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    GENE:

    MECOM (MDS1 And EVI1 Complex Locus)

    i
    Other names: MECOM, MDS1 And EVI1 Complex Locus, PRDM3, Ecotropic Virus Integration Site 1 Protein Homolog, Myelodysplasia Syndrome-Associated Protein 1, Histone-Lysine N-Methyltransferase MECOM, PR Domain 3, MDS1-EVI1, KMT8E, EVI1, MDS1, MDS1 And EVI1 Complex Locus Protein EVI1, MDS1 And EVI1 Complex Locus Protein MDS1, MDS1 And EVI1 Complex Locus Protein, Ecotropic Viral Integration Site 1, Myelodysplasia Syndrome 1 Protein, Myelodysplasia Syndrome 1, AML1-EVI-1 Fusion Protein, Zinc Finger Protein Evi1, Oncogene EVI1, AML1-EVI-1, RUSAT2, EVI-1
    3d
    The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis. (PubMed, Front Immunol)
    Clinically, EVI1 overexpression is one of the most robust independent indicators of poor prognosis, associated with therapy resistance and reduced overall survival. This review provides a detailed discussion of the mechanisms underlying EVI1's activation, its complex molecular functions in hematopoietic transformation, and its profound clinical implications in hematological malignancies.
    Review • Journal
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    PTEN (Phosphatase and tensin homolog) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • MECOM (MDS1 And EVI1 Complex Locus) • GATA2 (GATA Binding Protein 2) • TGFB1 (Transforming Growth Factor Beta 1)
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    MLL rearrangement
    4d
    SPINK2 silencing suppresses leukemic proliferation and restores myeloid commitment via MECOM downregulation in acute myeloid leukaemia. (PubMed, Cell Death Discov)
    Moreover, SPINK2-deficient FUJIOKA cells revealed a significant association between SPINK2 and MECOM expression, consistent with findings in patients harbouring complex karyotypes, yet absent in other AML subsets from the TARGET-AML cohort. Our findings suggest a novel potential correlation between SPINK2 and MECOM expression in complex karyotype leukemias and warrant further investigation into the underlying molecular mechanisms through which the SPINK2-MECOM axis enforces aberrant self-renewal and the development of novel targeted approaches aimed at modulating its expression in complex karyotypic AML.
    Journal
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    MECOM (MDS1 And EVI1 Complex Locus) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2)
    16d
    Aberrant epithelial differentiation may contribute to endometrial polyp formation: insights from single-cell analysis. (PubMed, Syst Biol Reprod Med)
    Study limitations include scRNA-seq restricted to the proliferative phase, which may limit generalizability. Nevertheless, future functional studies using primary epithelial organoids derived from EPs may provide a physiologically relevant model to evaluate targeted therapeutic strategies including hormonal interventions with potential applications in infertility management.
    Journal
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    MECOM (MDS1 And EVI1 Complex Locus) • KMT2B (Lysine Methyltransferase 2B)
    24d
    Prognostic Model Combining Mutational and Cytogenetic Profiles in Acute Myeloid Leukemia Treated with Venetoclax and Hypomethylating Agents. (PubMed, Blood Cancer Discov)
    Compared to existing HMA/VEN-specific models, our model demonstrated superior low- vs. intermediate-risk discrimination (31.9-month separation, p=0.002; HR=0.45, p=0.003), with comparable C-index. Our model supports personalized risk stratification for HMA/VEN-treated AML, pending broader validation.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • JAK2 (Janus kinase 2) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • MECOM (MDS1 And EVI1 Complex Locus)
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    TP53 mutation • KRAS mutation • CBL mutation
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    Venclexta (venetoclax)
    29d
    Mutant ASXL1 Drives Transcriptional Activation and Repression in Human Hematopoiesis. (PubMed, bioRxiv)
    Collectively, these studies highlight a highly reproducible model of mutant ASXL1 in the appropriate cell context. Further, they are the first to functionally describe the mutant ASXL1 interactome in the context of the human HSC, identifying new dependencies with therapeutic potential.
    Journal
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    ASXL1 (ASXL Transcriptional Regulator 1) • MECOM (MDS1 And EVI1 Complex Locus) • BRD4 (Bromodomain Containing 4)
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    ASXL1 mutation
    1m
    A rare cytogenetically cryptic MECOM rearrangement in a patient with myelodysplastic neoplasm and SF3B1 mutation identified by RNA sequencing: a case report. (PubMed, Front Oncol)
    Given the well-documented association between SF3B1 mutations and MECOM rearrangements, analysis of MECOM expression and RNA sequencing (RNA-seq) is crucial for SF3B1-mutated patients, even in the absence of elevated blast counts. Furthermore, this case underscores the need for further research into the synergistic biological role of spliceosome mutations and MECOM rearrangements in driving leukemia.
