ArticleCancer research2021
Recruitment of KMT2C/MLL3 to DNA Damage Sites Mediates DNA Damage Responses and Regulates PARP Inhibitor Sensitivity in Cancer.
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Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42citing papers in PubMed
5.0field-weighted citation impact, top 3% of its field
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
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- Multiregion profiling of genomic and transcriptional heterogeneity in head and neck squamous-cell carcinoma.ESMO open · 2026Article
- Genomic analysis of oesophageal carcinoma (EC) identifies recurrent mutations in histone methyltransferases as a distinctive subset.Oncogene · 2026Article
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
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- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Glutamine metabolism and its roles in tumor radiotherapy by regulating DNA damage repair.Frontiers in cell and developmental biology · 2026Review
- Molecular mechanisms of KMT2C alterations in gastrointestinal cancers: enhancer network destabilization, lineage plasticity, and clinical translation.Frontiers in immunology · 2026Review
- Genetic Characteristics of Disease Flare After Lenvatinib Discontinuation in Patients With Thymic Carcinoma: A Brief Report.JTO clinical and research reports · 2025Article
- Multidisciplinary management and molecular characterization of inferior vena cava leiomyosarcoma: a case report.World journal of surgical oncology · 2025Article
- KMT2C inactivation leads to PTEN downregulation and tolerance to DNA damage during cell cycle progression.NPJ precision oncology · 2025Article
- Identification of Anticancer Targets in Ovarian Cancer Using Genomic Drug Sensitivity Data.International journal of molecular sciences · 2025Article
- NAMPT haploinsufficiency is a collateral lethal therapeutic vulnerability in high-risk myeloid malignancies withBlood neoplasia · 2025Article
- Multiplex gene editing models of del(7q) reveal combinedBlood neoplasia · 2025Article
- USP51/GRP78/ABCB1 axis confers chemoresistance through decreasing doxorubicin accumulation in triple-negative breast cancer cells.Acta pharmaceutica Sinica. B · 2025Article
- Article
- Clinical, pathological and gene expression profiling of estrogen receptor discordance in breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Microarray analysis points to LMNB1 and JUN as potential target genes for predicting metastasis promotion by etoposide in colorectal cancer.Scientific reports · 2024Article
- Pan‑cancer analysis on the role of KMT2C expression in tumor progression and immunotherapy.Oncology letters · 2024Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Antao Chang *Department of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Liang Liu *Department of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.ORCID 0000-0001-8630-7430
Justin M AshbyDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Dan WuDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Yanan ChenNankai University School of Medicine, Tianjin, China.
Stacey S O'NeillDepartment of Pathology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Shan HuangDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Juan WangDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Guanwen WangDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Dongmei ChengDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Xiaoming TanDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
W J PettyDepartment of Internal Medicine, Division of Hematology and Oncology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.
Boris C PascheDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina.ORCID 0000-0002-3750-7898
Rong XiangNankai University School of Medicine, Tianjin, China.
Wei ZhangDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina. psun@wakehealth.edu wezhang@wakehealth.edu.
Peiqing SunDepartment of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Wake Forest Baptist Medical Center, Medical Center Blvd, Winston-Salem, North Carolina. psun@wakehealth.edu wezhang@wakehealth.edu.
Atrium Health Wake Forest Baptist · USNankai University · CN
Funding
Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4MTip60 in p38 and PRAK Mediated Oncogene-Induced Senescence and Tumor SuppressionR01CA131231 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUN, PEIQING · 2009 to 2018
$3.5MThe role of microRNA in oncogene-induced senescence and cancer developmentR01CA172115 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUN, PEIQING · 2014 to 2018
$1.8MNCI NIH HHS P30 CA012197NCI NIH HHS R01 CA131231NCI NIH HHS R01 CA172115
Abstract
When recruited to promoters, histone 3 lysine 4 (H3K4) methyltransferases KMT2 (KMT2A-D) activate transcription by opening chromatin through H3K4 methylation. Here, we report that
Indexed as
DNA DamageDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticMutationAnimalsApoptosisArgonaute ProteinsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell ProliferationDNA-Binding ProteinsFemaleHomologous RecombinationHumansLung NeoplasmsMiceAGO2 protein, humanArgonaute ProteinsBiomarkers, TumorDNA-Binding ProteinsKMT2C protein, humanPoly(ADP-ribose) Polymerase Inhibitors
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.