Fifteen continuous high-grade serous ovarian carcinoma patient-derived organoids are characterized by transcriptomic, genomic, and drug sensitivity assays to reveal that they comprise communities of clonal populations and represent models of different causes of chromosomal instability and degrees of genome complexity.

Extending the period of remission for cancer patients requires new knowledge of dormant, residual disease and Netrin signaling contributes to the survival of dormant cells in ovarian cancer.

GrimAge acceleration may increase the risk of colorectal cancer.

FOXM1 is co-expressed with its bidirectional gene partner RHNO1, and the two genes promote DNA repair, cell growth and survival, and chemotherapy resistance in ovarian cancer.

A certain type of primary cancer may cause another second primary cancer which would be of clinical importance to make a personalized screening plan for certain primary cancer patients.

Application of machine learning to serum miRNA profiles generated through next generation sequencing identifies a biologically relevant miRNA signature which can be deployed as a qPCR test to assist the diagnosis of epithelial ovarian cancer.

A functional ovarian-specific PAX8-centric regulon is susceptible to FDA-approved HDAC inhibitors, providing the rationale to target human cancers driven by lineage-survival oncogenes with epigenetic therapeutics perturbing the enhancer topology.

Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.