alberto kornblihttUltraviolet radiation from the sun can zap DNA, damage cells, and set the stage for the subsequent development of cancer. Scientists have now identified the built-in safety mechanism that forces some cells damaged by UV radiation to commit suicide so they do not perpetuate harmful mutations.

Alberto R. Kornblihtt, a Howard Hughes Medical Institute international research scholar at the University of Buenos Aires and the National Research Council of Argentina, has found that UV radiation causes human cells to create proteins that trigger cell death. It’s a built-in safety pathway whose precise mechanism had never been seen before.

by Monya Baker

Two papers point to how cancer cells go astray

A growing body of research in breast cancer, leukaemia and brain cancer shows that cancer stem cells co-opt the pathways of regular stem cells to maintain themselves and resist treatments. Two recent studies in acute myeloid leukaemia have used very different techniques that each point to the likelihood of uncovering strategies to target cancer stem cells while sparing healthy stem cells.

jpan massagueResearchers have uncovered the first genetic clues that suggest how invasive breast cancer cells pry their way into the tightly protected interior of the brain, where they can grow into new and lethal tumors. Howard Hughes Medical Institute researcher Joan Massagué and colleagues at Memorial Sloan-Kettering Cancer Center have identified three genes that work together to fuel the spread of breast cancer to the brain.

Their studies indicate that those renegade cancer cells use some of the same strategies that other breast cancer cells rely on to invade the lungs – but also need more specialized molecular tools to infiltrate the brain. The study is reported in an advance online publication on May 6, 2009, in the journal Nature.

by Monya Baker

Two research teams follow cancer to its source

According to two papers published in Nature this month, colon cancer tumours originate from normal stem cells. Both studies show that, when a cell-signaling pathway is misregulated, rare stem cells within the small intestine initiate cancer.

 Much cancer stem cell work sorts through human tumour cells and transplants them into mice to identify a subset capable of initiating tumours anew. Not only is this approach challenged by cross-species differences and other transplantation techniques, but also it does not identify the original 'bad apples' from which the cancerous cells arose. Now, working in genetically engineered mice, two teams of researchers have been able to find the source of these cells. Both systems track the formation of aberrant growths from the crypt stem cells of the small intestine.

by Monya Baker

The cell cycle inhibitor p21 gives cancer cells the chance to repair DNA

To sustain disease, leukemia stem cells have to keep on dividing. To do so cells require a counterintuitive resource: a protein that keeps cells from proliferating. Work reported in Nature this month shows that, by giving cancer stem cells a chance to slow down and repair DNA damage, the protein p21, a cell-cycle inhibitor, not only helps cancer maintain itself, it helps leukemia evade therapies designed to kill rapidly dividing cells. Drugs that inhibit p21 or DNA repair, then, might help leukemia speed up and self destruct.

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