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The discovery of WWP2 could lead to new drug advancements within the next decade  (Source:
Could lead to the development of new drugs for aggressive cancers within the next decade

University of East Anglia researchers may have found a way to prevent the spread of cancer through the discovery of a rogue gene. 

Andrew Chantry, study leader from the University of East Anglia's School of Biological Sciences, and Dr. Surinder Soond, of the University of East Anglia, have discovered a rogue gene that, if blocked by proper medication, could prevent the spread of cancer

The discovery of the rogue gene came about when the team of researchers was studying 'Smads,' which are natural cancer cell inhibitors in the human body. 

The rogue gene is called WWP2, and it is an enzymic bonding agent. It is found within cancer cells and helps the spread of cancer by attacking Smads in the human body, which are supposed to stop the spread of cancer. 

"The late stages of cancer involve a process known as metastasis - a critical phase in the progression of the disease that cannot currently be treated or prevented," said Chantry. "The challenge now is to identify a potent drug that will get inside cancer cells and destroy the activity of the rogue gene. This is a difficult but not impossible task, made easier by the deeper understanding of the biological processes revealed in this study."

In the lab, researchers found that the levels of the natural inhibitor increased when WWP2 was blocked. This caused the cancer cells to remain dormant. 

Chantry and Soond hope this research leads to the development of drugs that can block WWP2. This would allow Smads to prevent the spread of cancer, and doctors could perform surgery on primary tumors without worrying about the spread of the disease.  

According to Chantry, these drugs could be developed within the next decade, taking researchers one step closer to success in the war on cancer. They're aiming to stop the spread of some of the most aggressive cancers such as brain, colon, skin and breast cancer

This study was published in Oncogene.

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RE: Lets see
By mac2j on 1/24/2011 2:09:53 PM , Rating: 2
The FDA process is terrible, about 5x slower than it needs to be, and I would say as a doctor that hundreds of thousands of people die each year needlessly because of it.

We have a drug that showed the ability to cure cancer in otherwise untreatable animals 13 years ago. In clinical trials it can cure otherwise untreatable patients with widespread tumors and even those left uncured live substantially longer. BUT after 13 years the FDA is still thinking about it ... even after thousands of patients have now benefited from it in clinical trials. Some of the first patients given weeks to live are still alive, tumor-free 7+ years later.

Critically ill patients should at least be able to choose to try experimental medicines but they can't. The whole system needs to be revamped so that "lifestyle" medicines go through the current, stringent process and have post-approval follow-up (sorely lacking now) BUT life-saving medicines are made available ASAP.

RE: Lets see
By geddarkstorm on 1/24/2011 2:27:23 PM , Rating: 2
Really, and what drug is that?

The FDA does a vital role. They protect us from the companies just outputting a new snake oil once a week to fleece us with empty promises before we catch on. Think of Viocodin and Percocet which slipped by the FDA and were found to be deadly later on, and thus recalled. Without the FDA at all, that would be happening constantly.

You better believe we should be slow when it comes to drugs. Unintended consequences are the RULE and the NORM not the exception with drug design. And for very good biological reasons. We are all slightly chemically different, nothing will work for everyone, and there will always be side effects. It's a matter of balancing the good above the harm, and that's what the FDA process attempts to screen.

RE: Lets see
By jimhsu on 2/18/2011 2:11:46 PM , Rating: 2
#1 piece of advice for molecular animal studies: mice are not humans.

Just yesterday, our group discussed anthrax vaccine development and the suitability of the mouse model. There were a number of live attenuated and protein subunit vaccines that have AMAZING efficacy (near 100% survival against lethal challenge of anthrax spores) in mice, but are only weakly immunogenic in humans - thus you don't get much of an antibody response. Gamma tocopherols, a potent ROS/RNS and anti-inflammatory scavenger, on the other hand, have almost pathetic oral bioavailability in rats, but have reasonably bioavailability in humans, again due to any number of reasons.

Examples where animal studies do not translate into efficacious, well controlled human trials are everywhere. Literally thousands of anti-cancer drugs have been tried in animals, but failed to demonstrate safety, dose dependent therapeutic effects, or efficacy in humans. Just to get a reasonable example: AstraZeneca's zibotentan, a endothelial receptor inhibitor, passed all animal studies, safety, and even phase II, but failed to demonstrate prolonged survival in a phase III trial of prostate cancer ( ). These things literally happen every day.

Don't let anyone tell you that if something works in mice, it'll work in humans. But yes, people are desperate, and desperate people try these things. In fact, the FDA process allows critically ill, desperate patients to try these things ... and sometimes they do work. There's a reason they are experimental drugs though.

RE: Lets see
By jimhsu on 2/18/2011 2:17:01 PM , Rating: 2
Another example: PLX4032 ( ), a B-Raf inhibitor was a topic of a talk here a few months ago (about B-Raf). Promising results in animals, amazing results in humans against otherwise incurable melanoma cancers. Did people sign up? Of course. The only problem is that after 12 months or so, the tumor becomes resistant to PLX4032 inhibition and recurs. Is a 12 month increase in survival worth it? Of course, and it'll probably get FDA approved. But these things are by no means magic bullets.

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