Drug Combinations on AML Cell Lines' Treatment

Kalkan, Fatma; Wood, Ezgi Temamogullari; Farid, Micheal; Yildiz, Muhammed Sadik; Chung, Stephen S.; Toprak, Erdal

doi:10.1182/blood-2022-171100

Cited by 1 publication

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“…We found that the effects of β elemene and 5a were additive without any sign of antagonism ( Figure 2 ). Using a combination of drugs against AML has demonstrated promising results in earlier studies [ 34 ]. As the mutations in the FLT3 in AML pose significant problems with the current drug therapies, it is crucial to investigate alternative means of therapy that can target the mutated FLT3 oncoproteins.…”

Section: Discussionmentioning

confidence: 99%

Combination of an Oxindole Derivative with (−)-β-Elemene Alters Cell Death Pathways in FLT3/ITD+ Acute Myeloid Leukemia Cells

Alanazi,

Bender,

Dogan

et al. 2023

Molecules

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Acute myeloid leukemia (AML) is one of the cancers that grow most aggressively. The challenges in AML management are huge, despite many treatment options. Mutations in FLT3 tyrosine kinase receptors make the currently available therapies less responsive. Therefore, there is a need to find new lead molecules that can specifically target mutated FLT3 to block growth factor signaling and inhibit AML cell proliferation. Our previous studies on FLT3-mutated AML cells demonstrated that β-elemene and compound 5a showed strong inhibition of proliferation by blocking the mutated FLT3 receptor and altering the key apoptotic genes responsible for apoptosis. Furthermore, we hypothesized that both β-elemene and compound 5a could be therapeutically effective. Therefore, combining these drugs against mutated FLT3 cells could be promising. In this context, dose–matrix combination-based cellular inhibition analyses, cell morphology studies and profiling of 43 different apoptotic protein targets via combinatorial treatment were performed. Our studies provide strong evidence for the hypothesis that β-elemene and compound 5a combination considerably increased the therapeutic potential of both compounds by enhancing the activation of several key targets implicated in AML cell death.

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Section: Discussionmentioning

confidence: 99%