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For decades cancer biologists have thought of oncogenes in terms of their ability to prompt tumor growth and survival, acting within the cancer cell. That viewpoint is now changing to take into account data showing that oncogenes influence inflammation. Insights now emerge from work on Ras and the proinflammatory mediator interleukin-8, produced by tumor-infiltrating immune cells.
Three studies show that cells are protected against intracellular pathogens by autophagy, a process that degrades cytoplasmic components in bulk. The work may have implications for the development of vaccines against pathogens such as Mycobacterium tuberculosis, Streptococcus pyogenes and Shigella flexneri.
The BCL-6 oncogene can downregulate expression of the p53 tumor suppressor gene in B cell lymphoma. This pathway probably exists to protect normal germinal-center B cells from apoptosis induced by DNA mutations.
New mouse models of ovarian cancer and endometriosis have been created, defining the genetic relationship between these two gynecologic diseases (pages 63–70).
Apoptosis results in the oxidation of membrane lipids on the dying cell. Newly identified oxidized lipids play a dual role: they contribute to the recognition and phagocytosis of dying cells, but may also spur antibody production and inflammation.