2020
DOI: 10.3390/cancers12092461
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Comment on Aasebø, E., et al. “The Progression of Acute Myeloid Leukemia from First Diagnosis to Chemoresistant Relapse: A Comparison of Proteomic and Phosphoproteomic Profiles”. Cancers 2020, 12, 1466

Abstract: In a recent article published in this journal, Aasebø and colleagues reported [...]

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“…Also, genes directly involved in cell cycle control (CDK6) and soluble growth factors (HCF) had mutations in this tumor. Furthermore, trophic pathways related to surface receptors seem to be involved in our case, as suggested by mutations in CD36 (a lipid scavenger receptor) [14], LRP1B (a member of the low-density lipoprotein receptor family) [15] and FGFR2 (fibroblast growth factor receptor 2/CD332) [12]. Furthermore, additional epigenetic regulation may be represented by mutations in DNMT3A, a methyltransferase that may modulate gene expression by altering histones [16].…”
Section: Discussionmentioning
confidence: 82%
“…Also, genes directly involved in cell cycle control (CDK6) and soluble growth factors (HCF) had mutations in this tumor. Furthermore, trophic pathways related to surface receptors seem to be involved in our case, as suggested by mutations in CD36 (a lipid scavenger receptor) [14], LRP1B (a member of the low-density lipoprotein receptor family) [15] and FGFR2 (fibroblast growth factor receptor 2/CD332) [12]. Furthermore, additional epigenetic regulation may be represented by mutations in DNMT3A, a methyltransferase that may modulate gene expression by altering histones [16].…”
Section: Discussionmentioning
confidence: 82%