Department of Otorhinolaryngology

faculty photo

Devraj Basu, M.D., Ph.D., F.A.C.S.

Assistant Professor of Otorhinolaryngology: Head and Neck Surgery at the Hospital of the University of Pennsylvania and the Veteran's Administration Medical Center
Full Member, Abramson Cancer Center
Department: Otorhinolaryngology: Head and Neck Surgery

Contact information
5 Ravdin/Silverstein
Hospital of the University of Pennsylvania
3400 Spruce Street
Philadelphia, PA 19104
Sc.B (Biology)
Brown University, 1994.
M.D. (Medicine)
Washington University School of Medicine, 2001.
Ph.D. (Immunology)
Washington University School of Medicine, 2001.
Post-Graduate Training
Intern, Surgery, Barnes-Jewish Hospital, 2001-2002.
Resident, Otolaryngology, Barnes-Jewish Hospital, 2002-2005.
Chief Resident, Otolaryngology, Barnes-Jewish Hospital, 2005-2006.
Fellow, Head and Neck Surgery and Microvascular Reconstruction, Hospital of the University of Pennsylvania, 2006-2007.
American Board of Otolaryngology, 2007.
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Description of Research Expertise

As a head and neck surgeon-scientist, I both treat head and neck cancer patients and lead a laboratory focused on mechanisms by which some tumor cells evade modern cancer drugs. In doing so, I am seeking to establish novel approaches for lasting control of the most aggressive and treatment-refractory head and neck cancers. My work has pursued how multiple discrete subpopulations of malignant cells within a single tumor cooperatively resist therapy via both tumor cell autonomous mechanisms and crosstalk with the stromal microenvironment. In the process, I have developed the expertise for analyzing heterogeneity and phenotypic plasticity within cancer cell lines, patient-derived xenografts, and primary human cancer samples based on molecular and functional criteria. My group seeks precise molecular definition of the plasticity and heterogeneity within head and neck cancers in order to discretely target mechanisms supporting homeostasis of the subset of tumor cells that maintain long-term malignant potential. My most recent work focuses on the role of interaction between PI3K/Akt signals and the histone demethylase JARID1B in driving therapy resistance. These studies have integrated known PI3K inhibitor resistance mechanisms into a novel conceptual framework where PI3K signal dependence is regulated by flux between distinct cell states. Although the PI3K pathway is a major oncogenic driver of head and neck cancer, my work demonstrates that its activation is remarkably heterogeneous and plastic within any single tumor. As a result, rapid compensation to PI3K targeting occurs not only at the level of signaling networks in individual cells but also through dynamics among multiple cell states cooperatively sustaining cancer progression. We are presently exploiting such intra-tumor diversity as an innovative basis to improve the marginal efficacy of current targeted agents in head and neck cancer therapy with new drug combinations. In doing so, we seek to realize the potential of therapies integrating these drugs with rapidly emerging tools to target epigenetic regulation of cell state in order to achieve durable head and neck cancer control.

Description of Clinical Expertise

Surgical treatment of disorders of the head and neck
Benign and malignant tumors of the head and neck
Oral Cancer
Laryngeal Cancer
Salivary Cancer
Sinonasal Cancer
Skin Cancer
Thyroid and parathyroid surgery
Transoral laser surgery
Head and neck trauma
Endoscopic sinus surgery

Selected Publications

Facompre ND, Harmeyer KM, Sole X, Kabraji S, Belden Z, Sahu V, Whelan K, Tanaka K, Weinstein GS, Montone KT, Roesch A, Gimotty PA, Herlyn M, Rustgi AK, Nakagawa H, Ramaswamy S, Basu D.: JARID1B Enables Transit between Distinct States of the Stem-like Cell Population in Oral Cancers. Cancer Research 76(18): 5538-49, September 2016.

Basu D, Bewley AF, Sperry SM, Montone KT, Gimotty PA, Rasanen K, Facompre ND, Weinstein GS, Nakagawa H, Diehl JA, Rustgi AK, Herlyn M : EGFR Inhibition Promotes an Aggressive Invasion Pattern Mediated by Mesenchymal-like Tumor Cells within Squamous Cell Carcinomas. Mol. Cancer Ther. 12(10): 2176-87, October 2013.

Facompre N, Nakagawa H, Herlyn M, Basu D: Stem-like cells and therapy resistance in squamous cell carcinomas. Adv. Pharmacol. 65: 235-265, October 2012.

Basu D, Montone KT, Wang LP, Gimotty PA, Hammond R, Diehl JA, Rustgi AK, Lee JT, Rasanen K, Weinstein GS, Herlyn M. : Detecting and targeting mesenchymal-like subpopulations within squamous cell carcinomas. Cell Cycle 10(12): 2008-2016, June 2011.

Basu D, Ngyen TK, Montone KT, Zhang BS, Wang L, Diehl JA, Rustgi AK, Lee JT, Weinstein GS, Herlyn M: Evidence for mesenchymal-like subpopulations within squamous cell carcinomas possessing chemoresistance and phenotypic plasticity. Oncogene 29(29): 4170-4182, July 2010.

Roesch A,Fukunaga-Kalabis M, Schmidt EC, Zabierowski SE, Brafford PA, Vultur A, Basu D, Gimotty P, Vogt T,4 Herlyn M: A Temporarily Distinct Subpopulation of Slow-Cycling Melanoma Cells Is Required for Continuous Tumor Growth. Cell 141(4): 583-594, May 2010.

Kagawa S, Natsuizaka M, Whelan KA, Facompre N, Naganuma S, Ohashi S,Kinugasa G, Egloff AM, Basu D, Gimotty PA, Klein-Szanto AJ, Bass A, 12, Wong K, Diehl JA, Rustgi AK, Nakagawa H : Cellular senescence checkpoint function determines differential Notch1-dependent oncogenic and tumor suppressor activities. Oncogene 34(18): 2347-59, April 2015.

Karakasheva TA, Waldron TJ, Eruslanov E, Kim SB, Lee JS, O'Brien S, Hicks PD, Basu D, Singhal S, Malavasi F, Rustgi AK.: CD38-Expressing Myeloid-Derived Suppressor Cells Promote Tumor Growth in a Murine Model of Esophageal Cancer. Cancer Research 75(19): 4074-85, October 2015.

Rasanen K, Sriswasdi S, Valiga A, Tang HY, Zhang G, Perego M, Somasundaram R, Li L, Speicher K, Klein-Szanto A, Basu D, Rustgi AK, Speicher DW, Herlyn M.: Comparative secretome analysis of epithelial and mesenchymal subpopulations of head and neck squamous cell carcinoma identifies S100A4 as a potential therapeutic target. Mol Cell Proteomics 12(12): 3778-92, December 2013.

Ohashi S, Natsuizaka M, Naganuma S, Kagawa S, Kimura S, Itoh H, Kalman RA, Nakagawa M, Darling DS, Basu D, Gimotty PA, Klein-Szanto AJ, Diehl JA, Herlyn M, Nakagawa H.: A NOTCH3-mediated squamous cell differentiation program limits expansion of EMT competent cells that express the ZEB transcription factors. Cancer Research 71(21): 6836-47, November 2011.

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Last updated: 10/10/2016
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