Postdoctoral position - Mount Sinai Medical Center, New York NY

A postdoctoral position is available in the Sam Sidi laboratory, Mount Sinai Medical Center, New York City. Our lab focuses on genotype-based target discovery in cancer, combining genetic and drug screening in zebrafish, functional genomics in human cancer cell lines, and preclinical studies in mouse PDX models. Previous efforts have identified a series of novel compounds, targets and downstream signaling pathways that define novel therapeutic strategies in cancer (e.g., Sidi et al., Cell 2008; Ando et al., Mol Cell 2012; Thompson et al., Mol Cell 2015). 

The successful applicant will focus on novel compounds identified in a recent large-scale screen for suppressors of whole-body radioresistance in p53 mutant embryos. These compounds carry the hope of restoring tumor sensivity to radiation therapy across tumor spectrums. Such ‘radiosensitizer’ agents are lacking and are urgently needed in head-and-neck and other cancers where resistance to RT is the primary predictor of patient death.

The applicant will focus on target discovery and dissecting the mechanism of action of select compounds. The project will involve combinations of computational target prediction, SAR and genetic epistasis studies in live zebrafish, and preclinical studies in mammalian HNSCC models. The applicant will take advantage of the vibrant and collaborative environment at Mount Sinai and work with our collaborators in world-class bioinformatics, genomics, medicinal chemistry and pharmacology departments. Finally, the applicant will participate in the lab’s new drug screening efforts.

Please send cover letter and CV (including a minimum of two reference contacts) to samuel.sidi@mssm.edu

For more information, please check out our lab websites and relevant publications. 

http://drb.mssm.edu/labs/sidi.html

http://www.searlescholars.net/person/575

Thompson R, Shah RB, Liu PH, Gupta Y, Ando K, Aggarwal AK, and Sidi S. An inhibitor of PIDDosome formation. Mol Cell 58, 767-779, 2015. 

Ando K, Kernan JL, Liu PH, Sanda T, Logette E, Tschopp J, Look AT, Wang J, Bouchier-Hayes L, and Sidi S. PIDD death-domain phosphorylation by ATM controls prodeath versus prosurvival PIDDosome signaling. Mol Cell 47, 681-693, 2012.

Sidi S, Sanda T, Kennedy RD, Hagen AT, Jette CA, Hoffmans R, Pascual J, Imamura S, Kishi S, Amatruda JF, Kanki JP, Green DR, D’Andrea AA and Look AT. Chk1 suppresses a caspase-2 apoptotic response to DNA damage that bypasses p53, Bcl-2 and caspase-3. Cell 133:864-877, 2008.