This painkiller may slow the growth of cancer

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One of the most widely prescribed pain and anti-inflammation drug may also slow the growth rate of cancer, a new study has found. The study focused on the effects of celecoxib or Celebrex.
It targets an enzyme called "cyclooxygenase-2" (COX-2), which is linked to pain and inflammation, researchers said. This enzyme is also critical in the creation of prostaglandins, compounds that act like hormones and play a role in promoting tumour growth, they said. COX-2 expression is typically low in normal tissue, but high in multiple types of cancers, researchers said.

 "We were actually interested in determining what a particular signalling pathway does in cancer," said Joseph Kissil from The Scripps Research Institute (TSRI) in the US. "In the process, we found that it activates genes that promote survival of tumour cells and that they do so by turning on enzymes involved in inflammation, including COX2, which anti-inflammatory drugs like Celebrex inhibit," said Kissil.

Researchers conducted animal studies tracking the effects of celecoxib on the growth of cancer cells from a tumour type known as neurofibromatosis type II (NF2). In humans, NF2 is a relatively rare inherited form of cancer caused by mutations in the anti-tumour gene NF2, which leads to benign tumours of the auditory nerve, researchers said.

Animals received a daily dose of the drug, and tumour growth was followed by imaging. Analysis of the results showed a significantly slower tumour growth rate in celecoxib-treated models than in controls, they said. Using various approaches, the study also showed that a signalling cascade known as the Hippo-YAP pathway is involved in these results and that the protein YAP is required for the proliferation and survival of NF2 cells and tumour formation.

"Our study shows that COX2 inhibitors do have an effect on the tumour cells. They also have an impact on inflammatory responses that play a role in tumour growth," said William Guerrant from TSRI. "It is possible that in other cancers these effects might actually be stronger because of the drug's impact on inflammation," he said.

The findings were published in the journal Cancer Research.

New drug for inherited cancer identified

 Scientists have identified a new drug that can potentially treat an inherited form of cancer that has no cure.

 The new study showed the drug candidate - known as FRAX97 - slowed the proliferation and progression of tumour cells in animal models of Neurofibromatosis type 2.

This inherited type of cancer, caused by mutations in the anti-tumour gene NF2, leads to tumours of the auditory nerve that connects the inner ear to the brain.

 The new compound, originally developed to treat neuro-degenerative disease, targets a protein family known as p21-activated kinases or PAKs.

 These kinases (enzymes that add a phosphate group to other proteins and change their function) play a critical role in the development of Neurofibromatosis type 2. PAK1 has also been implicated in the growth of breast and lung cancers.

 "Our study shows that if we inhibit these kinases we can counter the formation of tumours in this brain disease," said an  associate professor who led the study.

 In the new study, researchers showed that the inhibitor slows down progression of Neurofibromatosis type 2 in animal models and reduces more than 80 per cent of PAK1 activity.

They noted a key challenge in developing drug candidates is finding potential agents that are both potent and highly selective for their targets - limiting its action to the desired arena and reducing unwanted side effects.

 "This inhibitor turned out to be both potent and highly selective," he said.

 "The real question is why. We were able to show that it works through a unique mechanism," he said.

 While the binding site on PAK1 is quite large, it also contains a smaller pocket, a kind of back-room that juts off the larger site.

 The inhibitor not only takes up space in the larger site, but enters the back pocket as well. That extra binding gives the inhibitor its strong selectivity.

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