New Finding on Correlation Between Angiogenesis, Breast Cancer and Inflammation

As detailed in the August edition of Cell, Dr. Mien-Chie Hung discovered that a specific inflammatory protein produces an enzyme that renders two tumor-suppressing genes useless. As a result, the body starts rapidly producing new blood vessels to feed the cancer sells.

“This is a completely new pathway for inflammation-induced cancer and may provide new targets for clinical interventions,” said Hung, who is the chair of M.D. Anderson's Department of Molecular and Cellular Oncology. “What we found is a previously unrecognized role for IKKbeta, a protein kinase activated by TNFa,” he continued.

Inflammation has been tied to gastrointestinal tract cancers, liver and breast cancer. The team of researchers working on the project confirmed their hypothesis using lab mice, the started testing their findings in people. 116 breast cancer patients were studied, and the what the doctors working on the study found could have a significant impact on the cancer community.

When the patients had tumors that blocked their TSC1/TSC2 tumor suppressor complex, the survival rate was 46 percent at 60 months. On the other hand, patients who had an active TSC1/TSC2 had a significantly larger chance of living (the study showed a 65 percent survival rate at 60 months).

The study went on to show that IKKa phosphorylates CBP in the center of the cell, the nucleus, and promotes cell growth. Unphosphorylated CBP helps to suppress the cancer, forcing the bad cells into apoptosis, a programmed death of sorts for the cell. “If you can control IKKa, you get a double-dip effect,” said Hung. “You can think of them as a good guy and a bad guy, with a gun lying between them. Who gets the gun, and how does one get it?”

He went on to describe that when IKKa is controlled, “You not only activate p53, the good guy, you keep the bad guy out of the contest.”

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