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BIOMARKER:

KDM6A mutation

i
Other names: KDM6A, Lysine Demethylase 6A, KABUK2
Entrez ID:
Related biomarkers:
2ms
We characterize mutational features and clinical outcomes of RA-MIBC. These patients exhibited significantly worse PFS and OS compared to primary MIBC. Although these tumors share mutations known to be associated with primary bladder tumors, we identified unique features associated with prior radiation therapy that may represent a biologically distinct entity compared to primary non-radiation associated bladder cancer.
BRCA Biomarker
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TP53 (Tumor protein P53) • BRCA2 (Breast cancer 2, early onset) • BRCA1 (Breast cancer 1, early onset) • MSH6 (MutS homolog 6) • CHEK2 (Checkpoint kinase 2) • FANCA (FA Complementation Group A) • KDM6A (Lysine Demethylase 6A)
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TP53 mutation • BRCA1 mutation • BRCA2 mutation • CHEK2 mutation • FANCA mutation • KDM6A mutation
4ms
Overall, we conclude that KDM6A mutation is frequent in BC and promotes tumour immune escape, which may serve as a novel biomarker to predict the immune response.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR3 (Fibroblast growth factor receptor 3) • ARID1A (AT-rich interaction domain 1A) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • RB1 (RB Transcriptional Corepressor 1) • STAG2 (Stromal Antigen 2) • EP300 (E1A binding protein p300) • KDM6A (Lysine Demethylase 6A) • MUC16 (Mucin 16, Cell Surface Associated) • CSMD3 (CUB And Sushi Multiple Domains 3)
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TP53 mutation • PIK3CA mutation • STAG2 mutation • ERBB3 mutation • KDM6A mutation • KDM6A expression
5ms
Advantaged gene mutations in KDM6A expand dramatically by crypt fission but not fusion. The crypt diffusion process enables accommodation of the additional crypts up to a threshold value, beyond which polyp growth may occur. The fission rate associated with KRAS mutations offers a potential explanation for KRAS-initiated polyps.
Journal • Tumor Mutational Burden
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KRAS (KRAS proto-oncogene GTPase) • TMB (Tumor Mutational Burden) • KDM6A (Lysine Demethylase 6A)
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KRAS mutation • KDM6A mutation
5ms
These data quantify the contribution of BC risk factors to mutational burden and suggest different signature enrichments among never, former, and current smokers.
Clinical • Journal • Tumor Mutational Burden
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TMB (Tumor Mutational Burden) • ERCC2 (Excision repair cross-complementation group 2) • KDM6A (Lysine Demethylase 6A)
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KDM6A mutation
9ms
This study provides new insights into the correlation between the TMB and the immune microenvironment in urothelial carcinoma. The result may be a reference to immunotherapy.
Tumor Mutational Burden • MSi-H Biomarker • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • CD8 (cluster of differentiation 8) • KMT2D (Lysine Methyltransferase 2D) • KDM6A (Lysine Demethylase 6A)
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PD-L1 expression • TP53 mutation • TMB-H • MSI-H/dMMR • KMT2D mutation • KDM6A mutation
9ms
These findings provide direct genetic evidence that HNF1A deficiency promotes PDAC. They also connect the tumor-suppressive role of KDM6A deficiency with a cell-specific molecular mechanism that underlies PDAC subtype definition.
Journal
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KRAS (KRAS proto-oncogene GTPase) • KDM6A (Lysine Demethylase 6A)
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KRAS mutation • KDM6A mutation
11ms
Again, our findings indicate the loss of Kdm6a causes germinal center hyperplasia, enhances plasma cell differentiation, and likely impairs class switch recombination (CSR). Taken together, our data shows that Kdm6a plays an important, but complex, role in B-cell transiting in the GC reaction and that loss of Kdm6a causes germinal center hyperplasia and impedes the B-cell immune response in a specific manner that may contribute to infection and B-cell malignancies.
IO biomarker
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CD19 (CD19 Molecule) • KDM6A (Lysine Demethylase 6A) • CD27 • FAS (Fas cell surface death receptor) • SDC1 (Syndecan 1)
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KDM6A mutation
1year
In male, gastric cancer patients with stage Ⅲ, intestinal type, diffuse type, simple surgical treatment and fluorouracil chemotherapy, the expression of KDM6A is related to the patient's overall survival time (all P<0.05)... The survival time of gastric cancer patients with KDM6A mutation or low expression is shorter. The mutation and expression of KDM6A are related to clinical pathological factors, which may become a potential target for the diagnosis and treatment of gastric cancer.
Retrospective data • Journal
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KDM6A (Lysine Demethylase 6A)
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KDM6A mutation
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fluorouracil topical
1year
© RSNA, 2020 Online supplemental material is available for this article. See also the editorial by Choyke in this issue
Journal
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR3 (Fibroblast growth factor receptor 3) • ARID1A (AT-rich interaction domain 1A) • RB1 (RB Transcriptional Corepressor 1) • TSC1 (TSC complex subunit 1) • STAG2 (Stromal Antigen 2) • KDM6A (Lysine Demethylase 6A)
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TP53 mutation • PIK3CA mutation • ARID1A mutation • FGFR3 mutation • RB1 mutation • TSC1 mutation • STAG2 mutation • KDM6A mutation
over1year
Our findings provide insights into multistep carcinogenic processes of BC and suggest molecular targeted therapeutic approaches for BC patients with Kdm6a dysfunction.
IL6 (Interleukin 6) • KDM6A (Lysine Demethylase 6A) • CCL2 (Chemokine (C-C motif) ligand 2)
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KDM6A mutation