• Researcher Profile

    Mary-Ellen Taplin, MD

    Mary-Ellen Taplin, MD

    Top Doctor

    Chair, Executive Committee for Clinical Research
    Director of Clinical Research, Lank Center for Genitourinary Oncology
    Institute Physician

    Professor of Medicine, Harvard Medical School


    Genitourinary Oncology

    Office phone: 617-582-7221
    Fax: 617-632-2165

    Preferred contact method: appointment phone

    View Physician Profile

    Research Department

    Medical Oncology/Solid Tumor Oncology


    Prostate cancer, Clinical trials, Testis cancer, Bladder cancer, Kidney cancer, Hormone and chemotherapy

    Area of Research

    Clinical and Translational Trials in Prostate Cancer

    Dana-Farber Cancer Institute
    450 Brookline Avenue
    Dana 1232C
    Boston, MA 02215


    Dr. Taplin received her MD in 1986 from the University of Massachusetts, Worcester. She completed a residency in internal medicine and chief residency at the University of Massachusetts Medical Center and an oncology-hematology fellowship at Beth Israel Hospital and Harvard Medical School.

    Dr. Taplin was on staff in medical oncology-hematology as an assistant and then associate professor of medicine at the University of Massachusetts from 1993 to 2003, when she joined Dana-Farber Cancer Institute.


    Clinical and Translational Trials in Prostate Cancer

    Over the past eighteen years, I have been involved in prostate cancer research, in particular clinical trials, and molecular investigations of mechanisms of prostate cancer resistance involving the androgen receptor growth pathway. Collaborators and I have demonstrated that the bone marrow is a useful source of metastatic prostate tumor for correlative analysis, and we have defined the parameters in which a tumor-positive marrow is most likely to be obtained.

    Through a Cancer and Leukemia Group B study, we have collected a bone marrow bank of 198 biopsies from patients with prostate cancer. In this work, we have shown that AR mutations occur in androgen-independent prostate cancer and that the frequency of mutations ranges from 10% to 30%, depending on sample selection. AR mutations in prostate cancer are commonly single point mutations in the hormone-binding domain, and exon A mutations are uncommon. Mutant AR from clinical samples have different functional properties compared to wild-type AR and can be stimulated by ligands such as estrogens, progestins, and antiandrogens. In a study of 50 patients, we were unable to associate the antiandrogen withdrawal response with AR mutation and have hypothesized that the antiandrogen withdrawal response may be secondary to alterations in the AR coregulatory molecule. We have also shown that estrogen receptor-beta is overexpressed in hormone refractory prostate cancer (HRPC).

    The metastatic prostate cancer from bone marrow specimens are being evaluated for AR signaling, splice varients, alterations in androgen synthesis and metabolism pathway. The molecular profiles will be correlated with response to ketoconazole. We are assembling a large bank of metastatic prostate cancer samples from bone biopsies with the aim of peronalizing treatment approaches and we will use these valuable samples to further our understanding of treatment response and resistance to develop new therapies.

    Another area of interest has been clinical trials in prostate cancer, which included novel, second-line hormone therapy and chemotherapy trials in castration resistant prostate cancer. We have completed trials evaluating high dose casodex, estrogens, mifepristone, ketoconazole combined with dutasteride, RAD001/bicalutamide, MDV3100 and abiraterone in castration resistant patients. We are now involved in trials of novel approaches to androgen deprivation including abiraterone, TOK-001, MDV3100, combined abiraterone and dutasteride and ketoconazole and lapatinib.

    In a multi-institutional phase II trial of early chemotherapy and hormone therapy for men with biochemical failure, we demonstrated prolonged remission in approximately 30% of patients. We have ongoing trials evaluating early taxotere chemotherapy combined with VEGF inhibitors and androgen deprivation therapy with or without a VEGF inhibitor. We investigated the use of an mTOR inhibitor (RAD001) in combination with docetaxel, with correlative analysis of PET scans and bone marrow tumor for gene expression.

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