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    GENE:

    MGA (MAX Dimerization Protein MGA)

    i
    Other names: MAX Dimerization Protein MGA, MAD5, MAX Gene-Associated Protein, MAX Dimerization Protein 5, MXD5, MGA, MAX Dimerization Protein, MAX Gene Associated, FLJ12634, MGA
    1m
    Chromosome 15q15 Deletion Drives Brain Metastasis in Non-Small Cell Lung Cancer. (PubMed, J Thorac Oncol)
    The 15q15 deletion promotes BM development through aberrant MYC signaling and the subsequent reprogramming of carbohydrate metabolism.
    Journal
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    EGFR (Epidermal growth factor receptor) • MGA (MAX Dimerization Protein MGA)
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    EGFR mutation
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    elesclomol (STA-4783)
    1year
    In vivo CRISPR screens identify Mga as an immunotherapy target in triple-negative breast cancer. (PubMed, Proc Natl Acad Sci U S A)
    Interestingly, we observed that low MGA expression in breast cancer patients correlates with a favorable prognosis, particularly in those with active interferon-γ signaling. These observations provide insights into tumor immune escape mechanisms and suggest that further exploration of MGA's function could potentially lead to effective therapeutic strategies in TNBC.
    Preclinical • Journal • IO biomarker
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    IFNG (Interferon, gamma) • MGA (MAX Dimerization Protein MGA)
    almost2years
    Functional characterization of cooperating MGA mutations in RUNX1::RUNX1T1 acute myeloid leukemia. (PubMed, Leukemia)
    RUNX1::RUNX1T1 expression in Mga-deficient murine hematopoietic cells leads to a more aggressive AML with a significantly shortened latency. These data show that MGA regulates multiple pro-proliferative pathways in hematopoietic cells and cooperates with the RUNX1::RUNX1T1 fusion oncoprotein to enhance leukemogenesis.
    Journal
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • MGA (MAX Dimerization Protein MGA)
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    RUNX1 mutation • RUNX1-RUNX1T1 fusion • MGA mutation
    2years
    High-Grade Spindle Cell Sarcoma of the Scalp With an MGA::NUTM1 Gene Fusion in a Pediatric Patient. (PubMed, Am J Dermatopathol)
    In contrast to typical cases of spindle cell carcinomas or NC, NUTM1 fusion-positive sarcomas are associated with a better prognosis. This report highlights the importance of diagnostic workup of undifferentiated neoplasms, as identification of the MGA::NUTM1 fusion in spindle cell sarcoma could be used in treatment algorithms and lead to better outcomes, to the benefit of patients.
    Journal
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    BRD4 (Bromodomain Containing 4) • MGA (MAX Dimerization Protein MGA) • NUTM1 (NUT Midline Carcinoma Family Member 1) • BRD3 (Bromodomain Containing 3)
    2years
    Whole Genome and Transcriptome Sequencing of 21 Paired Chronic and Blast Phase CML Cases: Acquisition of Genomic Alterations, Changes in the Transcriptomic Profiles and Occurrence of B-Cell Receptor Rearrangements (ASH 2023)
    1) Extensive genetic profiling indicated a substantial clonal evolution in the progression from CP to BP CML including loss of ASXL1 mutations, expansion of RUNX1 mutated clones, multiple CNA, and the frequent acquisition of a BCR rearrangement in BP with a transcriptomic phenotype resembling B-ALL. 2) A subset of CML cases in CP already showed a transcriptomic phenotype resembling acute leukemia indicating a rapid progression to BP. 3) The presence of a RUNX1 mutated subclone or a clonal BCR rearrangement seem to represent a warning signal in CML CP.
    Clinical
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    ABL1 (ABL proto-oncogene 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • TET2 (Tet Methylcytosine Dioxygenase 2) • IKZF1 (IKAROS Family Zinc Finger 1) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • WT1 (WT1 Transcription Factor) • BCOR (BCL6 Corepressor) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • MECOM (MDS1 And EVI1 Complex Locus) • MGA (MAX Dimerization Protein MGA) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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    DNMT3A mutation • RUNX1 mutation • ASXL1 mutation • CDKN2A deletion • TET2 mutation • MLL rearrangement • BCOR mutation • IKZF1 deletion • WT1 mutation • MECOM rearrangement • SETD2 mutation • ABL1 fusion • MGA mutation • MLL3 mutation
    over2years
    Mucous Gland Adenoma of the Lung: A Neoplastic Counterpart of Mucinous Bronchial Glands. (PubMed, Mod Pathol)
    In conclusion, the gene expression profile, taken together with the histological similarity between MGA and bronchial glands, and the preferred location of the tumors (proximal airways with submucosal glands) suggest that MGA is a neoplastic counterpart of mucinous bronchial glands. NKX3.1 immunohistochemistry can be a sensitive and specific ancillary marker that distinguishes MGA from other histologic mimics.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • MGA (MAX Dimerization Protein MGA) • NKX3-1 (NK3 homeobox 1)
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    BRAF V600E • KRAS mutation • BRAF V600 • AKT1 mutation • MGA mutation
    over2years
    Mutational Spectrum and Prognosis Analysis of Young Patients with Diffuse Large B-Cell Lymphoma Based on Next-Generation Sequencing (PubMed, Zhongguo Shi Yan Xue Ye Xue Za Zhi)
    The aaIPI staging combination with molecular biology markers is more conducive to accurately judging the prognosis of young DLBCL patients. TP53, POU2AF1 and CCND3 mutations predict worse survival in the patients with the aaIPI high-risk group.
