• Researcher Profile

    Barrett J. Rollins, MD, PhD

    Chief Scientific Officer

    Linde Family Professor of Medicine, Harvard Medical School

    Office phone: 617-632-3896
    Fax: 617-632-5998
    Email: barrett_rollins@dfci.harvard.edu
    Website: Barrett Rollins Laboratory

    Preferred contact method: email

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    Research Department

    Medical Oncology/Molecular and Cellular

    Area of Research

    Control of Leukocyte Migration by Chemokines

    Dana-Farber Cancer Institute
    450 Brookline Avenue
    Smith 758
    Boston, MA 02215


    After graduating from Amherst College, Dr. Rollins received his MD in 1979 and PhD in 1980 from Case Western Reserve University. He completed his internship and residency in internal medicine at Beth Israel Hospital, Boston. He then served a clinical fellowship in medical oncology at DFCI and a postdoctoral research fellowship with Dr. Charles Stiles. Since joining DFCI in 1989, Dr. Rollins has worked in the area of white blood cell trafficking and the interactions between inflammation and cancer.

    Recent Awards

    • Association of American Physicians, 2004
    • American Society for Clinical Investigation, 1996
    • Scholar, Leukemia Society of America, 1995


    Control of Leukocyte Migration by Chemokines

    Leukocyte Trafficking
    White blood cells are the first line of host defense against invaders from without (e.g., microbial pathogens) or within (e.g., tumors). To be effective, leukocytes must engage in complex trafficking patterns. Some travel to the site of the initial breach to fight the invasion nonspecifically. Others sample the invasion site and carry bits of information back to lymph nodes where they initiate an immune response that directs the migration of effector cells back to the invasion site. We now know that these movements are controlled by a family of small secreted proteins called chemokines.
    One approach our laboratory takes to understanding chemokines is to study one in detail, namely monocyte chemoattractant protein-1 (MCP-1). We have dissected the molecular determinants of its function by structure-activity analyses and have attempted to understand its physiology using genetically modified mice. For example, studies in MCP-1-deficient mice show that this chemokine is essential for monocyte recruitment in inflammation, including diseases with inflammatory components such as atherosclerosis.
    We have also discovered that MCP-1 is required for the development of type 2 T helper cell-polarized immune responses, that is, those that fight parasites and are involved in allergies. Current efforts are directed toward understanding the molecular basis for this effect. We are also interested in the interface between chemokines and cancer. Chemokines can stimulate leukocytes to engage in host antitumor activity, but some chemokines can affect tumor cells directly. Recently, we demonstrated that ambient chemokines stimulate anti-apoptotic responses in tumor cells. In fact, some tumors secrete chemokines that act in an autocrine manner to inhibit apoptosis - a powerful and direct mechanism whereby inflammation can promote cancer.
    Finally, a new area of research involves the Langerhans cell histiocytoses, a family of diseases in which chemokine abnormalities may play a role in determining patterns of organ involvement. We have demonstrated that pathologic Langerhans cells aberrantly express chemokine receptors in a manner that could explain patterns of tissue involvement in the histiocytoses.
    Cell Cycle Control
    In addition to leukocyte trafficking, our laboratory studies cell cycle control. In particular, we have demonstrated that cyclin C, an understudied regulator of the cell cycle, combines with cdk3 to promote exit from the G0 state by phosphorylation of pRb, the product of the retinoblastoma susceptibility gene. These new insights into the G0 resting state may have important implications for cancer treatment.


    • Ren, Shengjun, PhD
    • Xuguang, Chen, PhD
    • Mrigank, Srivastava, PhD
    • Gayane, Badalian, MD, PhD
    • David, Nelson, PhD
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