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Nobel laureate James Watson publishes novel hypothesis on curing late-stage cancers
Date:1/8/2013

eat Britain's Royal Society.

He proposes that the cell-killing ability of currently used anti-cancer therapies toxic chemotherapeutic agents such as Taxol as well as radiation treatment is mainly due to the action of ROS to induce apoptosis, or programmed cell death. This would explain "why cancers that become resistant to chemotherapeutic control become equally resistant to radiotherapy." The common feature would be their common dependence upon a ROS-mediated cell-killing mechanism.

Watson, who is Chancellor Emeritus of Cold Spring Harbor Laboratory, then takes up the case of cancer cells largely driven by mutant proteins such as RAS and MYC. These, he notes, are often hardest to get to respond to treatment. He suggests this could be due to their high levels of ROS-destroying antioxidants. He cites recent research showing up-regulation of a gene transcription factor called Nrf2 when cells proliferate as well as when oncogenes such as RAS, MYC and RAF are active. Nrf2 controls the synthesis of antioxidants, and "this makes sense because we want antioxidants present when DNA functions to make more of itself," Watson writes.

In calling for "a much faster timetable for developing anti-metastatic drugs," the Nobel laureate wants those reading his new paper to consider a proposition he considers grossly underexplored: "Unless we can find ways of reducing antioxidant levels, late-stage cancer 10 years from now will be as incurable as it is today."


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Contact: Peter Tarr
tarr@cshl.edu
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert

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