Tumor Biology

Program Leadership

Christopher Counter, PhD
Ann Marie Pendergast, PhD

Program Overview

The Tumor Biology Program serves as one of the main epicenters of basic cancer research in the Duke Cancer Institute (DCI). The Program is led by Ann Marie Pendergast, PhD, and Christopher Counter, PhD, and is partitioned into two focus groups: Cell Metabolism and Signal Transduction.

The research encompassed by this program spans the spectrum of cancers, with active research studies in all the major human cancers, including but not limited to:

The program is comprised of faculty actively engaged in basic research in signaling pathways and phenotypic features characteristic of cancer cells. Program members employ molecular, biochemical and cell biology strategies to understand the molecular pathways dysregulated in cancer in both in vitro as well as in vivo models, with the goal of identifying novel targets for development by site based and translational programs within the DCI.

Specific Aims

The two main specific aims of the Tumor Biology program are to 1) foster innovative, high-impact basic approaches to elucidate the molecular mechanisms underpinning cancer and 2) promote collaborative and transdisciplinary research in the field of cancer biology through programmatic seminars, programmatic work-in-progress meetings, annual programmatic retreats, transdisciplinary joint retreats, and training initiatives. 

Focus Areas

  • Cell Metabolism Focus Group
  • Signal Transduction Focus Group

Scientific Highlights

Brady, DC, Crowe, MS, Turski, ML, Hobbs, GA, Yao, X, Chaikuad, A, Knapp, S, Xiao, K, Campbell, SL, Thiele, DJ, and Counter, CM. "Copper is required for oncogenic BRAF signalling and tumorigenesis."  Nature 509, no. 7501 (May 2014): 492-496. [PMC4138975]

Wang, H, Sun, T, Hu, J, Zhang, R, Rao, Y, Wang, S, Chen, R, McLendon, RE, Friedman, AH, Keir, ST, Bigner, DD, Li, QJ, Wang, H, and Wang, XF. "miR-33a promotes glioma-initiating cell self-renewal via PKA and NOTCH pathways."  The Journal of Clinical Investigation 124, no. 10 (October 2014): 4489-4502. [PMC4191031]

Sourbier, C, Ricketts, CJ, Matsumoto, S, Crooks, DR, Liao, PJ, Mannes, PZ, Yang, Y, Wei, MH, Srivastava, G, Ghosh, S, Chen, V, Vocke, CD, Merino, M, Srinivasan, R, Krishna, MC, Mitchell, JB, Pendergast, AM, Rouault, TA, Neckers, L, and Linehan, WM. "Targeting ABL1-mediated oxidative stress adaptation in fumarate hydratase-deficient cancer."  Cancer Cell 26, no. 6 (December 2014): 840-850. [PMC4386283]

Macintyre, AN, Gerriets, VA, Nichols, AG, Michalek, RD, Rudolph, MC, Deoliveira, D, Anderson, SM, Abel, ED, Chen, BJ, Hale, LP, and Rathmell, JC. "The glucose transporter Glut1 is selectively essential for CD4 T cell activation and effector function."  Cell Metabolism 20, no. 1 (July 2014): 61-72.   [PMC4079750]

Clinical Trials