Pathophysiology of ANKRD26-related thrombocytopenia and B-ALL recurrence after blinatumomab
カートのアイテムが多すぎます
カートに追加できませんでした。
ウィッシュリストに追加できませんでした。
ほしい物リストの削除に失敗しました。
ポッドキャストのフォローに失敗しました
ポッドキャストのフォロー解除に失敗しました
Pathophysiology of ANKRD26-related thrombocytopenia and B-ALL recurrence after blinatumomab
-
ナレーター：
-
著者：
In this week's episode, Blood editor Dr. Laurie Sehn interviews Drs. Shengwen Calvin Li and Hrishi Krishna Srinagesh on their latest articles published in Blood. Dr. Li discusses "Single-cell profiling of ANKRD26 thrombocytopenia reveals progenitor expansion and polyploid apoptosis via JUNB-p21". The study identifies reproducible abnormalities in progenitor expansion and increased apoptosis of polyploid megakaryocytes, and they propose a novel mechanism in which centrosomal over-expression of ANKRD26 drives polyploid megakaryocyte apoptosis through JUNB-mediated induction of p21 transcription. Dr. Srinagesh discusses "Blinatumomab nonresponse correlates with poor survival after brexucabtagene autoleucel in B-cell ALL" in which data collected by the Real-World Outcomes Collaborative of CAR-T in Adult ALL consortium showed that prior nonresponse to blinatumomab was associated with inferior survival after brexucabtagene in comparison to blinatumomab-naïve patients. Early CAR-T responses were uniformly high regardless of prior exposure or response. This highlights that resistance to blinatumomab may identify patients at higher risk of post–CAR T relapse despite excellent initial responses.