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This Week in Science: Mar 21, 2014

Researchers from the Lunenfeld-Tanenbaum Research Institute at Toronto's Mount Sinai Hospital report in Science this week that mitotic cells inhibit DNA double-strand break repair to prevent telomere fusions. They found that mitotic kinases phosphorylate the E3 ubiquitin ligase RNF8 as well as the non-homologous end-joining factor 53BP1 to prevent them from being recruited to DSB sites. When they restored this function they found that repair resumed, but was deleterious as it led to Aurora B-dependent sister telomere fusions. "We conclude that cells must suppress DSB repair in mitosis because M-phase telomeres are prone to fusions," the researchers say.

Also in Science, Danish and Australian scientists provide an overview of mass spectrometry's development as a tool to study ancient proteins. Given that proteins degrade less rapidly than DNA and because some disease processes are characterized by unique protein expression patterns, mass spec technology has enabled researchers to study new aspects of disease pathologies that could not be looked at in DNA studies. Still, challenges remain for the analysis of ancient proteins, including the need to adapt methodologies currently used to examine modern proteins, contamination, and the lack of reference databases for proteins in extinct species, the researchers note.

In Science Translational Medicine, researchers in Paris and their colleagues examine the tumor microenvironment, with a particular focus on cytokines in colorectal cancers. The local expression of 13 cytokines changed in the disease, the researchers found, adding that metastatic patients in particular were more likely to have deletions of cytokines from chromosome 4. Deletion of interleukin 15 was linked not only to decreased IL15 expression, but also to a higher recurrence risk and lower patient survival, the researchers say. Further, decreased IL15 expression affects the local proliferation of both B and T lymphocytes, the researchers report, noting that patients with B and T cells proliferating at the invasive margin and within the middle of the tumor had longer disease-free survival times. "These results delineate chromosomal instability as a mechanism of modulating local cytokine expression in human tumors and underline the major role of IL15," the researchers say.