Now Statin poisons which cause can Cancer are promoted to aid Cancer, all for PROFIT
HOW STATINS BEAT CANCER
A daily dose of statins could be the key to beating cancer
Friday January 20,2012
By Jo Willey
A DAILY dose of the cholesterol- busting heart pills called statins could be the key to beating cancer.
The tablets, which are already taken by millions every day to stave off heart attacks and stroke, have been shown to block the growth and spread of tumours.
The discovery, which has been hailed as having “great implications”, means that the cheap and effective daily pills could play a major role in slashing Britain’s cancer death toll.
Costing as little as 40p a day, they could also be a simple way of lowering the financial burden of the disease on the NHS.
If the latest findings are confirmed in clinical trials, it means patients could be given statins to help treat their tumours or even to prevent cancer striking in the first place.
Experts said they were “excited” by the findings, which could revolutionise treatment of the disease. Although the study was carried out on breast cancer, it is believed that statins could be effective against many other types of cancer. Researchers at Columbia University in New York, led by Dr Carol Prives, looked at the mutation of a gene called p53 that suppresses tumours.
Saying that statins are a potential new cancer treatment oversimplifies a very complicated picture
Because it has been identified as the most frequent abnormality detected in cancer, they believe understanding how it works could provide valuable information for treating or preventing the disease.
The scientists found a link between a cholesterol-building mechanism in the body and the disorganised cell growth which is characteristic of breast cancer.
Both involved defective versions of p53. More than half of all human cancers carry mutations in the gene. Many of these mutations do not simply disrupt the normal function of p53, they also give it new functions that fuel, instead of inhibit, the formation of cancer.
By studying cancer cells grown in an artificial system that resembles the human breast, the researchers learned that cells carrying mutant p53 grow in a haphazard and invasive manner, just like breast cancer.
When levels of the mutant gene were lowered, the cells grew more normally. And when cells which contained mutant p53 were treated with cholesterol-lowering statins, they stopped their invasive growth and in some cases even died.
Analysis of breast cancer tissue taken from patients then confirmed that p53 mutations and increased activity of cholesterol-building genes went hand-in-hand in human tumours.
Dr Prives said: “The data raises the possibility that we might identify patients whose tumours may respond to statins. Of course we can’t make any definitive conclusions until we know more.
“There are great implications. Perhaps one could do a clinical trial, and that may support these findings, or it may be more complicated.” The research is published in the journal Cell. Dr Caitlin Palframan, of the charity Breakthrough Breast Cancer, said: “We are excited that existing drugs, like statins, are showing potential in the fight against breast cancer.
“This research identifies a relatively large group of breast cancer patients who could be targeted with statins, though we will need to see the results of clinical trials to know whether this will work.” Artery-clearing statins are already credited with saving tens of thousands of lives each year from heart disease and stroke.
More than six million people take them every day to reduce harmful levels of “bad” cholesterol.
Cancer kills more than 156,000 people in Britain each year.
Studies have shown that women who develop a breast tumour are 30 per cent less likely to suffer a relapse if they take a specific type of statin called simvastatin. The pills have also been revealed to prevent prostate cancer from returning.
Dr Joanna Owens, of Cancer Research UK, said: “Saying that statins are a potential new cancer treatment oversimplifies a very complicated picture. The p53 protein is faulty in many types of cancer, but these faults can have several different effects alongside those studied in this research.
“These are laboratory findings and, as the researchers themselves point out, there’s a long way to go to find out if they apply to patients.”