Issue Archive

In this month’s CME article, the authors review the pattern of response to checkpoint inhibitors in lymphoma, dividing lymphoma subtypes into “inflamed” lymphomas (eg, Hodgkin lymphoma and primary mediastinal B-cell lymphoma), which have high response rates to PD-1 inhibition, and “noninflamed” lymphomas (eg, follicular lymphoma and diffuse large B-cell lymphoma), which do not.

Acquisition of BCR-ABL kinase domain (KD) mutations is an important cause of tyrosine kinase inhibitor (TKI) resistance in chronic lymphocytic leukemia (CML). Soverini et al demonstrate that next-generation sequencing (NGS) for KD mutations markedly increases detection of low-level mutations over Sanger sequencing, potentially allowing earlier change to an alternative TKI to decrease the risk of treatment failure.

Iron overload in thalassemia syndromes is caused in part by suppression of hepcidin by erythroferrone (ERFE). Arezes and colleagues demonstrate that antibodies against the N terminus of ERFE block hepcidin suppression and elucidate the mechanism by which ERFE suppresses hepcidin transcription.

Ivanov et al elucidate a novel function of the putatively inactive zymogens of prekallikrein and factor XII, demonstrating that the zymogens both have background proteolytic activity that permits them to reciprocally activate one another.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been identified as a mediator of gastrointestinal (GI) inflammation in graft-versus-host disease (GVHD). The authors identify a specific subset of T lymphocytes that secrete GM-CSF and promote gut inflammation, linking innate and adaptive immunity and offering a potential therapeutic target to treat GI GVHD.

In a population-based analysis including a large database restricted to patients over age 70, the authors demonstrate that the A91V polymorphism in the familial hemophagocytic lymphohistiocytosis–related gene is a nonpathological polymorphism that confers no increase in cancer, death, or immunopathology.