Mary Jo Turk, PhD
Professor of Microbiology and Immunology
Co-Director, Immunology and Cancer Immunotherapy Program
Norris-Cotton Cancer Center
Microbiology and Immunology
Dr. Turk received her B.S. in Chemistry from John Carroll University, and her Ph.D. from Purdue University. Dr. Turk was a postoctoral research fellow in the Laboratory of Tumor Immunology at Memorial Sloan-Kettering Cancer Center. She joined the department of Microbiology and Immunology, as well as the Norris Cotton Cancer Center, as a faculty member, 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
Our laboratory's research focuses on generating durable memory T cell responses to cancer. What is known about generating immunological memory has historically derived from studies of infectious pathogens. Because tumors are an altered form of self-tissue, memory T cell responses to tumors have been characteristically difficult to generate, and mechanisms for their maintenance have not been well understood. Our laboratory has established that autoimmune disease is a critical determinant for the maintenance of T cell memory to tumor antigens. Over the past decade, we have found that autoimmune melanocyte destruction (known as vitiligo) is required to maintain protective T cell responses against melanoma. Our recent work shows that the most functional tumor-specific memory T cells reside in peripheral tissues, establishing that tissue-resident memory (TRM) cells are a critical component of long-lived immunity to cancer.
Oncogenic pathways are the fundamental basis for cancer, and our laboratory also studies the link between oncogenic signaling and host anti-tumor immunity. Our studies indicate that oncogenic BRAF signaling in melanoma cells promotes their ability to recruit and support immunosuppressive myeloid cells and regulatory T cels within the tumor microenvironment. We have demonstrated how inhibitor drugs that target BRAF can be optimally combined with immunotherapies that perturb immunosuppressive cells in tumors.
Tissue Resident CD8 Memory T Cell Responses in Cancer and Autoimmunity.
A Leukocyte Infiltration Score Defined by a Gene Signature Predicts Melanoma Patient Prognosis.
Oncogenic BRAF<sup>V600E</sup> Governs Regulatory T-cell Recruitment during Melanoma Tumorigenesis.
VISTA expression on tumor-infiltrating inflammatory cells in primary cutaneous melanoma correlates with poor disease-specific survival.
Age effects of distinct immune checkpoint blockade treatments in a mouse melanoma model.
Resident memory T cells in the skin mediate durable immunity to melanoma.
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.