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Cancer Drugs’ Secrets Discovered

October 7, 2009 by ·

cancer drug's secrets discovered_Scientists have discovered why a particular group of cancer drugs are so effective at fighting the disease. Although they have been used for years to treat certain tumors, researchers did not know exactly how they worked.

A team from Dundee University studied the NEDD8 molecule, known to play an important role in turning on p53, a gene which inhibits a cell’s growth.

They found that by blocking NEDD8, cancer drugs were able to switch on p53 causing the death of the cancer cells. Experts believe the discovery could allow the development of drugs to treat more cancers.

NEDD8 works by attaching itself to other proteins – a process called NEDDylation – to alter their properties.

The Dundee team, led by Dr Dimitris Xirodimas, found that NEDDylation stops certain proteins leaving a specialised area of the cell.

Impeding this allows the proteins to move and gives the signal for p53 to be activated, killing the cancer cells.

Dr Dimitris Xirodimas said the team were very excited about the findings. He added: “A pharmaceutical company has recently developed chemicals which block the NEDDylation reaction and these compounds are currently being tested in clinical trials for the treatment of cancer.

“Our research reinforces the value of this work and opens up avenues for the development of new ways to treat cancer.”

‘Potential therapies’

The findings, being presented by Cancer Research UK’s chief scientist Prof Sir David Lane at the NCRI Cancer Conference in Birmingham later, are published in EMBO Reports.

The study was funded by the Association for International Cancer Research (AICR). The charity’s, scientific advisor, Dr Mark Matfield said: “The significance of this discovery is that it could lead to drugs that would be effective against a wide range of cancers.\

“Over the last decade, many of the new cancer drugs have only been useful for a few, specific cancers.

“What we really need are effective broad range cancer therapies.”

Prof Sir David Lane, Cancer Research UK’s chief scientist said: “p53 is missing or faulty in almost half of all cancers and there are 270,000 new cases of cancer in the UK each year so by understanding potential therapies can switch it on and off is an important part of the search for new potential therapies.” BBC News.

Filed Under: Disease, Drugs, Medical Research & Study ·

Understanding DNA Defects Is Route To Better Cancer Therapy

October 5, 2009 by ·

understanding dna defects_Cancer is at its root a disease of the genes. Whether a tumour affects the lungs, brain or breast, it is the result of a cell that has acquired the capacity to divide unchecked because of mutations in its DNA.

These mutations can be inherited, they can be the result of environmental carcinogens such as cigarette smoke or they can accumulate through errors copied during cell division — all three routes, indeed, are often involved.

This genetic background to all cancers offers an exciting route to better therapy, because the precise pattern of DNA defects that drives a tumour will influence its growth, its spread and the way it responds to treatment.

Drugs such as Herceptin, for breast cancer, are already taking healthcare towards more personalised medicine. Herceptin is highly effective but only against breast tumours with a particular genetic profile, and it must be prescribed accordingly.

Oncologists will be able to select the most appropriate treatment for almost any patient by sequencing the DNA of his or her tumour, and then using the combination of drugs that is likely to be most effective.

Two major hurdles stand in the way, however. The first is the cost of sequencing the genome of a tumour — about $50,000 (£31,362), although this will likely drop to about $1,000 within two years.

The second is a lack of understanding about which mutations and combinations of mutations drive tumours, and how they affect susceptibility to drugs. This is where projects such as the drug database at St George’s, University of London, will be pivotal.

The aim is to help researchers to “mix and match” drugs and cancer mutations, to determine combinations of defects that predict whether a given medicine is likely to work.

Last year, The Times revealed the launch of a similar initiative from the Sanger Institute near Cambridge and Massachusetts General Hospital in Boston. It will examine 1,000 colonies of cancer cells with known genetic defects, which will be exposed to 400 chemical agents to identify which colonies are susceptible to which drugs.

Such studies also have the potential to “rescue” drugs that have failed clinical trials for broad-spectrum use, either because they do not work for enough patients, or cause serious side-effects for a minority.

Some of these may prove to be both safe and effective for patients with a particular genetic profile. It is interesting to note that one “rescued” drug — thalidomide — is among those on the St George’s database.

What is happening now for cancer is also likely, in the longer term, to change the way that many other medical conditions are treated. Cancer may be the most obvious common disease with a genetic root, but it is far from the only one: disorders such as type 2 diabetes and heart disease also have a strong genetic component, and the DNA you inherit also affects the way your body metabolises drugs.

As more of these genetic variations become understood, doctors will increasingly start to practise “pharmacogenomics” for all manner of diseases, precribing drugs and other treatments according to their patients’ DNA profiles. The days when computerised tools like the St George’s database are used routinely in healthcare are probably not far off.  By Mark Henderson, The Times.

Filed Under: Disease, Health, Medical Research & Study ·

Study Offers Clues On Diet Benefits Without The Diet

October 2, 2009 by ·

study offers clues on diet_Experiments which mimicked a low-calorie diet by tinkering with genes in mice extended their lives and prevented disease, and a drug that has the same effect could give people longer, healthier lives, scientists said on Thursday.

British researchers found that deleting a gene linked to nutrients and growth helped mice to live 20 percent longer on average, and partly explained why eating less appears to improve health and increase longevity.

The findings also offered a possible genetic drug target for protecting against aging-related diseases, they said.

“What we have shown is that this gene is one that regulates life span and also determines how healthy animals are in middle and late age,” said Dominic Withers of the Center for Diabetes and Endocrinology at University College London.

Withers and his colleagues used so-called knockout mice — mice bred with a certain gene removed or knocked out — in this case the ribosomal S6 protein kinase 1 (S6K1) gene.

Deleting S6K1 meant the mice’s bodies behaved in a similar way to mammals whose calorie intake is restricted, they said.

