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Teizo Yoshimura, M.D., Ph.D.

Portait Photo of Teizo Yoshimura
Laboratory of Molecular Immunoregulation
Chemoattractant Receptor and Signal Section
Staff Scientist
Center for Cancer Research
National Cancer Institute
(Office) Building 559, Room 2
(Lab) Building 560, Room 31-76
P.O. Box B
Frederick, MD 21702-1201
Phone:  
301-846-5518
Fax:  
301-846-6924
E-Mail:  
yoshimut@mail.nih.gov

Biography

Dr. Yoshimura obtained his M.D. degree from Kumamoto University School of Medicine, Kumamoto, Japan. He also obtained his Ph.D. in experimental pathology there, where he studied the mechanisms of macrophage infiltration into the sites of delayed-type hypersensitivity reactions with Professor Hideo Hayashi.

Research

Infiltration of leukocytes is a hallmark of inflammatory responses. It occurs in a number of human cancer and mouse cancer models. Although the exact role of tumor infiltrating leukocytes has not been completely understood, infiltrating leukocytes, such as tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) are generally immunosuppressive and provide a microenvironment that favors tumor growth. Therefore, identifying the mechanisms by which immunosuppressive leukocytes are recruited into tumors is critical and clinically relevant.

Monocyte chemoattractant protein-1 (MCP-1)/CCL2 is a chemokine that regulates the recruitment of monocytes into sites of inflammation and cancer. Accumulating evidence strongly suggest that the production of MCP-1 by tumors is responsible for the recruitment of immunosuppressive macrophages. In fact, recent studies demonstrated that neutralization of MCP-1 reduced the growth of prostate, breast and lung cancer in mice. Thus, MCP-1 is a molecular target of cancer treatment.

The role of MCP-1 in carcinogenesis was previously studied by others. In a chemically induced skin papilloma model, the number of papilloma in MCP-1-deficient mice was lower compared to that in wild-type mice. Recently, a vital role of MCP-1 in the initiation and progression of colitis-associated colon carcinogenesis was demonstrated by using CCR2-deficient mice and MCP-1 blocking agents. However, these studies were limited to defining the role for MCP-1 in cancer induction, and the role for this chemokine in later stages of tumor development, such as tumor growth and metastasis, remains unclear. To better define the role for MCP-1 in tumor growth and metastasis, I have generated systemic and conditional MCP-1-deficient mice.

In addition, we recently generated two new mouse models which are deficient in the classical chemoattractant receptors, formyl peptide rceceptor (FPR) 1 and 2, or cathelin-related antimicrobial peptide (CRAMP), a ligand for FPR2. A better understanding of the role of chemoattractants and chemoattractant receptors in cancer development may lead us to develop a novel strategy for cancer treatment.

This page was last updated on 7/10/2014.