Publications

SELECTED PUBLICATIONS

Synthetic Lethal Interaction of Combined BCL-XL and MEK Inhibition Promotes Tumor Regressions in KRAS Mutant Cancer Models.Corcoran RB, Cheng KA, Hata AN, Faber AC, Ebi H, Coffee EM, Greninger P, Brown RD, Godfrey JT, Cohoon TJ, Song Y, Lifshits E, Hung KE, Shioda T, Dias-Santagata D, Singh A, Settleman J, Benes CH, Mino-Kenudson M, Wong KK, Engelman JA. Cancer Cell. 2013 Jan 14; 23(1):121-128.

Singh A, Sweeney M, Burger A, Yu M, Greninger P, Benes C, Haber DA, Settleman J. TAK1 inhibition promotes apoptosis in KRAS-dependent colon cancers. Cell 2012. Feb 17;148(4):639-50. PMC3291475

Ebi H, Corcoran RB, Singh A, Chen Z, Song Y, Lifshits E, Ryan DP, Meyerhardt JA, Benes C, Settleman J, Wong KK, Cantley LC, Engelman JA. Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers. J Clin Invest. 2011 Oct 10.

Singh, A, Settleman J., EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer. Oncogene 2010 Aug 26;29(34):4741-51.

Singh, A, Settleman J, Oncogenic K-ras “addiction” and synthetic lethality. Cell Cycle 2009. Sep 1;8(17):2676-7.

Singh A, Greninger P, Rhodes D, Koopman L, Violette S, Bardeesy N and Settleman J. A gene expression signature associated with “K-Ras addiction” reveals regulators of EMT and tumor cell survival. Cancer Cell 2009 15(6):489-500.  Reviewed in “Therapeutics: Dependent on KRAS” – Nat. Rev. Cancer 2009 7(9):457 and “K-Ras’ Achilles’ heel” – Science Business Exchange 2009 2(23): 4-5. Cited by Martin Fernandez-Zapico: Faculty of 1000 Medicine, 2 Sep 2009 http://f1000medicine.com/article/id/1161238/evaluation. Featured in “2009: Signaling Breakthroughs of the Year” – E.M. Adler, Science Signaling, 5 January 2010.

Montagut C, Sharma SV, Shioda T, McDermott U, Ulman M, Ulkus LE, Dias-Santagata D, Stubbs H, Lee DY, Singh A, Drew L, Haber DA, Settleman J. Elevated CRAF as a potential mechanism of acquired resistance to BRAF inhibition in melanoma.  Cancer Res. 2008 68(12):4853-61.

Chin TM, Quinlan MP, Singh A, Sequist LV, Lynch TJ, Haber DA, Sharma SV, Settleman J. Reduced Erlotinib sensitivity of epidermal growth factor receptor-mutant non-small cell lung cancer following cisplatin exposure: a cell culture model of second-line erlotinib treatment.  Clin Cancer Res. 2008 14(21):6867-76.

Singh A, Boyer JL, Der CJ, Zohn IE. Transformation by a nucleotide-activated P2Y receptor is mediated by activation of Galphai, Galphaq and Rho-dependent signaling pathways. J Mol Signal. 2010 Jul 23;5(1):11.

Campbell PM, Singh A, Williams FJ, Frantz K, Ulku AS, Kelley GG, Der CJ. Genetic and pharmacologic dissection of ras effector utilization in oncogenesis.  Methods Enzymol 2005 407:195-217.

Singh A, Karnoub AE, Palmby TR, Lengyel E, Sondek J, and Der CJ. Rac1b, a tumor associated, constitutively active Rac1 splice variant, promotes cellular transformation. Oncogene 2004 23(58): 9369-80. Cited by Dr. Brent Cochran Faculty of 1000 Biology – 20th April 2005 http://www.f1000biology.com/article/id/1025284/evaluation.

Luquain C, Singh A, Wang L, Natarajan V, and Morris AJ. Role of phospholipase D in agonist-stimulated lysophosphatidic acid synthesis by ovarian cancer cells. J Lipid Res 2003 .44: 1963-75.

 

Book chapters

Singh A., S.V. Sharma and J. Settleman.  2009. Epidermal Growth Factor Receptor mutations and sensitivity to selective kinase inhibitors in human lung cancer. Genomics and Pharmacogenomics in Anticancer Drug Development and Clinical Response. Edited by Federico Innocenti.

Singh A., 2013. Deregulated Signaling Networks in Lung Cancer. Systems Biology of Cancer. Edited by Sam Thiagalingam. In press.