Publications
Included here is a list of publications from OCG programs. All published data are available to the research community through the program-specific data matrices.
* denotes publications from the CTD2 initiative that are results of intra-Network collaborations
Colon organoid culture functionally validated the microRNA miR-483 as a dominant driver oncogene at the IGF2 (insulin-like growth factor-2) 11p15.5 CRC amplicon, inducing dysplasia in vitro and tumorigenicity in vivo.
Investigators show that knockdown or deletion of Hipk2 in vitro and in vivo inhibits white adipose development and negatively affects metabolism.
Cross-species computational analysis of interactomes from mouse models and human prostate cancer identified FOXM1 and CENPF as synergystic master regulators of prostate malignancy/tumor growth.
Using a high-coverage genome-wide shRNA library, researchers identify the characterized protein TMEM129 and the ubiquitin-conjugated E2 enzyme UBE2J2 to be essential for US11-mediated HLA class I downregulation.
Researchers describe toxicity of three new acylated arylamine derivatives (1-3), carpatamides A-C against non-small-cell lung cancer cell lines HCC366, A549, and HCC44.
Researchers show that squamous cell carcinoma antigens 1 and 2 (SCCA1/2), members of the Serpin family of serine/cysteine protease inhibitors, are transcriptionally upregulated by oncogenic Ras via MAPK and the ETS family transcription factor PEA3.
A web-based tool for exploring genomic vulnerabilities in cancer is available at https://cbio.mskcc.org/cancergenomics/statius/.
In this publication, the authors describe the generation of two mouse strains that enable Cre-dependent, robust expression of reverse tet-transactivator 3, providing tissue-restricted and consistent induction of TRE-controlled transgenes.
Researchers discuss identify somatic mutations with archival formalin fixed and paraffin embedded tissue from gallbladder cancer.
This work identifies nuclear PRAS40 as a dual-input signaling checkpoint that links cell growth and proliferation to inhibition of cellular senescence.
Pages
