Issues

YTB323, a CD19-directed chimeric antigen receptor (CAR) T-cell therapy, retains T-cell stemness after a manufacturing process time of less than 2 days and demonstrates clinical antitumor activity at significantly lower doses than traditionally manufactured CAR T cells.

In patients with FGFR-driven urothelial cancer, resistance to selective FGFR inhibitors is largely explained by the emergence of FGFR kinase domain mutations and alterations in the PI3K–mTOR pathway.

Unlike pan-FGFR inhibitors, RLY-4008 was designed to be selective for FGFR2 and induces clinical responses in FGFR2-altered solid tumors without clinically significant FGFR1-mediated hyperphosphatemia and FGFR4-mediated diarrhea.

Analyses of leukemia stem cells (LSC) in human acute myeloid leukemia (AML) revealed a type of monocytic LSC, distinct from primitive LSCs, that is responsible for the relapse/refractory response of some patients with AML treated with the BCL2 inhibitor venetoclax.

In breast cancer, chemotherapy evasion is coupled to loss of glycosylation (sialylation), cellular quiescence, cluster formation of circulating tumor cells, and metastasis, with anti-PODXL–targeting approaches blocking these effects.

An investigation into the activity and metabolic consequences of patient fumarate hydratase (FH) variants showed that FH deficiency and fumarate accumulation render kidney cancer cells reliant on the purine salvage pathway for tumor growth.

Sex-biased T-cell exhaustion in glioblastoma is, in part, regulated by T cell–intrinsic factors, such as the X chromosome inactivation escape gene Kdm6a, which highlights the potential for a precision therapy approach based on patient biologic sex.