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Tag: cancer (page 3 of 4)

09.05.2012

new adrogen blocking drug approved for prostate cancer

From Elie Dolgin of Nature magazine covers the news:

Men with advanced prostate cancer now have another treatment option, thanks to the approval today by the US Food and Drug Administration (FDA) of a pill that blocks androgen-receptor signaling and prolongs patient survival.

“To see activity in a post-hormone treated, post-chemotherapy treated prostate cancer population with a drug that doesn’t have myelosuppression [a decrease in blood cell production] and does has a very favorable safety profile is extremely exciting,” says Howard Scher, a prostate cancer specialist at the Memorial Sloan-KetteringCancer Center in New York. “My patient who got the drug in July 2007 is still on it. I have chills actually. It’s pretty amazing.”

The newly approved agent—Xtandi (enzalutamide), developed by San Francisco’s Medivation and Japan’s Astellas Pharma—works by plugging up the receptors that bind androgens, including testosterone, to prevent those male hormones from fueling the growth of prostate cancer cells. In a phase 3 clinical trial involving around 1,200 men with prostate cancer that had spread despite prior chemo- and hormone-therapy, an international team led by Scher found that participants taking Xtandi lived a median of 18.4 months, compared to 13.6 months for those who received a placebo. The drug also significantly lowered levels of prostate-specific antigen and boosted the time of progression-free survival, with only minimal side effects of fatigue, diarrhea and rare seizures. The results were reported earlier this month in the New England Journal of Medicine.

Read the complete coverage here.

08.29.2012

using HIV to fight cancer

A model of HIV.

HIV, like other viruses, mutates rapidly in response to changes in its environment. This ability to rapidly change gives them the ability to evade the natural defense mechanisms our bodies trigger once we are infected. Researchers have found a way to exploit this property of HIV to generate proteins that will help fight cancer. From Popular Science:

As HIV replicates, it creates slightly new versions of itself over successive generations – this allows it to readily resist most of the drug cocktails and anti-viral treatments developed to fight it. But it could also allow HIV to serve as a sort of molecule factory, creating new iterations of compounds that work in slightly different ways.

The CNRS team modified the genome of HIV by inserting a human gene for a protein called deoxycytidine kinase (dCK). This protein is found in all cells and is important for activating anti-cancer drugs. Researchers would like to make a more potent form of dCK that would allow cancer drugs to work more effectively, which could in turn require less of them, causing fewer side effects and less toxicity.

The team multiplied this mutant HIV through several generations, yielding an entire library of mutant dCK proteins, about 80 in all. Ultimately, they found a variant that induces tumor cells to die. With just 1/300th the dose of cancer-killing drugs, this one-two protein punch is just as effective at stopping tumor growth.

For more read here. For the original research paper from PLoS Genetics go here.

03.27.2012

protein regulates spread of cancer cells

Every medical press release promises to hold the key to the world’s greatest therapy and this one is no different.  Scientists have found that a protein called S100PBP suppreses another protein, cathepsin Z, generating conditions that allow pancreatic cancer cells to spread into surrounding tissues. This will revolutionize therapeutics for pancreatic cancer, which is one of the hardest cancers to diagnose and treat. From Eureka Alert:

Researchers at Queen Mary, University of London have identified a new protein that makes pancreatic cancer cells less ‘sticky’ and therefore less able to attach to and invade other tissue.

The protein, known as S100PBP, does this by suppressing a second protein called cathepsin Z. The research team has shown that cathepsin Z makes pancreatic cancer cells sticky, allowing them to spread to their surrounding environment. Prior to this study nothing was known about the function of S100PBP in the body or the role that cathepsin Z plays in pancreactic cancer.

The findings, funded by the UK charity, Pancreatic Cancer Research Fund (PCRF), are reported today (26 March 2012) in TheAmerican Journal of Pathology.

Lead researcher Dr Tatjana Crnogorac-Jurcevic of Barts Cancer Institute at Queen Mary said: “We believe these findings are significant. A greater understanding of the role these proteins play in the adhesion and spread of pancreatic cancer to other organs, which is almost always the case in this deadly cancer, could help us to develop novel preventive and therapeutic targets.”

More here (press release) and here (abstract):

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