Mechanistic update of Trisenox in blood cancer

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 treatme...

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Published inCurrent research in pharmacology and drug discovery Vol. 5; p. 100166
Main Authors Ananta, Benerjee, Swati, Tchounwou, Paul B, Kumar, Sanjay
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier 2023
Subjects
APL cells
PML-RARα
Trisenox
Trisenox
PML-RARα
APL cells
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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.
AbstractList 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.
Acute promyelocytic leukemia (APL) /blood cancer is a M3 type of acute myeloid leukemia (AML) that is formed inside bone marrow as result of a chromosomal translocation mutation between chromosomes 15 and 17. It accounts for about 10% cases of AML worldwide. Trisenox (TX) is used in chemotherapy for the treatment of all age groups of APL patients, showing the highest efficacy and survival rate for a considerable time-period. High concentration of TX inhibits the growth of APL cells by diverse mechanisms. However, it is effective only on APL patients who have the PML-RARα fusion gene/oncogene. TX resistance has been reported worldwide for APL patients who have a different oncogenic make-up. This review summarizes the updated mechanisms of TX action via PML nuclear bodies formation, proteasomal degradation, autophagy, p53 activation, telomerase activity, heteromerization of pRb & E2F, and regulation of signaling mechanisms in APL cells. We have also provided important information on the molecular mechanisms of action of the combination therapy of TX and other drugs in acute leukemia cells. Taken together, this review highlights the new modes of action of TX action, and provides valuable information for finding new targets and advancing research in APL pathophysiology or designing new drugs for the treatment of TX-resistant APL patients.
ArticleNumber 100166
Author Tchounwou, Paul B
Ananta
Kumar, Sanjay
Benerjee, Swati
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APL cells
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Snippet Acute promyelocytic leukemia (APL)/blood cancer is M3 type of acute myeloid leukemia (AML) formed inside bone marrow through chromosomal translocation mutation...
Acute promyelocytic leukemia (APL) /blood cancer is a M3 type of acute myeloid leukemia (AML) that is formed inside bone marrow as result of a chromosomal...
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SubjectTerms APL cells
PML-RARα
Trisenox
Title Mechanistic update of Trisenox in blood cancer
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