Immunobiology of Cancer
To learn whether or not an Interferon defect in cell signaling, recently discovered in immune cells from melanoma patients as well as breast cancer patients, is common to all cancers.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Immunobiology of Cancer|
peripheral blood mononuclear cells
|Study Start Date:||October 2008|
|Study Completion Date:||October 2011|
We have previously demonstrated that tumor-specific T cells could be identified in >50% of patients with metastatic melanoma and these cells appeared to be rendered anergic in vivo [Nature Medicine 5:677, 1999]. Recently we discovered that there is a signaling defect in the Interferon (IFN) pathway in immune cells from melanoma patients [PLOS Medicine 4:897 2007]. Interestingly, preliminary studies are showing the same defect in immune cells from breast cancer patients (unpublished). We would like to expand our research to all types of cancer to determine whether these phenomena occur in different cancer types.
Our primary objective is to determine whether there is an IFN signaling defect in different types of cancers and to determine what is causing this defect.
The second objective is to determine whether these PBMCs are rendered anergic.
The study population will consist of patients who have been diagnosed with cancer, regardless of sex or ethnicity. Blood will be collected during the subjects regularly scheduled laboratory appointment and peripheral blood mononuclear cells (PBMCs) will be isolated for research purposes. These PBMCs will undergo studies, i.e. phosflow, qPCR, proliferation, survival, etc., to determine immune responses for T cells (CD4 and CD8), B cells (CD19), natural killer cells (CD16), and possibly monocytes (CD14).
Please refer to this study by its ClinicalTrials.gov identifier: NCT00767533
|United States, California|
|Stanford University School of Medicine|
|Stanford, California, United States, 94305|
|Principal Investigator:||Peter P Lee||Stanford University|