    Journal
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    SF3B1 (Splicing Factor 3b Subunit 1) • MECOM (MDS1 And EVI1 Complex Locus)
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    SF3B1 mutation
    1m
    Identification of cellular hierarchy in paediatric acute myeloid leukaemia: The Japan Children's Cancer Group trial (JCCG AML-12). (PubMed, Br J Haematol)
    LSPC-Cycle, FLT3-ITD and NUP98::KDM5A were considered independent prognostic factors in multivariate analysis. Findings indicate the prognostic relevance of cellular hierarchy and the importance of integrating hierarchy-specific molecular profiles for improved risk stratification and treatment formulation.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • MECOM (MDS1 And EVI1 Complex Locus) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • NUP214 (Nucleoporin 214) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • GATA1 (GATA Binding Protein 1) • GLIS2 (GLIS Family Zinc Finger 2) • KDM5A (Lysine Demethylase 5A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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    FLT3-ITD mutation
    2ms
    Highly effective combination of BRG1/BRM inhibitor with BET inhibitor or decitabine for high-risk MECOM-rearranged AML. (PubMed, Hemasphere)
    In AML with 3q26.2 rearrangements (r) the distal GATA2 hematopoietic enhancer becomes aberrantly relocated leading to activation of EVI1 expression. In patient-derived xenograft (PDX) models of AML with MECOM-r, compared to each drug alone, co-treatment with FHD-286 and BETi OTX015 significantly reduced AML burden and improved survival, without inducing significant toxicity. These findings highlight the FHD-286-based combinations as promising therapy of AML with chromosome 3q26.2 rearrangement and EVI1 overexpression.
    Journal
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • CDK4 (Cyclin-dependent kinase 4) • MECOM (MDS1 And EVI1 Complex Locus) • GATA2 (GATA Binding Protein 2) • SMARCA2 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 2)
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    decitabine • birabresib (OTX015) • camibirstat (FHD-286)
    2ms
    MECOM Function is Critical for AR-Driven Treatment-Resistant Prostate Cancer. (PubMed, Cancer Res)
    In prostate cancer, MECOM was exclusively overexpressed in both CRPC and enzalutamide-resistant CRPC and interacted with AR in the nucleus...These insights reveal the crucial role of EVI1 in regulating cell survival within the context of an AR-reprogrammed chromatin landscape. More importantly, the findings suggest that MECOM overexpression may be another biomarker that could significantly broaden the use of PARP inhibitors beyond those with HRR gene mutations.
    Journal • PARP Biomarker
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    HRD (Homologous Recombination Deficiency) • MECOM (MDS1 And EVI1 Complex Locus)
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    Xtandi (enzalutamide)
    2ms
    Optical genome mapping as a high-resolution tool for uncovering cytogenetic complex and cryptic alterations in a cohort of patients with MDS and AML. (PubMed, NPJ Precis Oncol)
    The identified abnormalities have shown significant and potential clinical implications. Additionally, the discovery of novel alterations could offer insights into previously unknown pathogenic mechanisms, enhancing our understanding of AML and MDS pathogenesis.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • MECOM (MDS1 And EVI1 Complex Locus)
    2ms
    Venetoclax Added to Fludarabine + Busulfan Prior to Transplant and to Maintenance Therapy for AML, MDS, and MDS/MPN (clinicaltrials.gov)
    P1, N=102, Active, not recruiting, Jacqueline Garcia, MD | Trial completion date: Feb 2026 --> Mar 2027 | Trial primary completion date: Dec 2025 --> May 2026
    Trial completion date • Trial primary completion date
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • BCR (BCR Activator Of RhoGEF And GTPase) • BCL2 (B-cell CLL/lymphoma 2) • NPM1 (Nucleophosmin 1) • NF1 (Neurofibromin 1) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • DEK (DEK Proto-Oncogene) • RIT1 (Ras Like Without CAAX 1) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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    TP53 mutation • KRAS mutation • NRAS mutation • RUNX1 mutation • RAS mutation • ASXL1 mutation • CBL mutation • Chr del(5q)
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    Venclexta (venetoclax) • azacitidine • Inqovi (decitabine/cedazuridine) • fludarabine IV • busulfan
    3ms
    Pemigatinib After Chemotherapy for the Treatment of Newly Diagnosed Acute Myeloid Leukemia (clinicaltrials.gov)
    P1, N=32, Recruiting, OHSU Knight Cancer Institute | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026
    Trial completion date • Trial primary completion date
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    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • DEK (DEK Proto-Oncogene) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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    TP53 mutation • FLT3 mutation • RUNX1 mutation • ASXL1 mutation • EZH2 mutation • SRSF2 mutation • Chr del(5q)
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    cytarabine • Pemazyre (pemigatinib) • daunorubicin • Starasid (cytarabine ocfosfate)