Kris Cameron Wood

Kris Cameron Wood

Assistant Professor of Pharmacology & Cancer Biology

Appointments and Affiliations

  • Assistant Professor of Pharmacology & Cancer Biology
  • Assistant Professor of Biomedical Engineering
  • Member of the Duke Cancer Institute

Contact Information

  • Email Address:
  • Websites:


  • Ph.D. Massachusetts Institute of Technology, 2007
  • B.S. University of Kentucky at Lexington, 2002

Research Interests

More effective anticancer therapeutic strategies, many of which are based on functional genomics. Examples of projects include: a miniaturized screening platform, tools to systematically map the signaling pathways controlling anticancer drug responses, high-throughput computational methods to discover anticancer drug combinations, design of therapeutic strategies to reverse or prevent drug resistance, and systematic credentialing of mutations uncovered through cancer genome sequencing projects.

Courses Taught

  • CMB 710D: Cell & Molecular Biology Module IV
  • MOLCAN 780: Graduate Student Seminar
  • MOLCAN 818: Molecular Mechanisms of Oncogenesis
  • PHARM 393: Research Independent Study
  • PHARM 394: Research Independent Study
  • PHARM 493: Research Independent Study
  • PHARM 494: Research Independent Study
  • PHARM 780S: Graduate Student Seminar
  • PHARM 818: Molecular Mechanisms of Oncogenesis
  • UPGEN 778E: University Program in Genetics and Genomics Biological Solutions Module V

In the News

Representative Publications

  • Winter, PS; Wood, KC, Mapping Effector-Phenotype Landscapes in KRAS-Driven Cancers, Trends in cancer (2018) [10.1016/j.trecan.2018.02.004] [abs].
  • Singleton, KR; Crawford, L; Tsui, E; Manchester, HE; Maertens, O; Liu, X; Liberti, MV; Magpusao, AN; Stein, EM; Tingley, JP; Frederick, DT; Boland, GM; Flaherty, KT; McCall, SJ; Krepler, C; Sproesser, K; Herlyn, M; Adams, DJ; Locasale, JW; Cichowski, K; Mukherjee, S; Wood, KC, Melanoma Therapeutic Strategies that Select against Resistance by Exploiting MYC-Driven Evolutionary Convergence., Cell Reports, vol 21 no. 10 (2017), pp. 2796-2812 [10.1016/j.celrep.2017.11.022] [abs].
  • Anderson, GR; Winter, PS; Lin, KH; Nussbaum, DP; Cakir, M; Stein, EM; Soderquist, RS; Crawford, L; Leeds, JC; Newcomb, R; Stepp, P; Yip, C; Wardell, SE; Tingley, JP; Ali, M; Xu, M; Ryan, M; McCall, SJ; McRee, AJ; Counter, CM; Der, CJ; Wood, KC, A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution., Cell Reports, vol 20 no. 4 (2017), pp. 999-1015 [10.1016/j.celrep.2017.07.006] [abs].
  • Ali, M; Kaltenbrun, E; Anderson, GR; Stephens, SJ; Arena, S; Bardelli, A; Counter, CM; Wood, KC, Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance., Nature Communications, vol 8 (2017) [10.1038/ncomms15617] [abs].
  • Price, AM; Dai, J; Bazot, Q; Patel, L; Nikitin, PA; Djavadian, R; Winter, PS; Salinas, CA; Barry, AP; Wood, KC; Johannsen, EC; Letai, A; Allday, MJ; Luftig, MA, Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection., eLife, vol 6 (2017) [10.7554/elife.22509] [abs].