14 articles
This paper made me think differently about T-cell metabolism because it argues that one small metabolite, phosphoenolpyruvate, can directly shape signaling and antitumor function.
This paper helped define intratumoral T-cell dysfunction as a mitochondrial problem, not just an exhaustion-marker problem.
Solid tumors have resisted both CAR-T therapy and antibody-drug conjugates for different reasons. This study collapses that divide, engineering CAR-T cells that deliver chemotherapy directly within the tumor microenvironment.
This paper is one of the clearest demonstrations that long-term remission after CAR T therapy is not just about expansion. It is about persistence, cell state, and the kind of T cell that survives.
Solid tumors have resisted both CAR-T therapy and antibody-drug conjugates for different reasons. This study collapses that divide, engineering CAR-T cells that deliver chemotherapy directly within the tumor microenvironment.
Solid tumors have resisted both CAR-T therapy and antibody-drug conjugates for different reasons. This study collapses that divide, engineering CAR-T cells that deliver chemotherapy directly within the tumor microenvironment.
Solid tumors have resisted both CAR-T therapy and antibody-drug conjugates for different reasons. This study collapses that divide, engineering CAR-T cells that deliver chemotherapy directly within the tumor microenvironment.
Solid tumors have resisted both CAR-T therapy and antibody-drug conjugates for different reasons. This study collapses that divide, engineering CAR-T cells that deliver chemotherapy directly within the tumor microenvironment.
Solid tumors have resisted both CAR-T therapy and antibody-drug conjugates for different reasons. This study collapses that divide, engineering CAR-T cells that deliver chemotherapy directly within the tumor microenvironment.
This preprint treats one of solid-tumor CAR-T’s biggest problems as a movement problem, engineering “velocity receptors” that push T cells into a more migratory state and improve infiltration, tumor control, and survival in preclinical models.
This mini-review is less about a single experiment and more about building a translational map for risankizumab, tying IL-23 biology to dosing, pharmacokinetics, biomarkers, and pivotal efficacy data across psoriasis, psoriatic arthritis, and Crohn’s disease.
In a phase 2 study of mismatch repair-deficient locally advanced rectal cancer, single-agent dostarlimab produced a clinical complete response in every evaluable patient reported, with no patient proceeding to chemoradiotherapy or surgery during the follow-up window.
This paper argues that tumors do not only evade immunity with checkpoints and suppressive ligands. They may also win by taking the fuel first.
Why do CAR-NK therapies work… until they don’t? This post looks at a paper by the Rezvani Lab that argues relapse isn’t just the tumor getting smarter, but immune cells slowly running out of energy.