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    GENE:

    KMT2C (Lysine Methyltransferase 2C)

    i
    Other names: KMT2C, MLL3, Lysine Methyltransferase 2C, Histone-Lysine N-Methyltransferase 2C, Myeloid/Lymphoid Or Mixed-Lineage Leukemia Protein 3, Lysine (K)-Specific Methyltransferase 2C, Histone-Lysine N-Methyltransferase, H3 Lysine-4 Specific, Myeloid/Lymphoid Or Mixed-Lineage Leukemia 3, Histone-Lysine N-Methyltransferase MLL3, Lysine N-Methyltransferase 2C, ALR-Like Protein, KLEFS2
    6d
    Recruitment of BRD4 to the ASXL1 genomic targets depends on the extra-terminal domain of BRD4. (PubMed, Nat Commun)
    Genomic data from six cancer types reveals a strong positive ASXL1-BRD4 relationship, with BRD4 occupying the ASXL1 promoter and thus pointing to a possible feed-forward mechanism. Our findings provide mechanistic details by which ASXL1 associates with BRD4 and shed light on the biological significance of this association.
    Journal
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    ASXL1 (ASXL Transcriptional Regulator 1) • KMT2C (Lysine Methyltransferase 2C) • BRD4 (Bromodomain Containing 4)
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    ASXL1 mutation
    9d
    ELOC-mutated Renal Cell Carcinoma: Clinicopathologic, Immunohistochemical, and Molecular Genetic Analysis of 35 Cases. (PubMed, Mod Pathol)
    All patients with follow-up data were alive without evidence of disease progression. Our findings expand the clinical, histologic, immunohistochemical, and molecular spectrum of ELOC-mutated RCC and further support its classification as a distinct renal neoplasm.
    Journal
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    KMT2C (Lysine Methyltransferase 2C) • CA9 (Carbonic anhydrase 9) • MME (Membrane Metalloendopeptidase) • GPNMB (Glycoprotein Nmb) • CDH23 (Cadherin Related 23)
    11d
    Targeting lysine methyltransferase 2C deficiency: New frontiers in breast cancer therapy and prognosis. (PubMed, Clin Transl Med)
    Furthermore, we discuss emerging therapeutic strategies for KMT2C-deficient breast cancers, such as epigenetic modulators (EZH2 inhibitors, KDM6A inhibitors, and BET inhibitors), DNA damage response (DDR)-targeting agents, and pathway-specific inhibitors. These insights not only elucidate the complex biological functions of KMT2C in breast cancer but also provide a rationale for developing precision therapies tailored to KMT2C-mutant tumours.
    Review • Journal
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    IFNG (Interferon, gamma) • KMT2C (Lysine Methyltransferase 2C) • KDM6A (Lysine Demethylase 6A) • MMP3 (Matrix metallopeptidase 3)
    13d
    Chronic lymphocytic leukemia with IGH/BCL2 fusion and clonal heterogeneity: phenotypic and molecular profiling analysis of a rare case. (PubMed, Ann Hematol)
    NGS revealed that a common progenitor cell with BCL2-IgH translocation and mutations in TP53, KMT2A, KMT2C, and KMT2D gave rise to two distinct subclones: one (CD5 + CD23+CD200+) CLL driven by mutations in TNFAIP3 and BCORL1, and the other (CD5-CD23-CD200-) driven by mutations in EP300, NOTCH1, and BCL2. This case highlights the significance of clonal heterogeneity in CLL and underscores the crucial role of MFC, flow sorting, and molecular genetics in diagnosing and understanding the complex evolution of this disease.
    Journal • IO biomarker
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    TP53 (Tumor protein P53) • BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • KMT2A (Lysine Methyltransferase 2A) • IGH (Immunoglobulin Heavy Locus) • KMT2D (Lysine Methyltransferase 2D) • KMT2C (Lysine Methyltransferase 2C) • EP300 (E1A binding protein p300) • TNFAIP3 (TNF Alpha Induced Protein 3) • CD5 (CD5 Molecule) • CD200 (CD200 Molecule) • BCORL1 (BCL6 Corepressor Like 1) • FCER2 (Fc Fragment Of IgE Receptor II)
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    TP53 mutation • IGH mutation • MLL mutation
    13d
    Genomic and clinicopathological characteristics of low oncotype recurrent score breast cancers with subsequent metastasis. (PubMed, Histopathology)
    Using real-world CGP of tumour tissue and ctDNA, we identified key molecular features associated with endocrine resistance in patients with low RS who later developed metastases. PIK3CA mutation and other ER group-related mutations contributed to the low RS. Tissue CGP provides baseline for interpreting ctDNA, and ctDNA monitoring PIK3CA, TP53, ESR1 and other pathogenic or driver mutations in the early course of low RS cases may represent an excellent non-invasive option for identifying targets and early intervention to prevent disease progression, though a large validation study is needed.
