A5085901987- MicroRNA in disease regulation
- Acute Myeloid Leukemia Research
- Histone Deacetylase Inhibitors Research
- Autophagy in Disease and Therapy
- Cancer-related molecular mechanisms research
- Protein Degradation and Inhibitors
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Computational Drug Discovery Methods
- Cancer Genomics and Diagnostics
- Metal complexes synthesis and properties
New York University
2023
NYU Langone Health
2023
NYU Langone’s Laura and Isaac Perlmutter Cancer Center
2023
Abstract BH3 mimetics are used as an efficient strategy to induce cell death in several blood malignancies, including acute myeloid leukemia (AML). Venetoclax, a potent BCL-2 antagonist, is clinically combination with hypomethylating agents for the treatment of AML. Moreover, MCL1 or dual BCL-2/BCL-xL antagonists under investigation. Yet, resistance single combinatorial BH3-mimetic therapies eventually ensues. Integration multiple genome-wide CRISPR/Cas9 screens revealed that loss mitophagy...
<p>Supplementary Methods, Tables, and References</p>
<p>Supplementary Methods, Tables, and References</p>
<div>Abstract<p>BH3-mimetics are used as an efficient strategy to induce cell death in several blood malignancies, including acute myeloid leukemia (AML). Venetoclax, a potent BCL-2 antagonist, is clinically combination with hypomethylating agents for the treatment of AML. Moreover, MCL-1 or dual BCL-2/BCL-xL antagonists under investigation. Yet, resistance single combinatorial BH3-mimetics therapies eventually ensues. Integration multiple genome-wide CRISPR/Cas9 screens revealed...
<p>Supplemental Figure S1 shows the integration of CRISPR/Cas9 loss-of-function screens to identify dependencies and liabilities in BH3-mimetics treatments. Supplemental S2 demonstrates that increased mitochondria-ER interactions contribute resistance. S3 mitophagy affects responsiveness AML cells BH3-mimetics. S4 reveals enhanced autophagic clearance mitochondria as a mechanism resistance AML. S5 exhibits synergism between macroautophagy inhibition human S6 deletion MFN2 or MARCH5...
<p>Supplemental Figure S1 shows the integration of CRISPR/Cas9 loss-of-function screens to identify dependencies and liabilities in BH3-mimetics treatments. Supplemental S2 demonstrates that increased mitochondria-ER interactions contribute resistance. S3 mitophagy affects responsiveness AML cells BH3-mimetics. S4 reveals enhanced autophagic clearance mitochondria as a mechanism resistance AML. S5 exhibits synergism between macroautophagy inhibition human S6 deletion MFN2 or MARCH5...
<div>Abstract<p>BH3-mimetics are used as an efficient strategy to induce cell death in several blood malignancies, including acute myeloid leukemia (AML). Venetoclax, a potent BCL-2 antagonist, is clinically combination with hypomethylating agents for the treatment of AML. Moreover, MCL-1 or dual BCL-2/BCL-xL antagonists under investigation. Yet, resistance single combinatorial BH3-mimetics therapies eventually ensues. Integration multiple genome-wide CRISPR/Cas9 screens revealed...
<p>Supplemental Figure S1 shows the integration of CRISPR/Cas9 loss-of-function screens to identify dependencies and liabilities in BH3-mimetics treatments. Supplemental S2 demonstrates that increased mitochondria-ER interactions contribute resistance. S3 mitophagy affects responsiveness AML cells BH3-mimetics. S4 reveals enhanced autophagic clearance mitochondria as a mechanism resistance AML. S5 exhibits synergism between macroautophagy inhibition human S6 deletion MFN2 or MARCH5...
<div>Abstract<p>BH3 mimetics are used as an efficient strategy to induce cell death in several blood malignancies, including acute myeloid leukemia (AML). Venetoclax, a potent BCL-2 antagonist, is clinically combination with hypomethylating agents for the treatment of AML. Moreover, MCL1 or dual BCL-2/BCL-xL antagonists under investigation. Yet, resistance single combinatorial BH3-mimetic therapies eventually ensues. Integration multiple genome-wide CRISPR/Cas9 screens revealed...
<p>Supplemental Figure S1 shows the integration of CRISPR/Cas9 loss-of-function screens to identify dependencies and liabilities in BH3-mimetics treatments. Supplemental S2 demonstrates that increased mitochondria-ER interactions contribute resistance. S3 mitophagy affects responsiveness AML cells BH3-mimetics. S4 reveals enhanced autophagic clearance mitochondria as a mechanism resistance AML. S5 exhibits synergism between macroautophagy inhibition human S6 deletion MFN2 or MARCH5...