Ranjini K. Sundaram

TL;DR: It is reported that IDH1/2 mutations induce a homologous recombination defect that renders tumor cells exquisitely sensitive to poly(adenosine 5′-diphosphate–ribose) polymerase (PARP) inhibitors, and an unexpected link between oncometabolites, altered DNA repair, and genetic instability is uncovered.

TL;DR: Combination therapies targeting iNKT cells may be of benefit toward prevention of cancer in humans and synergistic activation of several innate immune cells by this combination and the capacity to mediate tumor regression are demonstrated.

TL;DR: Findings define a dNTPase-independent function for SAMHD1 in HR-mediated DSB repair by facilitating CtIP accrual to promote DNA end resection, providing insight into how SAM HD1 promotes genome integrity.

TL;DR: It is reported that fumarate and succinate both suppress the homologous recombination DNA-repair pathway required for the resolution of DNA double-strand breaks (DSBs) and for the maintenance of genomic integrity, thus rendering tumor cells vulnerable to synthetic-lethal targeting with poly(ADP)-ribose polymerase (PARP) inhibitors.

TL;DR: Analysis of antigen-specific B/T-cell immunity, immune composition of the tumor microenvironment, and expression of a panel of ICPs on tumor and tumor-infiltrating immune cells in 305 patients with asymptomatic monoclonal gammopathy suggest that stem-cell antigens and PD-L1 may be targeted for immunoprevention of myeloma.