ArticleOncogene2021
Large-scale analysis of KMT2 mutations defines a distinctive molecular subset with treatment implication in gastric cancer.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Pucotenlimab in patients with advanced mismatch repair-deficient or microsatellite instability-high solid tumors: A multicenter phase 2 study.Cell reports. Medicine · 2023Trial
- Genomic analysis of oesophageal carcinoma (EC) identifies recurrent mutations in histone methyltransferases as a distinctive subset.Oncogene · 2026Article
- Loss of Kmt2c/d promotes gastric cancer and confers vulnerability to mTORC1 and PD-1 inhibition.The Journal of clinical investigation · 2026Article
- Histone lysine methyltransferases KMT2C and KMT2D join the all-star tumor suppressor team in gastrointestinal cancer.The Journal of clinical investigation · 2026Article
- Review
- DNA Methylation in Gastric Cancer and Preneoplastic Lesions: Emerging Insights and Future Directions.Cancers · 2026Review
- Genomic Landscape of Poorly Differentiated Gastric Carcinoma: An AACR GENIELife (Basel, Switzerland) · 2026Article
- Non-catalytic role of SETD1A promotes gastric cancer cell proliferation through the E2F4-TAF6 axis in the cell cycle.Cell death & disease · 2025Article
- Multi-omic characterization of early-onset esophagogastric cancer.NPJ precision oncology · 2025Article
- CD2AP shapes a stromal reduced tumor microenvironment and contributes to immunotherapy in gastric cancer.BMC cancer · 2025Article
- Advancements in research leveraging phage display technology for gastric cancer diagnosis and treatment.Frontiers in microbiology · 2025Review
- KHSRP promotes cancer stem cell maintenance, tumorigenesis, and suppresses anti-tumor immunity in gastric cancer.Oncology research · 2025Article
- Utility ofInternational journal of nanomedicine · 2025Article
- Gastric Cancer in the Era of Epigenetics.International journal of molecular sciences · 2024Review
- Chromatin Remodeling-Related PRDM1 Increases Stomach Cancer Proliferation and Is Counteracted by Bromodomain Inhibitor.Journal of personalized medicine · 2024Article
- SL-scan identifies synthetic lethal interactions in cancer using metabolic networks.Scientific reports · 2023Article
- Gastric cancer treatment: recent progress and future perspectives.Journal of hematology & oncology · 2023Review
- Molecular Subtypes of Head and Neck Cancer in Patients of African Ancestry.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- PD-L1 expression-related PI3K pathway correlates with immunotherapy efficacy in gastric cancer.Therapeutic advances in medical oncology · 2023Article
- Chromatin and noncoding RNA-mediated mechanisms of gastric tumorigenesis.Experimental & molecular medicine · 2023Review
Corrections and comments
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Authors and funding
21 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frequent mutations of genes in the histone-lysine N-methyltransferase 2 (KMT2) family members were identified in gastric cancers (GCs). Understanding how gene mutations of KMT2 family affect cancer progression and tumor immune microenvironment may provide new treatment strategies. A total of 1245 GCs were analyzed using next-generation sequencing, whole transcriptome sequencing, immunohistochemistry (Caris Life Sciences, Phoenix, AZ). The overall mutation rate of genes in the KMT2 family was 10.6%. Compared to KMT2-wild-type GCs, genes involved in epigenetic modification, receptor tyrosine kinases/MAPK/PI3K, and DNA damage repair (DDR) pathways had higher mutation rates in KMT2-mutant GCs (p < 0.05). Significantly higher rates of high tumor mutational burden, microsatellite instability-high/mismatch-repair deficiency (dMMR), and PD-L1 positivity were observed in KMT2-mutant GCs (p < 0.01), compared to KMT2-wild-type GCs. The association between PD-L1 positivity and KMT2 mutations remained significant in the proficient-MMR and microsatellite stable subgroup. Based on transcriptome data from the TCGA, cell cycle, metabolism, and interferon-α/β response pathways were significantly upregulated in KMT2-mutant GCs than in KMT2-wild-type GCs. Patients with KMT2 mutation treated with immune checkpoint inhibitors had longer median overall survival compared to KMT2-wild-type patients with metastatic solid tumors (35 vs. 16 months, HR = 0.73, 95% CI: 0.62-0.87, p = 0.0003). In conclusion, this is the largest study to investigate the distinct molecular features between KMT2-mutant and KMT2-wild-type GCs to date. Our data indicate that GC patients with KMT2 mutations may benefit from ICIs and drugs targeting DDR, MAPK/PI3K, metabolism, and cell cycle pathways.
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