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.

The percentage of a tumor’s genome with alterations in copy number is correlated with increased mortality across a range of tumor types and can be measured using a clinically approved sequencing assay.

Cell culture models widely used in cancer research do not reflect metabolism in tumors; by altering culture systems to better model tumor metabolism we find that environmental cystine promotes tumor glutamine metabolism.

The HOXB13 binding partner MEIS1 suppresses prostate cancer proliferation, invasion, and metastasis by promoting expression of the anti-oncogenic extracellular proteoglycan Decorin.

GrimAge acceleration may increase the risk of colorectal cancer.

Breast cancer resistant to either doxorubicin or epirubicin relies on distinct primary metabolic processes, which can be targeted to reduce cancer progression.

Gene copy number provides more prognostic information than gene mutation status in cancer.

In lung adenocarcinoma, deleting one glucose transporter, whether it is Glut1 or Glut3 is insufficient, whereas their dual deletion reduces tumor growth.

Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.

Many tumors are depleted of mitochondrial DNA; this depletion is associated with changes in gene expression and with the incidence of critical somatic mutations and alterations.