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This Week in Cancer Cell: Jan 27, 2012


In Cancer Cell this week, a team of US researchers reports a study of tumor growth potential in mouse models of glioma. High expression of Id1 in glioma identifies tumor cells with a high capacity for self-renewal, and while low expression of Id1 identifies tumor cells with limited capacity for self-renewal, such cells also have potential for proliferation. "Surprisingly, Id1low cells generate tumors more rapidly and with higher penetrance than Id1high cells," the authors write. "Further, eliminating tumor cell self-renewal through deletion of Id1 has modest effects on animal survival, while knockdown of Olig2 within Id1low cells has a significant survival benefit, underscoring the importance of non-self-renewing lineages in disease progression."

Also in Cancer Cell this week, researchers in the US and Germany report that bile acid and inflammation can activate gastric cardia stem cells in a mouse model of Barrett's esophagus. In a mouse model of the pre-cancerous condition, the team found that esophageal over-expression of interleukin-1β "phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and [esophageal adenocarcinoma]." In addition, the authors write, the development of Barrett's esophagus and esophageal cancer was accelerated by exposure to bile acids.

Finally in Cancer Cell this week, an international team of researchers reports on the differences between HIF-1α and HIF-2α in their regulation of metastasis. The team found that loss of HIF-1α in endothelial cells reduces the synthesis of nitric oxide, slows tumor cell migration through the endothelial layers, and restricts tumor cell metastasis. In addition, the loss of HIF-2α has the opposite effect. "This results from differential regulation of [nitric oxide] homeostasis that in turn regulates vascular endothelial growth factor expression in an NO-dependent feedback loop," the authors write. "These opposing roles for the two HIF factors indicate that both they and endothelial cells regulate metastasis as malignancy progresses."

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