CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice

Lange, Ana Paula Alencar de Lima; Almeida, Luciana Yamamoto; Silva, Cleide Lúcia Araújo; Scheucher, Priscila Santos; Chahud, Fernando; Krause, Alexandre; Bohlander, Stefan K.; Rego, Eduardo Magalhães

doi:10.1590/1414-431x20198424

Cited by 2 publications

(1 citation statement)

References 18 publications

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“…AML1-ETO fusion protein related to AML with t (8; 21) has been shown to trigger the transcription of BCL-2 [ 27 ]. In addition, BCL-2 expression is likely to be induced by transcription factor CCAAT/enhancer binding protein α, encoded by the CEBPA gene, which is mutated in about 10% of AML patients [ 30 , 51 , 52 ].…”

Section: An Overview Of the Impact Of Dysregulation In The Expression...mentioning

confidence: 99%

Targeting Apoptosis in AML: Where Do We Stand?

Krawiec

Strzałka²,

Czemerska³

et al. 2022

Cancers

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More than 97% of patients with acute myeloid leukemia (AML) demonstrate genetic mutations leading to excessive proliferation combined with the evasion of regulated cell death (RCD). The most prominent and well-defined form of RCD is apoptosis, which serves as a defense mechanism against the emergence of cancer cells. Apoptosis is regulated in part by the BCL-2 family of pro- and anti-apoptotic proteins, whose balance can significantly determine cell survival. Apoptosis evasion plays a key role in tumorigenesis and drug resistance, and thus in the development and progression of AML. Research on the structural and biochemical aspects of apoptosis proteins and their regulators offers promise for new classes of targeted therapies and strategies for therapeutic intervention. This review provides a comprehensive overview of current AML treatment options related to the mechanism of apoptosis, particularly its mitochondrial pathway, and other promising concepts such as neddylation. It pays particular attention to clinically-relevant aspects of current and future AML treatment approaches, highlighting the molecular basis of individual therapies.

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Section: An Overview Of the Impact Of Dysregulation In The Expression...mentioning

confidence: 99%

Targeting Apoptosis in AML: Where Do We Stand?

Krawiec

Strzałka²,

Czemerska³

et al. 2022

Cancers

View full text Add to dashboard Cite

show abstract

Zebrafish models of acute leukemias: Current models and future directions

Molina

Chavez

Grainger

2020

WIREs Developmental Biology

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Acute myeloid leukemias (AML) and acute lymphoid leukemias (ALL) are heterogenous diseases encompassing a wide array of genetic mutations with both loss and gain of function phenotypes. Ultimately, these both result in the clonal overgrowth of blast cells in the bone marrow, peripheral blood, and other tissues. As a consequence of this, normal hematopoietic stem cell function is severely hampered. Technologies allowing for the early detection of genetic alterations and understanding of these varied molecular pathologies have helped to advance our treatment regimens toward personalized targeted therapies. In spite of this, both AML and ALL continue to be a major cause of morbidity and mortality worldwide, in part because molecular therapies for the plethora of genetic abnormalities have not been developed. This underscores the current need for better model systems for therapy development. This article reviews the current zebrafish models of AML and ALL and discusses how novel gene editing tools can be implemented to generate better models of acute leukemias.

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CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice

Cited by 2 publications

References 18 publications

Targeting Apoptosis in AML: Where Do We Stand?

Targeting Apoptosis in AML: Where Do We Stand?

Zebrafish models of acute leukemias: Current models and future directions

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