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Cancer Cell

Scientists from the University of Southern California say fasting for short periods may help to combat cancer and boost the effectiveness of treatments.

Their study found fasting slowed the growth and spread of tumors and cured some cancers when it was combined with chemotherapy.

It is hoped that the discovery will prompt the development of more effective treatment plans and further research is now under way.

The study, published in the journal Science Translational Medicine, found that tumor cells responded differently to the stress of fasting compared to normal cells.

Instead of entering a dormant state similar to hibernation, the cells kept growing and dividing, in the end destroying themselves.

Lead researcher Professor Valter Longo, from the University of Southern California said: “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.”

Prof. Valter Longo and his team looked at the impact fasting had on breast, urinary tract and ovarian cancers in mice.

Fasting without chemotherapy was shown to slow the growth of breast cancer, melanoma skin cancer, glioma brain cancer and neuroblastoma – a cancer that forms in the nerve tissue.

In every case, combining fasting with chemotherapy made the cancer treatment more effective.

Multiple cycles of fasting combined with chemotherapy cured 20% of those with a highly aggressive form of cancer while 40% with a limited spread of the same cancer were cured.

None of the mice survived if they were treated with chemotherapy alone.

Researchers are already investigating the effects of fasting on human patients, but only a clinical trial lasting several years will confirm if human cancer patients really can benefit from calorie restriction.

However, they highlight that fasting could be dangerous for patients who have already lost a lot of weight or are affected by other risk factors, such as diabetes.

Results of a preliminary clinical trial will be presented at an annual meeting of the American Society of Cancer Oncologists (ASCO) in Chicago this June.

Prof. Valter Longo points out that the study only tests if patients could tolerate short fasts of two days before and one day after chemotherapy.

“We don’t know whether in humans it’s effective,” he said.

“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.”

Previous research led by Prof. Valter Longo showed that fasting protected normal cells from the effects of chemotherapy but it did not look at cancer cells.

It is now though fasting may be one way to make tumor cells weaker and more vulnerable.

Prof. Valter Longo added: “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.”

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Medical scientists have found a new form of mechanism leading to hereditary cancer susceptibility, demonstrating that minor changes in certain anti-cancer genes might work as magnets to draw altering “biochemical tags”.

The tags successfully switch these genes off as well as predispose families to a higher risk associated with the condition. The researchers, from the University of New South Wales (UNSW),  consider that a minor spelling error affecting just one letter in the DNA sequence close to the beginning of the gene is actually what draws in the biochemical marking, named methylation. This methylation switches genes off, thus has specific influences on the DNA.

“Methylation sits on top of our DNA, and provides the instructions to turn the gene off,” pointed out Dr Megan Hitchins.

In one well studied cause of hereditary cancer, alterations in the cancer-prevention gene MLH1 are transferred from mother or father to children. This situation generates up to 80 percent risk of developing bowel cancer, uterine cancer and other malignancies.

On the other hand, a number of family members with hereditary cancer do not have spelling mistakes in MLH1, but alternatively possess methylation placed on the gene.

“When the methylation attaches to the MLH1 gene in these families, it causes it to be completely switched off and as a consequence cancer develops,” affirmed head of the adult cancer program at the Lowy Cancer Research Centre, Professor Robyn Ward. “But until now, we did not understand how these methylation tags were being passed from parent to child.”

Hereditary cancer study

Hereditary cancer study: certain anti-cancer genes act like a magnet for methylation that disappears in semen or ova and reappears in child

In the study the researchers investigated three generations of a large family, who had experienced cancer at young age, but in whom no spelling mistakes characteristic for this kind of inherited cancer syndrome had been identified. Noticeably a number of family members from all generations had methylation tags on their gene.

“In this family, biochemical tags attached to the MLH1 gene were present in all three generations. This was intriguing since these markers are usually removed during the production of eggs and sperm. What we found was that a subtle change near the gene was acting like a magnet to attract methylation. So it was not the methylation itself that was being passed from parent to child, but rather the DNA change, and this acted as a methyl magnet,” Dr Megan Hitchins said.

The methylation had disappeared in the semen and ova and after that regenerated in every brand-new generation, the researchers explained.

Professor Robyn Ward said the study had specified the trigger of cancer in this family and it had provided new options for genetic diagnosis, counselling as well as early treatment in other families vulnerable to hereditary cancer.

The group is additionally studying the utilization of specific medications (Epigenetic Reversal Drugs) to remove the methylation in cancer, thus to switch the anti-cancer genes back on again. Later on these medicines might be administered in order to create a more specific method of cancer therapy and perhaps prevention.

Additional scientists linked to this research have been the Genetic Services of Western Australia and School of Paediatrics and Child Health, University of Western Australia.

The study on hereditary cancer was  published in the primary international journal “Cancer Cell”.