Steven M. Frisch, PhD

Professor

Organization:

West Virginia University School of Medicine

Department:

Biochemistry

Classification:

Faculty

Member
Member

Organization:

West Virginia University WVU Cancer Institute

Department:

WVU Cancer Institute Research Programs

Classification:

Faculty

• PhD, University of California, Berkeley

Anoikis: how the extracellular matrix regulates life-or-death decisions. Frisch, S.M., Editor. Springer Publications, 2021

Interferon-I and related pathways in cell senescence. Aging Cell 2020 Sep 12:e13234. doi: 10.1111/acel.13234. Online ahead of print. PMID: 32918364  Frisch, S.M. and MacFawn, I. 

Grainyhead-like-2 confers NK-sensitivity through interactions with epigenetic modifiers.  Molecular Immunology.  105:  137-149, 2019 MacFawn,I, Wilson,H, Selth,LA, Leighton,I, Serebriiskii,I, Bleackley,RC, Elzamzamy,O, Farris,J, Pifer,PM, Richer,J and Frisch,SM.

Mechanisms and context underlying the role of autophagy in cancer metastasis.
Dower CM, Wills CA, Frisch SM, Wang HG.
Autophagy. 2018; 14(7): 1110-1128.
PMC6103720

Roles of Grainyhead-like transcription factors in cancer.
Frisch SM, Farris JC, Pifer PM.
Oncogene. 2017; 36(44): 6067-6073.

Grainyhead-like-2 inhibits the coactivator p300, suppressing tubulogenesis and the epithelial-mesenchymal transition.
Pifer PM, Farris JC, Thomas AL, Stoilov P, Denvir J, Smith DM, Frisch SM.
Mol Biol Cell. 2016; 27(15): 2479-2492.
PMC4966987

Grainyhead-like 2 reverses the metabolic changes induced by the oncogenic epithelial-mesenchymal transition: effects on anoikis.
Farris JC, Pifer PM, Zheng L, Gottlieb E, Denvir J, Frisch SM.
Mol Cancer Res. 2016; 14(6): 528-538.
PMC4912396

CD44S-hyaluronan interactions protect cells resulting from EMT against anoikis.
Cieply B, Koontz C, Frisch SM.
Matrix Biol. 2015; 48(55): 65.
PMC4851163

The wind god promotes lung cancer.
Frisch SM, Schaller MD.
Cancer Cell. 2014; 25(5): 551-552.

Regulation of anoikis by deleted in breast cancer-1 (DBC1) through NF-kappaB.
Park SH, Riley P, Frisch SM.
Apoptosis. 2013; 18(8): 949-962.
PMC3691317

Mechanisms that link the oncogenic epithelial-mesenchymal transition to suppression of anoikis.
Frisch SM, Schaller MD, Cieply B.
J Cell Sci. 2013; 126(Pt 1): 21-29.
PMC3603508

Epithelial-mesenchymal transition and tumor suppression are controlled by a reciprocal feedback loop between ZEB1 and Grainyhead-like-2.
Cieply B, Farris JC, Denvir J, Ford HL, Frisch SM.
Cancer Res. 2013; 15(73): 6299-6309.
PMC3806457

Suppression of the epithelial-mesenchymal transition by Grainyhead-like-2.
Cieply B, Riley P, Pifer PM, Widmeyer J, Addison JB, Ivanov AV, Denvir J, Frisch SM.
Cancer Res. 2012; 72(9): 2440-2453.
PMC3342427

Dean’s Award for Excellence in Research, 2008

Post Doctorate Fellowship: Center for Cancer Research, MIT

Mechanisms of Metastasis & Therapeutic Response Program (MMTR)

Our lab has contributed to an understanding of cancer biology in two areas.  The first involves transcription factors that promote or suppress the oncogenic Epithelial-Mesenchymal Transition (EMT).  EMT is a gene expression program that confers tumor cell invasion, metastasis, drug-resistance and cancer stemness. Currently, we are focusing on a newly discovered factor that ubiquitously reverses EMT.  The second area stems from our discovery that normal epithelial cells –but not tumor cells that have undergone EMT – die via apoptosis when detached from their extracellular matrix. This process, called “anoikis”, safeguards against tumor metastasis. We are currently investigating intracellular metabolic changes accompanying EMT that impact upon anoikis.  A recent, major focus area in the Frisch lab is the control of epigenetic marks, especially histone modifications, during EMT, and how these impact upon drug resistance and tumor recurrence. We are also interested in how the tumor cell differentiation state affects the ability of various immune cells to target the tumor, especially with regard to interferon responses. Our projects are highly translational, with discoveries informing the development of novel drugs to suppress metastasis and tumor recurrence in patients.