Cancer is a consequence of the release of basal cellular functions inherited from our unicellular ancestors from the control of regulatory networks that evolved during the emergence of multicellularity.

Knocking out Folliculin (FLCN) in human renal epithelial cells activates STAT1/2-mediated gene expression, independent of interferon, uncovering a tissue-specific process potentially relevant in the cancer syndrome Birt-Hogg-Dubé (BHD).

AIDPS derived by 76 machine-learning algorithm combinations in 13 independent multicenter cohorts exhibited superior capability than clinical traits and 86 published prognostic signatures and could serve as an ideal biomarker for stratified management and individualized treatment of pancreatic cancer.

ZHX2 controls HIF1α oncogenic signaling and tumorigenesis in triple-negative breast cancer.

Building on previous work (Reznik et al., 2016), independent measurements of mitochondrial genome copy number and expression indicate that several solid tumor types suppress respiratory metabolism compared to normal tissue.

The apical polarity protein CRB3 is crucial for regulating vesicle trafficking in γ-tubulin ring complex assembly during ciliogenesis and cilium-related Hedgehog and Wnt signaling pathways in tumorigenesis.

Molecular biology experiments identified a cleaved METTL3, which mediates the METTL3–METTL3 interaction, a prerequisite step for recruitment of WTAP in MTC assembly, controlling m6A deposition and cancer progression.

Identification of a pro-tumorigenic and pro-metastatic role of EHD2 protein in triple-negative breast cancer (TNBC) through the store-operated calcium entry (SOCE) pathway provides a rationale for potential targeting of EHD2-overexpressing TNBC with SOCE inhibitors.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.