David G. Kirsch

This study identifies integrin signaling and cell-cycle deregulation as key drivers of SMARCB1-deficient epithelioid sarcoma and highlights therapeutic targets.

The paper identifies BAP1 as a tumor suppressor in soft tissue sarcoma using an in vivo CRISPR screen and shows that PLK1 inhibition can suppress tumor growth in BAP1-deficient models.

This study shows Lgr5+ stem cells maintain intestinal epithelial homeostasis and drive regeneration after injury through WNT signaling.

This paper develops a new mouse model of CIC::DUX4 sarcoma and identifies Minnelide as a selective inhibitor effective in preclinical models.

The paper compares radiation response in autochthonous and transplant sarcomas in mice with and without adaptive immunity, finding higher cure rates in transplant tumors with immune function.

This study shows that disrupting ATM enhances radiation therapy efficacy in p53-mutant DMGs but not p53-wildtype DMGs using mouse models.

This study shows that loss of Atrx in a mouse sarcoma model activates the ALT telomere maintenance pathway independently of telomerase, leading to telomere instability and APB formation.

The paper investigates a p53 mutation that causes mis-splicing and loss of function in vitro and in vivo, challenging the classical view of p53 tumor suppression.

This study shows that combining radiotherapy with CpG, a TLR9 agonist, enhances tumor response in a mouse sarcoma model by boosting CD8 T cell activity.

This study generates genetically engineered mouse models of CIC-DUX4 sarcoma that spontaneously develop tumors and express the fusion protein, validating CIC-DUX4 as a transcriptional activator.

This study shows that p53 TAD1 regulates the DNA damage response in endothelial cells to prevent radiation-induced cardiac injury.

The paper quantitatively analyzes the physiological contributions of glucose to the TCA cycle using isotope-labeling data and metabolic flux analysis, showing glucose is the major nutrient source across tissues and conditions.

This study shows that dietary methionine restriction affects one carbon metabolism in humans and produces therapeutic responses in cancer by altering metabolic pathways.

The paper shows that glucose metabolism generates acetate through two mechanisms and demonstrates its role in maintaining Ac-CoA pools and cell proliferation under specific metabolic conditions.