DEPARTMENT OF DEFENSE - CONGRESSIONALLY DIRECTED MEDICAL RESEARCH PROGRAMS

Posted September 5, 2013
Scott Abrams, Ph.D., Health Research Inc., Roswell Park Division, New York State Department of Health

Scott Abrams, Ph.D. While scientists and clinicians recognize that the immune system may be involved in cancer progression, there is still much to learn about how and when it is harmful and helpful for a given tumor. Dr. Scott Abrams was awarded a Pilot Award in fiscal year 2010 to investigate the secretion of immune factors from ovarian cancers, and the role these chemical signals play in recruiting immune cells that suppress additional immune response. According to Dr. Abrams, he "hypothesized that a key target of such tumor-derived signals is the bone marrow, the birthplace of the immune army," where it may promote a precursor of white blood cells, called myeloid cells. These specialized cells in turn prevent the rest of the immune system from attacking the tumor, as the cancer "takes hostage of the very institutions commissioned to provide host defense." Dr. Abrams and his team implanted human ovarian cancer cell lines in a mouse model and identified six potential myelopoeitic factors (chemical signals for the myeloid cells). One of these, interleukin 6 (IL-6), was found to be significantly higher in ovarian cancer patients than in healthy controls, correlated with the accumulation of myeloid populations, and inversely associated with patient outcome (i.e., higher levels were associated with poorer outcomes). The level of IL-6 was measured primarily from ascites but also sera taken from the mice. While the results are preliminary, these types of studies are needed to justify the use of resources to pursue potential biomarkers for disease detection and monitoring. Dr. Abrams hopes that the findings will also help "uncover novel treatment options that ambush the disease process in underappreciated or unconventional ways."

Links:

Public and Technical Abstracts: Granulopoietic Growth Factor Secretion in Ovarian Carcinoma as a Mechanism for the Emergence of Immune Suppressive Myeloid Subsets

Top of Page