决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Possible Roles for Purinergic Receptor P2RX4 in Breast and Prostate Cancers.
嘌呤能受体 P2RX4 参与乳腺癌和前列腺癌的恶性行为。
嘌呤能受体P2RX4参与乳腺癌和前列腺癌的恶性行为,在这些肿瘤中表达上调,并通过上皮-间质转化(EMT)、自噬及促恶性溶酶体内容物释放等机制促进肿瘤进展。P2RX4还可通过与癌基因和肿瘤抑制因子相互作用影响细胞信号通路。某些P2RX4遗传变异与乳腺癌和前列腺癌患病风险增加相关。因此,靶向P2RX4是一种有前景的治疗思路,潜在策略包括抗体疗法、CAR-T细胞疗法及开发小分子抑制剂。仍需进一步研究充分阐明P2RX4促进癌症进展的分子机制,并将相关发现转化为有效且安全的临床疗法。
The purinergic receptor P2RX4 contributes to the malignant behavior of breast and prostate cancers. It is upregulated in these malignancies and promotes tumor progression through mechanisms involving EMT, autophagy, and the release of pro-malignant lysosomal contents. P2RX4 also influences cellular signaling pathways by interacting with oncogenes and tumor suppressors. Certain genetic variants of P2RX4 are associated with an increased risk of developing these cancers. Hence, targeting P2RX4 represents a promising therapeutic approach, with potential strategies including antibody and CAR-T cell therapies and the development of small-molecule inhibitors. Further investigation is needed to fully elucidate the molecular mechanisms by which P2RX4 drives cancer progression and to translate these findings into effective and safe clinical therapies.
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