubated different cancer cell lines in serum collected from mice that underwent 48 hour fasts or were allowed to eat as much as they liked. Breast cancer cells that were cultured in serum from animals that underwent fasting showed greater susceptibility to standard chemotherapies (doxorubicin and cyclophosphamide) compared to cells incubated in serum from non-fasted animals. When cancer cells were incubated in cultures containing glucose levels and growth factors comparable to those of fasted mice, proliferation and cell death increased in comparison to that observed in cells cultured in media that mimicked normally fed mice. Glucose and growth factor restriction sensitized 15 of 17 cancer cell lines to doxorubicin and/or cyclophosphamide, an effect that was reversed by treatment with insulin-like growth factor-1 in an experiment with one of the cell lines.

In studies with live mice that received implanted human and animal cancer tumors, animals that had access to only water for 48 to 60 hours experienced benefits in some cases that were comparable to chemotherapy, however, the greatest benefits were observed in animals that underwent both chemotherapy and fasting. In two experiments with mice injected with neuroblastoma cells, approximately 25 and 42 percent of fasted animals that received chemotherapy achieved long term survival, in contrast with zero chemotherapy-treated animals that consumed a normal diet.

Concerning the effects of fasting on cancer cells observed in the current series of experiments, Dr Longo explained that "The cell is, in fact, committing cellular suicide. What we're seeing is that the cancer cell tries to compensate for the lack of all these things missing in the blood after fasting. It may be trying to replace them, but it can't."

"A way to beat cancer cells may not be to try to find drugs that kill them specifically but to confuse them by generating extreme environments, such as fasting that only normal cells can quickly respond to," he added.

"We don't know whether in humans it's effective," Dr Longo cautioned. "It should be off limits to patients, but a patient should be able to go to their oncologist and say, 'What about fasting with chemotherapy or without if chemotherapy was not recommended or considered?"

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Metformin helps prevent breast cancer growth fueled by estrogen and other compounds

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An article published on November 23, 2011 in the journal PLoS One reports the finding of South Korean researchers of a protective benefit for the diabetes drug metformin against breast cancer cell growth stimulated by exposure to natural and synthetic chemicals.

James Trosko and his associates at Seoul National University's College of Veterinary Medicine studied the effects of metformin in miniature human breast cancer tumors grown in culture. The cells were exposed to the breast tumor-promoting hormone estrogen and the endocrine disruptors TCDD and bisphenol-A (BPA), resulting in an increase in tumor growth as well as increased expression of OCT4, a marker of cancer stem cells. Cancer stem cells have been recently demonstrated to sustain tumor growth and are resistant to anticancer therapies.

The addition of metformin resulted in a reduction in tumor size and number. In estrogen and TCDD-treated tumors, expression of OCT4 was also reduced.

"People with type-2 diabetes are known to be at high risk for several diabetes-associated cancers, such as breast, liver and pancreatic cancers," stated Dr Trosko, who is also a professor at Michigan State University College of Human Medicine's Department of Pediatrics and Human Development. "While metformin has been shown in population studies to reduce the risk of these cancers, there was no evidence of how it worked."

"While future studies are needed to understand the exact mechanism by which metformin works to reduce the growth of breast cancers, this study reveals the need to determine if the drug might be used as a preventive drug and for individuals who have no indication of any existing cancers," he added. "Though we still do not know the exact molecular mechanism by which it works, metformin seems to dramatically affect how estrogen and endocrine-disrupting chemicals cause the pre-existing breast cancers to grow."

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