“These mice were resistant to type 2 diabetes … and they also appeared to have reduced incidence of the mouse-equivalent of osteoporosis — so they had stronger bones,” Withers said.

Balance, strength and coordination all improved in the knockout mice, and they were more inquisitive, suggesting their brains were healthier.

“Our results demonstrate that S6K1 influences healthy mammalian life span,” the researchers wrote in their study published in the journal Science.

Most calorie restriction studies have found that a lifetime of deprivation is needed to achieve the longer-life benefits, and many researchers are working on ways to replicate the findings with drugs.

Withers said he knew of various pharmaceutical companies looking at developing drugs that could manipulate the S6K1 pathway, and his study showed they may also prove useful in age-related diseases, assuming they are safe in the long term.

But he also noted that his study had shown that another well-known target, known as AMP-activated protein kinase or AMPK, was on the same pathway as S6K1, meaning existing drugs could be explored to see if they might have the same effect.

Metformin — a common diabetes drug that works by stimulating AMPK, a master circuit for energy metabolism in the body — could be examined in this context, he said.

Since people live far longer than mice, it is almost impossible to study fully the effects of restricting calories in humans, but this study in mice and another recently in monkeys offer good clues for humans, Withers said.

“The big implication is that intervening in aging protects against a broad spectrum of aging-related diseases, and there is now a druggable pathway providing a means to do this which could be used, in principle, in people,” he said.

Researchers reported in August that the antibiotic rapamycin, sold by Wyeth under brand Rapamune to suppress the immune system in transplant patients, showed promise at slowing age-related disease in older mice, but it is not clear how it works. By China Daily.

Filed Under: Health, Medical Research & Study ·

Killer Prostate Cancer Test Hope

September 25, 2009 by ·

prostate cancer_Scientists have discovered a protein that predicts survival from prostate cancer at diagnosis. A University of Liverpool team found the presence of heat shock protein-27 (Hsp-27) was a key marker of how prostate cancer would progress.

Men who tested positive for Hsp-27 at diagnosis were almost twice as likely to die from the disease in the next 15 years than those who did not.

The study features in the British Journal of Cancer. Aggressive prostate cancer can kill rapidly, and requires immediate treatment.

However, prostate tumours can also be very slow-growing, and people who develop them often end up dying of unrelated conditions.

It can be difficult to distinguish between the two forms of the disease, and consequently many men end up unnecessarily undergoing intensive treatment which carries a risk of side effects.

The Liverpool team analysed tissue samples taken from 553 men at the time they were diagnosed with prostate cancer.

Their findings suggest testing for Hsp-27 might be a more reliable way of determining whether a tumour is aggressive or not.

Lead researcher Professor Chris Foster said: “Our study shows that this protein marker can give us a reliable and accurate indication of whether individual cancers will become aggressive.

“Currently, we are working on developing this finding into a blood test to monitor men with prostate cancer in order to determine when their individual disease needs treatment.” Hsp-27 is a key component of signalling pathways that control the movement of cells around the body.

The study also suggests that new drugs could be developed to block these signals and halt the spread of prostate cancer cells.

Important step

Dr Lesley Walker, director of cancer information at the charity Cancer Research UK, said: “These results are an important step towards tackling the long-standing question of how to treat men with prostate cancer once it has been diagnosed.

“The need for treatment varies greatly between patients – men with non-aggressive cancer can live with it for many years without needing therapy, while aggressive cancers require prompt treatment with combinations of surgery, radiotherapy and chemotherapy.

“A marker molecule which identifies aggressive prostate cancer would help us target active treatment to patients who need it – avoiding unnecessary therapy, which can have side effects, to those who don’t.”

Jon Neate, chief executive of the Prostate Cancer Charity, said much research was under way to try to develop a more accurate diagnostic test.

He said: “It is critically important to develop a test for prostate cancer which is able to distinguish reliably between aggressive and slow growing forms of the disease.”

Prostate cancer is the most common cancer in men in the UK, with about 34,000 new cases diagnosed every year.

About 10,000 men die from the disease each year in the UK. Several tests are currently used to diagnose prostate cancer, including testing for levels of a protein called prostate-specific antigen (PSA).

A high level of PSA can be a sign of cancer – but average levels tend to rise with age, and so the test can be unreliable. BBC News.

Filed Under: Health News, Medical Research & Study ·

Vegetarian Diet ‘Weakens Bones’

September 20, 2009 by ·

vegetarian diet 'weakens bones'_People who live on vegetarian diets have slightly weaker bones than their meat-eating counterparts, Australian researchers said Thursday.

A joint Australian-Vietnamese study of links between the bones and diet of more than 2,700 people found that vegetarians had bones five percent less dense than meat-eaters, said lead researcher Tuan Nguyen.

The issue was most pronounced in vegans, who excluded all animal products from their diet and whose bones were six percent weaker, Nguyen said.

There was “practically no difference” between the bones of meat-eaters and ovolactovegetarians, who excluded meat and seafood but ate eggs and dairy products, he said.

“The results suggest that vegetarian diets, particularly vegan diets, are associated with lower bone mineral density,” Nguyen wrote in the study, which was published Thursday in the American Journal of Clinical Nutrition.

“But the magnitude of the association is clinically insignificant,” he added.

Nguyen, who is from Sydney’s Garvan Institute for Medical Research and collaborated on the project with the Pham Ngoc Thach University of Medicine in Ho Chi Minh City, said the question of whether the lower density bones translated to increased fracture risk was yet to be answered.

“Given the rising number of vegetarians, roughly five percent (of people) in western countries, and the widespread incidence of osteoporosis, the issue is worth resolving,” he said. By Canada.com

Filed Under: Food, Medical Research & Study ·