Mary Jo Turk, PhD
Associate Professor of Microbiology and Immunology
Microbiology and Immunology
Dr. Turk received her B.S. in Chemistry in 1995 from John Carroll University, and her Ph.D. in 2001, from the Department of Chemistry at Purdue University. From 2001 through September of 2004, Dr. Turk was a postoctoral research fellow in the Laboratory of Tumor Immunology at Memorial Sloan-Kettering Cancer Center in New York City. She joined the department of Immunology and Microbiology, as well as the Norris Cotton Cancer Center as an Assistant Professor in October of 2004.
Molecular and Cellular Biology Graduate Programs
Norris Cotton Cancer Center
One Medical Center Drive
Rubin Building 732, HB 7937
Lebanon NH 03756
Office: Rubin 732
Asst. Phone: 603-653-9952
Research in the Turk Laboratory focuses on understanding how the immune system responds to poorly immunogenic tumors, and in using this knowledge to design effective immunotherapies against cancer. We employ a century-old model (first discovered in 1906) known as Concomitant Tumor Immunity, whereby immunity to a progressively growing tumor is monitored by measuring growth of a secondary tumor given several days later. Using this model, we have recently shown that, in the absence of CD4 CD25 regulatory T cells, progressively growing tumors themselves induce robust anti-tumor immunity against subsequent tumors. In hosts with melanoma, this protection is mediated by CD8 T cells which recognize unaltered self proteins that are expressed by both melanoma cells and normal melanocytes. These findings are intriguing because they demonstrate that tumors are able to break immunological tolerance to self proteins when regulatory T cells are disabled. Our research goals involve elucidating the mechanisms by which tumors prime these T cell responses, devising effective strategies for blockade of regulatory T cells, and developing vaccines which will boost this inherent immunity against cancer.
Myeloid Cells That Impair Immunotherapy Are Restored in Melanomas with Acquired Resistance to BRAF Inhibitors.
Tumor-Intrinsic PD-L1 Signals Regulate Cell Growth, Pathogenesis, and Autophagy in Ovarian Cancer and Melanoma.
The mitogen-activated protein kinase pathway plays a critical role in regulating immunological properties of BRAF mutant cutaneous melanoma cells.
Melanoma Induces, and Adenosine Suppresses, CXCR3-Cognate Chemokine Production and T-cell Infiltration of Lungs Bearing Metastatic-like Disease.
BRAF-inhibition and tumor immune suppression.
BRAF inhibition alleviates immune suppression in murine autochthonous melanoma.
Local hyperthermia treatment of tumors induces CD8(+) T cell-mediated resistance against distal and secondary tumors.
Multiple murine BRaf(V600E) melanoma cell lines with sensitivity to PLX4032.
Autoimmune vitiligo does not require the ongoing priming of naive CD8 T cells for disease progression or associated protection against melanoma.
Adenocarcinoma contains more immune tolerance regulatory t-cell lymphocytes (versus squamous carcinoma) in non-small-cell lung cancer.