This page provides study documentation for BA6. For description of the specimen results, see Specimen Results Description (open to public). Data sets of the specimen results are included in the existing WHI datasets located on the WHI Data on this site (sign in and a completed Data Distribution Agreement are required; see details on the Data site).
Investigator Names and Contact Information
Jianfeng Xu, M.D., Dr. P.H., Wake Forest University School of Medicine, Winston-Salem, NC
An association between inflammation and cancer has been appreciated for over a century. Two hypotheses have been proposed concerning the role of the immune system in tumorigenesis. In the tumor surveillance hypothesis, tumor-infiltrating leukocytes control tumor growth and eradicate newly forming tumors, and failure of this surveillance permits tumor establishment. In contrast to the immune surveillance hypothesis, there is abundant evidence emerging suggesting that immune-mediated inflammation promotes tumorigenesis. Immune-mediated inflammation is thought to contribute to tumorigenesis by a variety of mechanisms: 1) induction of hyperplasia by either release of growth factors or disruption of tissue homeostasis by destruction of a large portion of the tissue; 2) release of reactive oxygen species (ROS) resulting in DNA damage-mutation; 3) promoting vascularization as part of “normal” tissue repair processes; 4) releasing of anti-inflammatory mediators by innate immune cells to suppress the tumor surveillance system.