    Journal
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    HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • KMT2C (Lysine Methyltransferase 2C) • MAP3K1 (Mitogen-Activated Protein Kinase Kinase Kinase 1) • EMSY (EMSY Transcriptional Repressor BRCA2 Interacting)
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    TP53 mutation • HR positive • HER-2 negative • PIK3CA mutation • ESR1 mutation
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    Oncotype DX Breast Recurrence Score®Test
    17d
    Taking the direct route: menin inhibitors go straight to the frontline in KMT2A-rearranged acute leukaemia. (PubMed, Exp Hematol)
    Menin inhibitors disrupt oncogenic transcription in KMT2A-rearranged leukaemias, but responses are heterogeneous. Mahdavi et al highlight the role of non-genetic resistance driven by altered chromatin context, including loss of KMT2C/D-UTX activity, underscoring the need for broader epigenetic profiling to guide therapy timing and combination strategy selection.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • KMT2C (Lysine Methyltransferase 2C)
    18d
    Clinicopathological and molecular features of acquired cystic disease-associated renal cell carcinoma (PubMed, Zhonghua Bing Li Xue Za Zhi)
    ACD-RCC is a rare renal cell carcinoma that occurs in patients with end-stage renal disease and has unique morphological features. It is often associated with favorable prognosis and alterations in genes related to the MTOR/TSC pathway or chromatin modification.
    Journal
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    ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • KMT2C (Lysine Methyltransferase 2C) • TSC2 (TSC complex subunit 2) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • SDHB (Succinate Dehydrogenase Complex Iron Sulfur Subunit B) • TSC1 (TSC complex subunit 1) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • TFE3 (Transcription Factor Binding To IGHM Enhancer 3) • MME (Membrane Metalloendopeptidase) • KMT2B (Lysine Methyltransferase 2B) • GATA3 (GATA binding protein 3) • PAX8 (Paired box 8) • TFEB (Transcription Factor EB 2)
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    TP53 mutation
    18d
    KMT2C Loss Promotes NF2-Wildtype Meningioma Progression and Ferroptosis Sensitivity via Epigenetic Repression of Hippo Signaling. (PubMed, Adv Sci (Weinh))
    Pharmacological restoration of histone acetylation with the HDAC inhibitor Trichostatin A (TSA) effectively suppressed tumor growth. Collectively, our findings identify KMT2C as a key epigenetic regulator linking promoter histone acetylation, NF2-Hippo pathway activity, and ferroptosis susceptibility. These results provide mechanistic insights into high-grade meningioma progression and highlight ferroptosis induction and epigenetic modulation as promising therapeutic strategies for NF2-wild-type, KMT2C-deficient meningiomas.
    Journal
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    KMT2C (Lysine Methyltransferase 2C) • EP300 (E1A binding protein p300)
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    trichostatin A (VTR-297)
    24d
    Harnessing AACR Project GENIE to Define the Molecular Features of Desmoplastic Small Round Cell Tumor. (PubMed, Curr Issues Mol Biol)
    Our data highlights mutational variation across demographic cohorts. These patterns are vital to future studies into identifying diagnostic markers or therapeutic targets.
    Journal
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    TP53 (Tumor protein P53) • ARID1A (AT-rich interaction domain 1A) • FGFR4 (Fibroblast growth factor receptor 4) • KMT2C (Lysine Methyltransferase 2C) • WT1 (WT1 Transcription Factor) • EP300 (E1A binding protein p300) • FIP1L1 (Factor Interacting With PAPOLA And CPSF1) • ANKRD1 (Ankyrin Repeat Domain 1) • TRAF1 (TNF Receptor Associated Factor 1) • PCLO (Piccolo Presynaptic Cytomatrix Protein)
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    TP53 mutation • ATM mutation • ARID1A mutation
    29d
    A tryptophane-phenylalanine binding motif for the histone methyltransferases MLL4 and MLL3. (PubMed, J Biol Chem)
    A high correlation of expression of MLL4/MLL3 and the motif containing proteins in several tumor types suggests shared roles in oncogenic transcriptional programs. In conclusion, our findings highlight a potential relationship between the MLL4/MLL3 methyltransferases and diverse motif-containing epigenetic coregulators.
    Journal
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    KMT2D (Lysine Methyltransferase 2D) • KMT2C (Lysine Methyltransferase 2C)
    1m
    A novel oncogenic nonsense mutation of SMARCA4 and genetic characteristic analysis of SMARCA4 (BRG1)-deficient undifferentiated tumor of the bladder. (PubMed, Virchows Arch)
    This suggests that besides SMARCA4 deficiency, alterations in other genes may cooperatively contribute to the tumorigenesis of bladder undifferentiated tumors. These findings provide a reference for subsequent exploration of precise diagnostic and prognostic assessment and treatment strategies for this disease.
    Journal • IO biomarker
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    TP53 (Tumor protein P53) • CCND1 (Cyclin D1) • FGF19 (Fibroblast growth factor 19) • KMT2D (Lysine Methyltransferase 2D) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • KMT2C (Lysine Methyltransferase 2C) • FGF3 (Fibroblast growth factor 3) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • FGF4 (Fibroblast growth factor 4) • GLI1 (GLI Family Zinc Finger 1) • STAG2 (Stromal Antigen 2) • FLT4 (Fms-related tyrosine kinase 4) • RICTOR (RPTOR Independent Companion Of MTOR Complex 2) • EPHA3 (EPH receptor A3)
    1m
    A comparative analysis of mutational profiles between triple-negative breast cancer and non-triple-negative breast cancer. (PubMed, Discov Oncol)
    Our study delineates the distinct genomic mutational landscapes between TNBC and non-TNBC cohorts, and reveals somatic interactions, driver genes, mutational signatures and pathway enrichment. These findings highlight the distinct molecular features of TNBC, which may contribute to its aggressive clinical behavior.
    Journal • Tumor mutational burden
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    TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • KMT2C (Lysine Methyltransferase 2C) • MAP3K1 (Mitogen-Activated Protein Kinase Kinase Kinase 1) • TGFB1 (Transforming Growth Factor Beta 1) • GATA3 (GATA binding protein 3)
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    TP53 mutation • PIK3CA mutation