Mechanistic update of Trisenox in blood cancer

Q2 Agricultural and Biological Sciences Current Research in Pharmacology and Drug Discovery Pub Date : 2023-01-01 DOI:10.1016/j.crphar.2023.100166

Ananta , Swati Benerjee , Paul B. Tchounwou , Sanjay Kumar

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Abstract

Acute promyelocytic leukemia (APL)/blood cancer is M3 type of acute myeloid leukemia (AML) formed inside bone marrow through chromosomal translocation mutation usually between chromosome 15 & 17. It accounts around 10% cases of AML worldwide. Trisenox (TX/ATO) is used in chemotherapy for treatment of all age group of APL patients with highest efficacy and survival rate for longer period. High concentration of TX inhibits growth of APL cells by diverse mechanism however, it cures only PML-RARα fusion gene/oncogene containing APL patients. TX resistant APL patients (different oncogenic make up) have been reported from worldwide. This review summarizes updated mechanism of TX action via PML nuclear bodies formation, proteasomal degradation, autophagy, p53 activation, telomerase activity, heteromerization of pRb & E2F, and regulation of signaling mechanism in APL cells. We have also provided important information of combination therapy of TX with other molecules mechanism of action in acute leukemia cells. It provides updated information of TX action for researcher which may help finding new target for further research in APL pathophysiology or new TX resistant APL patients drug designing.

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Trisenox治疗血癌的机制研究进展

急性早幼粒细胞白血病(Acute promyelocytic leukemia, APL)/血癌是一种M3型的急性髓性白血病(Acute myeloid leukemia, AML)，通常在骨髓内发生染色体易位突变。17. 它占全球AML病例的10%左右。Trisenox (TX/ATO)用于化疗治疗所有年龄组APL患者，疗效最高，生存率较长。高浓度TX通过多种机制抑制APL细胞的生长，但仅对PML-RARα融合基因/含癌基因的APL患者有效。在世界范围内，已经报道了TX耐药APL患者(不同的致癌成分)。本文综述了TX在PML核小体形成、蛋白酶体降解、自噬、p53激活、端粒酶活性、pRb和amp异聚化等方面的最新作用机制。E2F与APL细胞信号机制的调控。我们还提供了TX与其他分子联合治疗急性白血病细胞的作用机制的重要信息。为研究人员提供了TX作用的最新信息，有助于寻找新的靶点，进一步开展APL病理生理学研究或设计新的TX耐药APL患者的药物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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