Steven B. McMahon

Steven B. McMahon, PhD

Contact Dr. McMahon

233 South 10th Street
Bluemle Life Sciences Building Room 331
Philadelphia, PA 19107

(215) 503-9064


PhD, Immunology, University of Pennsylvania
MS, Physiology, Temple University
BS, Biology, Albright College

Labsite: Steven McMahon

Universtiy Appointments

Associate Dean, Basic Science Research
Senior Associate Provost for Programmatic Science

Chair, Biochemistry and Molecular Biology - 2017
Senior Associate Provost, Programmatic Science

Vice Chair, Cancer Biology
Deputy Director, Basic Science
Associate Professor, Cancer Biology - 2006

Awards & Achievements

  • Sidney Kimmel Cancer Center Mentorship Award
  • Ralph and Marian Falk Medical Research Trust Catalyst Award
  • Gertrude Elion Award, American Association for Cancer Research
  • Special Fellow Award, Leukemia and Lymphoma Society
  • Research Scholar Award, American Cancer Society
  • Scholar Award, V Foundation for Cancer Research

Expertise & Research Interests

Our group has a longstanding interest in understanding the biochemical events that are deregulated to cause alterations in broad transcriptional programs in human cancer. As such, our research focuses on the two most commonly mutated transcription factors, MYC and p53, that are critical to cancer progression. We are currently focused on defining precisely how MYC and p53 are regulated in cancer cells, how the transcription programs they control are altered in cancer, and ultimately what essential cellular processes are impacted by these changes.  Collectively, these studies have identified previously unknown nodes in these pathways that may represent potential therapeutic targets.

Current Research Projects

  • Understand the role of altered mitochondrial transcription in the ability of MYC to reprogram cellular metabolism during malignant transformation.
  • Identify the mechanism by which post-translational modifications control the ability of the p53 tumor suppressor to selectively activate distinct transcriptomes.
  • Define the contribution of genetic lesions in subunits of the human SAGA coactivator complex to human cancer.