Posted on 06/24/2009 11:33:12 PM PDT by CutePuppy
Just-released research about a new class of drugs called “PARP inhibitors” is the most exciting development in cancer research in a decade or more. In just a few years it could save thousands of lives.
In the longer term, the drugs could represent a transformational approach to understanding and treating several forms of the disease.
All this enthusiasm is based on a small report published today in the New England Journal of Medicine. It focuses on one clinical trial in its earliest stage in 60 patients with breast, ovarian and prostate cancer. Some — but not all — of the patients whose cancers seemed hopeless saw them shrink drastically or disappear. Many avoided the typical side effects — nausea, hair loss — associated with cancer treatment.
.....
PARP inhibitors kill cancer cells
The next big discovery came in 2005 when scientists found in lab experiments that they could make a drug, called a PARP inhibitor, that would interfere with the normal copy of the protein made from BRCA1 and BRCA2 genes. If cells have defective genes, when the drug is added, the DNA cannot be repaired at all. As a result, the cells die. And that is how PARP inhibitors kill cancer cells.
In experiments so far, the drugs have worked only in people with BRCA 1 and BRCA2 mutations resulting in breast, ovarian and prostate cancers. But there is evidence they may work in people without the mutations — particularly in cases of ovarian cancer for which better treatments are desperately needed.
The story of the PARP inhibitors is fine example of how research can move from the laboratory bench to the bedside, and it also shows how long and difficult journey can be.
(Excerpt) Read more at msnbc.msn.com ...
Yes, very smart, as opposed to the brute force approach of cooking cells or poisoning the body, hoping the cancer dies first.
The latest advances in RNA research (microRNA, rRNA, siRNA etc.) to treat various diseases and different forms of cancer are simply awesome.
Hmm... sounds alright... but wouldnt it be improved by adding some foetal stem cells, freshly harvested from fetuses? /s
Check out Dendreon’s prostate cancer immunotherapy for prostate cancer, it's almost there, with almost NO side effects. www.dendreon.com
And they have candidates ready for development or in clinical trials for breast, colon, head and neck.
If obi’s health care plans go through, they can drop all this expensive research and just let the patients die. Or even help them along a bit. Too expensive to take care of all those sick people.
I think / hope it’s less than 10 years, even with all the FDA bureaucracy. There are a number of companies (Dendreon and SiRNA Therapeutics/Merck including) with RNAI based drugs in Phase III and/or late stage Phase II programs.
Many of them are promising and a radical departure from brute force chemo / radiation therapies that take huge toll on the human system. That includes various forms of cancer and offshoots, like wet AMD, melanoma, pancreatic etc. which are notoriously difficult to treat now.
Thanks for linking the printer friendly version.
New Drug Targeting Cancer Weakness Shows Great Promise
Inhibition of Poly(ADP-Ribose) Polymerase in Tumors from BRCA Mutation Carriers
The New England Journal of Medicine article may require registration, not subscription. Did somebody say Nobel?
...interfere with the normal copy of the protein made from BRCA1 and BRCA2 genes. If cells have defective genes, when the drug is added, the DNA cannot be repaired at all. As a result, the cells die. And that is how PARP inhibitors kill cancer cells.What have they got for the Troubled Asset Relief Program (TARP)?
Olaparib was given to 19 patients with inherited forms of advanced breast, ovarian and prostate cancers caused by mutations of the BRCA1 and BRCA2 genes.
In 12 of the patients - none of whom had responded to other therapies - tumours shrank or stabilised.
The study, led by the Institute of Cancer Research, features in the New England Journal of Medicine.
CASE STUDY
Julian Lewis, 62, was treated with olaparib after being diagnosed with advanced prostate cancer.
Within a month or two levels of a key chemical marker of cancer went down to a low level, and have now stayed low for more than two years.
In addition, secondary tumours in his bones have almost disappeared.
He has experienced minor side-effects, such as stomach discomfort and mild nausea, but he said: "I hope to carry on with this for as long as possible. Partly the aim is the obvious one of keeping my cancer cells in check, but there's a broader goal too: to help find out how long this drug can be used safely in other people."
One of the first patients to be given the treatment is still in remission after two years.
Olaparib - a member of a new class of drug called PARP inhibitors - targets cancer cells, but leaves healthy cells relatively unscathed.
The researchers, working with the pharmaceutical company AstraZeneca, found that patients experienced very few side-effects, and some reported the treatment was "much easier than chemotherapy".
Researcher Dr Johann de Bono said the drug should now be tested in larger trials.
He said: "This drug showed very impressive results in shrinking patients' tumours.
"It's giving patients who have already tried many conventional treatments long periods of remission, free from the symptoms of cancer or major side-effects."
Olaparib is the first successful example of a new type of personalised medicine using a technique called "synthetic lethality" - a subtle way of exploiting the body's own molecular weaknesses for positive effect.
In this case the drug takes advantage of the fact that while normal cells have several different ways of repairing damage to their DNA, one of these pathways is disabled by the BRCA mutations in tumour cells.
Olaparib blocks one of the repair pathways by shutting down a key enzyme called PARP.
..... This does not affect normal cells because they can call on an alternative repair mechanism, controlled by their healthy BRCA genes.
..... But there is evidence that olaparib will also be effective in other cancers with different defects in the repair of DNA.
..... The researchers say the process of drug evaluation and registration may have to be revamped to take consideration of the fact that new generation cancer drugs target specific molecular defects, rather than types of cancer.
Dr Peter Sneddon, of the charity Cancer Research UK, said: "It is very encouraging to see the development of 'personalised treatment', tailored to the requirements of the individual patient, becoming a reality as it offers the opportunity to design new drugs that are truly selective. .....
I saw a short piece on the tube about this earlier today, so did some Googling.
PARP inhibitors work by turning off the DNA repair enzymes (or at least some of them). These seem to have a much worse effect on cancer cells because their DNA is typically more of a shambles than regular cells DNA.
So does this mean that it cures you from cancer but three years later, you die because all your (good) DNA has broken down?
Many times, extreme longitudinal studies seem to be overkill to me but in this case, I’d be real, real worried of the side effects.
Might turn out to be leprosy-in-a-pill.
Thnx. The articles I read didn’t mention alternative forms of DNA repair.
I read once that the guesstimate is that each strand of our DNA has 100,000 mutations per day, most caused by oxidants.
But most get repaired quickly, and even if they fail, well, heck, we’re diploid anyways!
Be they short or long, you gotta love proteins!
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