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High EVI1 expression predicts poor outcome in Acute myeloid leukemia with intermediate cytogenetic risk in patients receiving chemotherapy.
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The relationship between EVI1 and microRNAs in human malignancies. [review]
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Fisher's exact SubID was used to reveal EVI1 as a transcriptional regulator of INPP4B in AML; a finding which was validated in vitro. Next, we used CoxPH SubID to conduct a pan-cancer analysis of INPP4B's prognostic significance
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Letter/Case Report: ETV6/MECOM gene fusion in therapy-related acute myeloid leukemia with t(3;12) and monosomy 7.
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These findings highlight a novel mechanism for hepatitis B virus X-induced hepatocarcinogenesis through transcription factor EVI1 and its target lncRNAs
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Findings represent the first global genome-wide study of EVI1 DNA binding associated with whole transcriptome expression analysis. Results reveal several important genes with an ETS-like binding motif, is involved in terminal myeloid differentiation, cell cycle regulation and apoptosis
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The expression of EVI1 and SOX9 is associated with stem cell-like and metastasis signatures, and their depletion impairs the metastatic potential of breast cancer cells. These results establish the mechanistic link between resistance to mTOR inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR targeting failure
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EVI1 contributes to PCa progression by regulating different oncogenic functions. EVI1 regulates the PCa stem cell compartment responsible for disease initiation and also development of CRPC.
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oncogenic potential for EVI1 in modulating genomic stability
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EVI1 acts as a regulator of its own expression, highlighting the complex regulation of EVI1, and open new directions to better understand the mechanisms of EVI1 overexpressing leukemias.
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EVI1 overexpression alters cellular metabolism. EVI1 promotes CKMT1 expression by repressing the myeloid differentiation regulator RUNX1.
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EVI1 transcription is directly regulated by LEF1/beta-catenin complex in myeloid blast crisis of chronic myeloid leukemia. Loss of p53 function as a key regulator for beta-catenin-EVI1 in myeloid blast crisis of chronic myeloid leukemia.
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we demonstrated that miR-22 promoted monocyte/macrophage differentiation, and MECOM (EVI1) mRNA is a direct target of miR-22 and MECOM (EVI1) functions as a negative regulator in the differentiation.The miR-22-mediated MECOM degradation increased c-Jun but decreased GATA2 expression, which results in increased interaction between c-Jun and PU.1
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Results establish the oncogenic contributions of EVI1 in ER- and HER2-negative subsets of breast cancer.
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MECOM gene harbors both somatic frameshift mutations.
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Isochromosome 3q, especially MECOM abnormality, could play a key role in Persistent polyclonal binucleated B-cell lymphocytosis.
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MECOM deletion is associated with congenital thrombocytopenia.
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involvement of MECOM in patients with acute myeloid leukemia and myelodysplastic syndrome with various 3q abnormalities
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RUNX1-Evi-1 may promote proliferation and apoptosis resistance of primitive hematopoietic cell, and inhibit the differentiation of myeloid cells with the synergy of different pathways and factors.
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EVI1 overexpression has been revealed as an important independent adverse prognostic marker in adult acute myeloid leukemia and defines distinct risk categories in 11q23-rearranged AML.
