A well-known inflammatory protein spawns an enzyme that inactivates two tumor-suppressing genes, ultimately triggering production of new blood vessels to nourish breast cancer cells, researchers at The University of Texas M. D. Anderson Cancer Center report in the August edition of the journal Cell. "This is a completely new pathway for inflammation-induced cancer and may provide new targets for clinical intervention," senior author Mien-Chie Hung, Ph.D., professor and chair of M. D. Anderson's Department of Molecular and Cellular Oncology says of the chain of events described in the journal. Hung and colleagues showed that IKKa phosphorylates CBP in the nucleus, switching CBP's binding preference to the NF"B oncogene, promoting cell growth. Unphosphorylated CBP helps p53 do its job suppressing cancer by forcing defective cells to kill themselves, programmed cell death known as apoptosis.
Inflammation, Angiogenesis And Breast Cancer Linked In Chain Of Events
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