Manoj Pillai, MD Assistant Professor, Medical Oncology Education: All India Institute of Medical Sciences (AIIMS), NewDelhi, India 1998 University of Colorado at Denver School of Medicine Division of Medical Oncology 12801 E. 17th Ave., MS 8117, Aurora, CO  80045 Tel: (303) 724-2948, Fax: (303) 724-3889 e-mail: Manoj. Pillai@ucdenver.edu

Bio

Dr. Pillai joined the Division of Medical Oncology in July, 2008, in the Section of Hematological Malignancies and Bone Marrow Transplantation (BMT). Dr. Pillai completed his residency in Internal Medicine from Baylor College of Medicine, Houston, TX in 2002 and fellowship in Medical Oncology from the Fred Hutchinson Cancer Research Center (FHCRC) and the University of Washington, Seattle, WA in 2005. He joined the laboratory of Dr. Beverly Torok-Storb following the first year of clinical training and continued under her mentorship till joining untill joining UCD. In Dr. Torok-Storb’s lab, his work focused on the regulation of hematopoiesis and the contribution of monocytes/ macrophages to this regulation in normal physiology and in clonal myeloid disorders like MDS (Myelodysplastic Syndrome).

Research

Dr. Pillai’s primary research interest is to dissect out the role of stromal cells and monocytes/ macrophages in regulating diverse tissue microenvironments (MEs) particularly, the hematopoietic and tumor MEs. This is pursued in both human in-vitro as well as murine in-vivo models. Cloned stromal cell lines and peripheral blood monocytes (CD14 isolated) are used in human in-vitro work. A novel transgenic tetracycline inducible mouse utilizing a macrophage promoter (CD68 promoter) and a new generation reverse tetracycline activator (rtTA-M2) was generated and characterized, this will allow for the expression of various transgenes of interest at- will in a reversible fashion. This model will be extended to the study of macrophages in the hematopoietic ME as well as tumor associated macrophages (TAMs) in appropriate mouse models of cancer (lung, breast). By defining the nature of macrophage factors involved in diverse tissue MEs, it is hoped that the more effective therapeutic strategies can be devised in clinical scenarios where macrophage dysfunction is thought to contribute to the pathogenesis itself or its progression.