Targeted Therapies and Druggable Genetic Anomalies in Acute Myeloid Leukemia: From Diagnostic Tools to Therapeutic Interventions

Lanza, Francesco; Bazarbachi, Ali

doi:10.3390/cancers13184698

Cancers

2021

DOI: 10.3390/cancers13184698

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Targeted Therapies and Druggable Genetic Anomalies in Acute Myeloid Leukemia: From Diagnostic Tools to Therapeutic Interventions

Francesco Lanza

Ali Bazarbachi

Abstract: Acute myeloid leukemia (AML) is a clonal disorder resulting from acquired somatic mutations in hematopoietic progenitor cells that lead to the dysregulation of differentiation and the proliferation of hematopoietic cells [...]

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Cited by 4 publications

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References 34 publications

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“…Interestingly, the immunophenotype of KMT2A-rearranged AML was found to be different from other AML Rondoni Michela [Color figure can be viewed at wileyonlinelibrary.com] subcategories. KMT2A-rearranged AML is an aggressive subtype of AML with frequent monocytic or myelomonocytic differentiation, and some cases can present with lineage switch to acute lymphoblastic leukemia (Collins et al, 2020;Lanza & Bazarbachi, 2021). Interestingly, some cases of KMT2A-rearranged AML have an APL-like immunophenotype.…”

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Lanza

Rondoni

2022

Cytometry Part B Clinical

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mentioning

confidence: 99%

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Lanza

Rondoni

2022

Cytometry Part B Clinical

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PHF6 loss reduces leukemia stem cell activity in an acute myeloid leukemia mouse model

Yuan,

Gao,

Wang

et al. 2024

Cancer Cell Int

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Acute myeloid leukemia (AML) is a malignant hematologic disease caused by gene mutations and genomic rearrangements in hematologic progenitors. The PHF6 (PHD finger protein 6) gene is highly conserved and located on the X chromosome in humans and mice. We found that PHF6 was highly expressed in AML cells with MLL rearrangement and was related to the shortened survival time of AML patients. In our study, we knocked out the Phf6 gene at different disease stages in the AML mice model. Moreover, we knocked down PHF6 by shRNA in two AML cell lines and examined the cell growth, apoptosis, and cell cycle. We found that PHF6 deletion significantly inhibited the proliferation of leukemic cells and prolonged the survival time of AML mice. Interestingly, the deletion of PHF6 at a later stage of the disease displayed a better anti-leukemia effect. The expressions of genes related to cell differentiation were increased, while genes that inhibit cell differentiation were decreased with PHF6 knockout. It is very important to analyze the maintenance role of PHF6 in AML, which is different from its tumor-suppressing function in T-cell acute lymphoblastic leukemia (T-ALL). Our study showed that inhibiting PHF6 expression may be a potential therapeutic strategy targeting AML patients.

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Novel insights and therapeutic approaches in secondary AML

Marconi,

Rondoni,

Zannetti

et al. 2024

Front. Oncol.

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Secondary acute myeloid leukemia (sAML) presents as a complex and multifaceted ensemble of disorders, positioning itself as both a challenge and an intriguing frontier within hematologic oncology. Its origins are diverse, stemming from antecedent hematologic conditions, germline predisposing mutations, or the sequelae of cytotoxic therapies, and its development is driven by intricate genetic and epigenetic modifications. This complexity necessitates a diverse array of therapeutic strategies, each meticulously tailored to address the distinctive challenges sAML introduces. Such strategies require a personalized approach, considering the variegated clinical backgrounds of patients and the inherent intricacies of the disease. Allogeneic stem cell transplantation stands as a cornerstone, offering the potential for curative outcomes. This is complemented by the emergence of innovative treatments such as CPX-351, venetoclax, and glasdegib, which have demonstrated promising results in enhancing prognosis. The evolving landscape of sAML treatment underscores the importance of continued research and innovation in the field, aiming not only to improve patient outcomes but also to deepen our understanding of the disease’s biological underpinnings, thereby illuminating pathways toward more effective and individualized therapies.

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Targeted Therapies and Druggable Genetic Anomalies in Acute Myeloid Leukemia: From Diagnostic Tools to Therapeutic Interventions

Abstract: Acute myeloid leukemia (AML) is a clonal disorder resulting from acquired somatic mutations in hematopoietic progenitor cells that lead to the dysregulation of differentiation and the proliferation of hematopoietic cells [...]

Cited by 4 publications

References 34 publications

Issue Highlights—July 2022

Issue Highlights—July 2022

PHF6 loss reduces leukemia stem cell activity in an acute myeloid leukemia mouse model

Novel insights and therapeutic approaches in secondary AML

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