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
This study shows that transient overexpression of cyclin E in mammary epithelial cells generated chromosomal copy number alterations (CNAs) signatures. These CNAs can be translated to changes in gene expression patterns that drive tumor growth.
Small-molecule and genome-scale CRISPR knock-out screens revealed that receptor tyrosine kinases and small heterodimer partner2 are vulnerabilities in rhabdoid tumor cell lines.
Scientists at UCSF developed a new analytical framework, GI manifold, for mapping and understanding genetic interactions. This approach describes the transcriptional states that a cell can occupy upon perturbation and could help in identifying synthetic lethal genetic interactions in cancer.
Saturated mutagenesis screen showed that p53 missense mutations in the DNA-binding domain exert a dominant-negative effect. This is a primary unit of selection for TP53 missense mutations.
UCSD researchers developed a framework to simulate population dynamics of heterogeneous tumor cells with a reversible mechanism of resistance. The study provides insights to optimal cancer treatment methods and may guide the development of therapeutic strategies to evade drug resistance.
Researchers at the Emory CTD2 Center showed transcription factor, SOX4, knockdown induced WNT5a expression and increased WNT5a expression are associated with decreased invasive ability in bladder cancer cells.
Study reports that the third-generation pan-FGFR inhibitor, TAS-120, overcomes resistance to several FGFR2 mutations; leads to personalized targeted therapy in FGFR-activated intrahepatic cholangiocarcinoma.
Bioinformatic approach, MethylMix analysis, refines nominations for epigenetic driver genes by leveraging quantitative high-throughput proteomic data to select only genes where DNA methylation is predictive of protein abundance.
UCSF scientists demonstrated that neomorphic fusion oncoprotein, CIC-DUX4, controls capicua-regulated transcriptional pathways to promote hallmark features of malignancy like tumor cell survival, growth, and metastasis.
Study identifies acetylation as a regulatory mechanism leading ribonucleotide reductase activity, an enzyme that catalyzes the de novo synthesis of precursors required for DNA synthesis.