Different types of epigenetic DNA modifications affect the likelihood of cytosine mutations in cancer.

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.

Assessing metabolites in renal cell carcinoma and kidney tissue suggests cancers adapt rather than dictate nutrient availability.

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

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.

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.

L-mimosine and dopamine protect against cisplatin-induced oto- and nephrotoxicity in zebrafish and human cell line models.

Multiple imaging modalities resolved the ultrastructure of single hematopoietic stem cells in their endogenous niche, allowing identification of dopamine beta-hydroxylase positive cells as a functional niche cell type.

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.

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