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This Week in Cancer Cell: Nov 17, 2011

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In Cancer Cell this week, researchers in the US and Japan elucidate the role of polycomb group protein CBX8 in the initiation and maintenance of MLL-AF9-induced leukemogenesis. Chromosomal translocations involving the mixed lineage leukemia gene AF9 usually lead to the develop of acute leukemias, the authors write. In this study, the team shows that CBX8 interacts with MLL-AF9 and is essential for leukemogenesis. The team also observed that CBX8 ablation and disruption of the CBX8 interaction with MLL-AF9 abolishes the gene's leukemic transformation. "Surprisingly, CBX8-deficient mice are viable and display no apparent hematopoietic defects," the authors add. "Together, our findings demonstrate that CBX8 plays an essential role in MLL-AF9 transcriptional regulation and leukemogenesis."

Also in Cancer Cell this week, MIT researchers write that direct signaling between platelets and cancer cells can promotes metastasis. Interactions between cancer cells and the primary tumor microenvironment can determine cancer progression, but it's still unclear whether there are additional pro-metastatic signals during intravascular transit of cancer cells to the site of metastasis, the authors write. For this study, the team shows that "platelet-tumor cell interactions are sufficient to prime tumor cells for subsequent metastasis." TGFβ derived from platelets and direct platelet-tumor cell contacts can activate the TGFβ-Smad and NF-κB pathways in cancer cells, which enhance metastasis in vivo. "Inhibition of NF-κB signaling in cancer cells or ablation of TGFβ1 expression solely in platelets protects against lung metastasis in vivo," the authors write. "Thus, cancer cells rely on platelet-derived signals outside of the primary tumor for efficient metastasis."

And finally in Cancer Cell this week, a team led by researchers at the Dana-Farber Cancer Institute has linked FOXM1 phosphorylation to suppression of senescence in cancer cells. CDK4 and CDK6 kinases are over-active in most human cancers, but it's unclear by which mechanisms them promote tumorigenesis. By performing a systematic screen for substrates of these kinases, the researchers identified the FOXM1 transcription factor as a phosphorylation target. "CDK4/6 stabilize and activate FOXM1, thereby maintain expression of G1/S phase genes, suppress the levels of reactive oxygen species, and protect cancer cells from senescence," the authors write. "Melanoma cells, unlike melanocytes, are highly reliant on CDK4/6-mediated senescence suppression, which makes them particularly susceptible to CDK4/6 inhibition."

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With genetic data from two large population cohorts and summary statistics from prior genome-wide association studies, researchers came up with 27 exposure polygenic risk scores in the American Journal of Human Genetics.