本实验室的初步试验显示致癌信号通路通过挟持干细胞的转录网络诱导癌症发生。这一点在几乎所有的癌症中均适用。比如本实验室研究的Kras致癌突变蛋白与干细胞转录组相辅相成，导致胰腺癌细胞的存活与繁衍。在胰腺癌以外，本实验室还将研究致癌信号通路和其他肠胃、食道癌干细胞转录组之间功能上的相互作用。为此，本实验室利用多种转基因小鼠模型以及人的类器官（organoid）来研究癌症生物学以及干细胞生物学的多方面重要研究领域。

2017 Memorial Sloan Kettering Postdoctoral Researcher Award

2017 NIH K22 Award

2010 John S. Newberry Award (Columbia University)

1. Li Y*, He Y*, Peng J*, …, Chen M, Zhao Y#, Wu W# andDavid CJ#(2021). Mutant Kras co-opts a proto-oncogenic enhancer network in inflammation-induced metaplastic progenitor cells to initiate pancreatic cancer.Nature Cancer2:49–65.

2.David CJ, Massagué J (2018). Contextual determinants of TGFβ action in development, immunity and cancer.Nature Reviews Molecular Cell Biology19:419-435.

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.Cell164(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 Development25: 972-83.

5.David CJ, Manley JL (2010). Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged.GenesandDevelopment24: 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.Nature463: 364-8.*Co-first author