W. K. Rathmell

The paper shows that fever increases inflammatory activity in CD4+ T cells but causes mitochondrial dysfunction and DNA damage specifically in Th1 cells, leading to p53-dependent apoptosis to prevent mutations.

This study shows obesity induces PD-1 on tumor-associated macrophages, which suppresses anti-tumor immunity by altering metabolic and functional properties of these cells.

This study shows that SETD2 loss leads to chromosome segregation errors and DNA bridging via isochromosome formation, contributing to genomic instability in cancer.

This study shows ACSS2 promotes HIF-2 stability by preventing its interaction with MUL1, and inhibiting ACSS2 reduces HIF-2 levels and suppresses ccRCC growth.

This study identifies the mitochondrial ATP synthase as the target of apoptolidin family glycomacrolides and demonstrates their efficacy in suppressing leukemia progression.

The paper uses computational analysis to identify mast cell signatures in ACC tumor microenvironment, finding anti-tumor associations with improved survival.

This study identifies immunosuppressive signatures in cortisol-secreting adrenocortical carcinoma (CS-ACC) through multiplatform immunogenomic analyses, linking these signatures to poor prognosis and immunotherapy resistance.

The paper investigates how SETD2 mutations in clear cell renal cell carcinoma affect protein methylation and translation, finding dysregulated translation linked to poor patient outcomes.

This study identifies the molecular mechanisms by which SETD2 methylates α-tubulin, revealing distinct substrate recognition and catalytic requirements for tubulin versus histone methylation.

The paper measures nutrient uptake in the tumor microenvironment using PET tracers and finds cancer cells prefer glutamine while myeloid cells consume most glucose.

This study identifies SETD2 as an actin lysine methyltransferase that regulates actin polymerization and cell migration through methylation of the actin cytoskeleton.