Home / Education / Faculty Team / School of Basic Medical Sciences / Tenure-track Faculty / Oncobiology / Content

David, Charles

E-mail: cdavid@tsinghua.edu.cn

  • Personal Profile

  • Research fields and main results

  • ​ Selected Publications

  • Other information

Searching for the transcriptional origin of cancer phenotypes

Charles David completed his Ph.D. at Columbia University under the mentorship of James L. Manley, where he worked on the mechanisms and regulation of pre-mRNA splicing in cancer and identified a mechanism linking transcription and splicing. He then proceeded to postdoctoral training with Joan Massagué at Memorial Sloan Kettering Cancer Center where he identified a novel tumor suppressive effect of TGF-beta in pancreatic cancer. Since joining the Tsinghua University School of Medicine, Dr. David has focused on the transcriptional mechanisms underlying pancreatic cancer initiation and progression.

Because transcriptional regulation underlies all biological processes, the David lab is focused on transcriptional changes that occur downstream of inflammation and oncogene activation, critical changes in the pancreas that result in cancer. The David laboratory is focused on the detailed mechanisms underlying the transcriptional changes during tumorigenesis, with a goal of identifying tractable drug targets for the treatment of pancreatic cancer.

In recent published work, the David lab identified an injury-induced progenitor state in pancreatic exocrine cells that can be rapidly transformed by mutant Kras, the driving oncogene of pancreatic cancer. Ongoing work in the David lab is focused on how transcriptional programs co-opted from these progenitor cells drive the highly aggressive nature of pancreatic cancer.

1.Li Y*, He Y*, Peng J*, …, Chen M, Zhao Y#, Wu W# and David CJ# (2021). Mutant Kras co-opts a proto-oncogenic enhancer network in inflammation-induced metaplastic progenitor cells to initiate pancreatic cancer. Nature Cancer 2:49–65.

2.David CJ, Massagué J (2018). Contextual determinants of TGFβ action in development, immunity and cancer. Nature Reviews Molecular Cell Biology 19:419-435.

3.David CJ, Huang YH, Chen M, Su J, Bardeesy N, Iacobuzio-Donahue CA, Massagué J (2016) TGF-β tumor suppression through a lethal EMT. Cell 164(5):1015-30.

4.David CJ, Boyne AB, Millhouse SR, Manley JL (2011). The RNA polymerase II C-terminal domain promotes splicing activation through recruitment of a U2AF65-Prp19 complex. Genes and Development 25: 972-83.

5.David CJ, Manley JL (2010). Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged. Genes and Development 24: 2324-64.

6.David CJ*, Chen M*, Assanah M, Canoll P, Manley JL (2010). HnRNP proteins controlled by c-Myc deregulate pyruvate kinase mRNA splicing in cancer. Nature 463: 364-8.*Co-first author.

Academic Awards

2018 Thousand Talents Program

2017 Postdoctoral Researcher Award, MSKCC

2011-2013 Translational Research in Oncology Training Program, MSKCC

2011 John S. Newberry Award (Outstanding Biology Graduate), Columbia University

2005-2007 NIH Training Grant, Columbia University

2001 Excellence in Plant Science Prize, Duke University

Offer courses

Medical Scientific Writing

Technology patent

US Patent WO2011109823A1

INHIBITORY RNAS TO RNA BINDING PROTEINS