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
Wnt/β-catenin signaling plays a key role in the pathogenesis of colon and other cancers; emerging evidence indicates that oncogenic β-catenin regulates several biological processes essential for cancer initiation and progression.
The study reported that alterations of the lymphoid transcription factor gene IKZF1 (IKAROS) are associated with a high risk of treatment failure in B-ALL and approximately 20% of B-ALL cases have genetic alterations that activate kinase signaling.
Researchers evaluate blocking the MET pathway to prevent post-bevacizumab treatment tumor recurrence, providing a strong rationale for using a combination of MET and VEGF receptor inhibitors to treat glioblastoma patients.
Researchers have developed an integrated systems-biology approach to identifying novel cancer genes contributing to endometrial tumorigenesis. Their results revealed 12 potential driver cancer genes including 10 tumor-suppressor candidates and two oncogene candidates.
Researchers created a mouse model of prostate cancer with inducuble PTEN disruption plus BRAF(V600E) expression.
A group of researchers, including a member of the CTD² network, has identified 56 candidate genes upon which cancer cells are uniquely dependent for survival.
The comprehensive characterization of a large number of cancer genomes will eventually lead to a compendium of genetic alterations in specific cancers.
Several of the novel alterations induced cancerous phenotypes in cell lines and mouse xenograft models and demonstrated sensitivity to tyrosine kinase inhibitors. Stratifying ALL patients may improve clinical outcomes through the use of therapies targeted to the specific genetic alteration.
Researchers describe emerging approaches that aim to determine which altered genes are actually contributing to cancer, as well as their potential as therapeutic targets.
Investigators screemed a library of kinases that lead to activation of the MAPK pathway and identified PAK1.
Pages