    Retrospective data • Journal • Next-generation sequencing
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    TP53 (Tumor protein P53) • B2M (Beta-2-microglobulin) • CARD11 (Caspase Recruitment Domain Family Member 11) • CCND3 (Cyclin D3) • MGA (MAX Dimerization Protein MGA) • POU2AF1 (POU Class 2 Homeobox Associating Factor 1)
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    CARD11 mutation • MGA mutation • SPEN mutation
    almost3years
    In vivo modeling of CLL transformation to Richter's syndrome reveals convergent evolutionary paths and therapeutic vulnerabilities. (PubMed, Blood Cancer Discov)
    Comparative human and murine RS analyses demonstrated tonic PI3K signaling as a key feature of transformed disease, with constitutive activation of the AKT and S6 kinases, down-modulation of the receptor phosphatase PTEN, and convergent activation of MYC/PI3K transcriptional programs underlying enhanced sensitivity to MYC/mTOR/PI3K inhibition. This robust experimental system presents a unique framework to study lymphoid biology and therapy.
    Preclinical • Journal
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    TP53 (Tumor protein P53) • PTEN (Phosphatase and tensin homolog) • MGA (MAX Dimerization Protein MGA) • CHD2 (Chromodomain Helicase DNA Binding Protein 2)
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    TP53 mutation • MGA mutation
    3years
    Disrupting MGA-MYC Driven Metabolic Reprogramming in Richter's Syndrome Pre-Clinical Models Via Novel Therapeutic Approaches (ASH 2022)
    In summary, our murine model reveals that MGA/MYC/NME1 axis drives RS through increased mitochondrial OXPHOS and ROS accumulation. Moreover, targeting this axis provides therapeutic benefits for RS, highlighting this pathway as a novel potential target for RS treatment.
    Preclinical
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • CD5 (CD5 Molecule) • EIF4EBP1 (Eukaryotic translation initiation factor 4E binding protein 1) • MGA (MAX Dimerization Protein MGA)
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    MYC overexpression • SF3B1 mutation • MYC expression • MGA mutation
    3years
    Rapid Generation of Murine CLL/Richter Syndrome Models By Multiplexed CRISPR/Cas9 Editing of Common CLL Driver Genes (ASH 2022)
    The effects of the introduced genetic lesions on leukemia cell growth and treatment resistance were investigated by analyzing the mutant allele frequency (MAF) of the injected cells and cells recovered from the spleens of untreated or venetoclax-treated mice... This study shows that multiplex CRISPR/Cas9 editing can be used to rapidly generate murine leukemias with the genetic make-up of human CLL or Richter Syndrome. These models can represent an important preclinical tool to study how individual genetic lesions cooperate during CLL development and progression and how they affect the response to treatment with novel therapeutic agents.
    Preclinical
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    TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • RB1 (RB Transcriptional Corepressor 1) • NOTCH1 (Notch 1) • CD19 (CD19 Molecule) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • BIRC3 (Baculoviral IAP repeat containing 3) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • CD5 (CD5 Molecule) • MGA (MAX Dimerization Protein MGA) • POT1 (Protection of telomeres 1) • NFKBIE (NFKB Inhibitor Epsilon) • CHD2 (Chromodomain Helicase DNA Binding Protein 2)
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    TP53 mutation • ATM mutation • NOTCH1 mutation • Chr del(13)(q14) • MGA mutation
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    Venclexta (venetoclax)
    almost4years
    MGA mutation status affect tumor immunomicroenvironment and predict the effect of immune check point inhibitor: From NSCLC to pan-cancers analysis (AACR 2022)
    This research investigated the immunotherapeutic value of MGA in pan-cancers, indicating that MGA-MUT could serve as a potential predictive biomarker for immune checkpoint inhibitors, and providing preliminary evidence regarding the function of MGA mutation and its role in anti-tumor immunity.
    Tumor Mutational Burden • IO biomarker • Pan tumor
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    TMB (Tumor Mutational Burden) • CD8 (cluster of differentiation 8) • MGA (MAX Dimerization Protein MGA)
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    MGA mutation