EXOSC1 acts as an endogenous source of mutation inkidney renalclear cell carcinoma via cleaving single-stranded DNA.

A distinct class of kidney tumors is characterized not by patterns of somatic mutations, but by a distinct metabolism.

Transcription beyond annotated gene boundaries expands the diversity of the cancer transcriptome with overexpressed oncogenes and RNA chimeras.

The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

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.

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.

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

Kidney-specific TFEB overexpression in transgenic mice closely recapitulates features observed in both TFEB- and TFE3-mediated human kidney tumors.

Faithful models of RMC require SMARCB1 loss for survival, and genetic and small-molecule screens identify inhibition of the ubiquitin-proteasome system (UPS) as a potential therapeutic approach for SMARCB1 deficient cancers.

Major secondary tumor suppressors in kidney cancer are required to maintain the activity of a tumor suppressive transcription factor after the loss of the primary tumor suppressor VHL.