Christopher M. Counter

About

Christopher M. Counter is the George Barth Geller Distinguished Professor of Pharmacology and a Professor of Pharmacology and Cancer Biology at Duke University School of Medicine. He also holds positions as an Assistant Professor in Radiation Oncology and as a Professor of Cell Biology. He is a member of the Duke Cancer Institute. His primary research focuses on pharmacology, cancer biology, and cell biology, contributing to the understanding of molecular mechanisms underlying cancer and therapeutic interventions. His academic and research roles are centered at Duke University, where he is involved in teaching and advancing research in these fields.

Research topics

• Genetics
• Biology
• Cancer research
• Cell biology
• Molecular biology

Selected publications

• Oncogenic KRAS is dependent upon an EFR3A-PI4KA signaling axis for potent tumorigenic activity

  Nature Communications · 2021 · 51 citations

  Senior authorCorresponding

  inhibitor sotorasib, suggesting a clinical path to exploit this pathway. In sum, we have discovered a distinct KRAS signaling axis with actionable therapeutic potential for the treatment of KRAS-mutant cancers.

  DOI

• Capturing the primordial Kras mutation initiating urethane carcinogenesis

  Nature Communications · 2020 · 30 citations

  Senior authorCorresponding

  L/R mutation in the gene Kras. Similarly, the frequency, isoform, position, and substitution of oncogenic RAS mutations are often unique to human cancers. To elucidate the principles underlying this RAS mutation tropism of urethane, we adapted an error-corrected, high-throughput sequencing approach to detect mutations in murine Ras genes at great sensitivity. This analysis not only captured the initiating Kras mutation days after urethane exposure, but revealed that the sequence specificity of u…

  PublisherOA PDFDOI

• p53 dosage can impede KrasG12D- and KrasQ61R-mediated tumorigenesis

  PLoS ONE · 2024-03-28 · 3 citations

  articleOpen accessSenior authorCorresponding

  Mice engineered with a G12D versus Q61R mutation in Kras exhibited differences in tumorigenesis. Namely, the incidence or grade of oral or forestomach squamous epithelial lesions was more prevalent in the KrasG12D background while hematolymphopoietic disease was more prevalent in the KrasQ61R background. Loss of the Trp53 gene encoding the tumor suppressor p53 enhances the ability of oncogenic Kras to initiate tumorigenesis in carcinogen and genetic models of lung cancer. Conversley, an extra co…

  PublisherOA PDFDOI

• KRASG12R-Mutant Pancreatic Cancer Features Limited ERK/MAPK Transcriptional Activity and a Distinctive Tumor Microenvironment

  Cancer Research · 2026-01-13 · 2 citations

  articleOpen access

  Patients with pancreatic ductal adenocarcinoma (PDAC) harboring KRASG12R mutations have increased overall survival relative to patients with KRASG12D/V mutations. To investigate the mechanisms underlying this differential outcome, we developed a genetically engineered mouse model (GEMM) harboring KrasG12R and Trp53R172H mutations (KrasLSL-G12R/+;Trp53LSL-R172H/+;p48Cre-ERTM). Unlike KrasG12D models, KrasG12R GEMMs exhibited limited tumorigenesis, with only 10% developing pancreatic tumors after…

  PublisherOA PDFDOI

• The essential clathrin adapter protein complex-2 is tumor suppressive specifically in vivo

  Nature Communications · 2025-03-06 · 1 citations

  articleOpen accessSenior authorCorresponding

  The microenvironment is a rich source of new cancer targets. We thus used a targeted single-guide RNA library to screen a panel of human pancreatic cancer lines for genes uniquely affecting tumorigenesis. Here we show inactivation of the Adapter Protein complex-2 of clathrin-mediated endocytosis reduces cell growth in vitro, but completely oppositely, promotes tumor growth in vivo. In culture, loss of the complex reduces transferrin endocytosis and iron import required for cell fitness. In tumor…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21CA126903

  NIH · $343k · 2009

• NIH Grant R01CA123031

  NIH · $3.5M · 2019

• NIH Grant R03CA165927

  NIH · $152k · 2014

Frequent coauthors

• Robert A. Weinberg

  Whitehead Institute for Biomedical Research

  38 shared

• Kian‐Huat Lim

  34 shared

• Silvia Bacchetti

  31 shared

• David F. Kashatus

  University of Virginia

  30 shared

• Calvin B. Harley

  28 shared

• Carol W. Greider

  University of California, Santa Cruz

  27 shared

• Donita C. Brady

  27 shared

• William C. Hahn

  Dana-Farber Cancer Institute

  26 shared

Labs

• Counter LabPI

Similar researchers at Duke University

• Blanche Capelh-107
• Staci D. Bilboh-73
• Vadim Y Arshavskyh-72