- PhD, University of California, Berkeley
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.
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.
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.
CD44S-hyaluronan interactions protect cells resulting from EMT against anoikis.
Cieply B, Koontz C, Frisch SM.
Matrix Biol. 2015; 48(55): 65.
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.
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.
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.
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.
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. Our projects are highly translational, with discoveries informing the development of novel drugs to suppress metastasis and tumor recurrence in patients.