Dancik, G.M.; Varisli, L.; Tolan, V.; Vlahopoulos, S. Aldehyde Dehydrogenase Genes as Prospective Actionable Targets in Acute Myeloid Leukemia. Genes2023, 14, 1807.
Dancik, G.M.; Varisli, L.; Tolan, V.; Vlahopoulos, S. Aldehyde Dehydrogenase Genes as Prospective Actionable Targets in Acute Myeloid Leukemia. Genes 2023, 14, 1807.
Dancik, G.M.; Varisli, L.; Tolan, V.; Vlahopoulos, S. Aldehyde Dehydrogenase Genes as Prospective Actionable Targets in Acute Myeloid Leukemia. Genes2023, 14, 1807.
Dancik, G.M.; Varisli, L.; Tolan, V.; Vlahopoulos, S. Aldehyde Dehydrogenase Genes as Prospective Actionable Targets in Acute Myeloid Leukemia. Genes 2023, 14, 1807.
Abstract
It has been previously shown that aldehyde dehydrogenase (ALDH) family member ALDH1A1 has a significant association with acute myeloid leukemia (AML) patient risk group classification, and that AML cells lacking ALDH1A1 expression can be readily killed by chemotherapy. In the past, however, a redundancy between the activities of subgroup members of the ALDH family has hampered conclusive evidence for addressing the role of specific ALDH genes. We here describe the bioinformatics evaluation of all nineteen member genes of the ALDH family as prospective actionable targets for the development of methods aimed to improve AML treatment. We implicate ALDH1A1 in the development of recurrent AML, and we show that from the nineteen members of the ALDH family, ALDH1A1 and ALDH2 have the strongest association with AML patient risk group classification. Furthermore, we discover that the sum of the expression values for RNA from the genes ALDH1A1 and ALDH2 has a stronger association with AML patient risk group classification and survival than either one gene alone. In conclusion, we identify ALDH1A1 and ALDH2 as prospective actionable targets for the treatment of AML in high risk patients. Substances that inhibit both enzymatic activities can constitute potentially effective pharmaceutics.
Keywords
cancer bioinformatics; aldehyde dehydrogenase; biomarkers; gene expression; leukemia; myeloid; acute
Subject
Medicine and Pharmacology, Oncology and Oncogenics
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
