Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

KDM6A Loss Triggers an Epigenetic Switch That Disrupts Urothelial Differentiation and Drives Cell Proliferation in Bladder Cancer

13 Jan 2023

Abstract excerpt

Disruption of KDM6A, a histone lysine demethylase, is one of the most common somatic alternations in bladder cancer. Insights into how KDM6A mutations affect the epigenetic landscape to promote carcinogenesis could help reveal potential new treatment approaches. Here, we demonstrated that KDM6A loss triggers an epigenetic switch that disrupts urothelial differentiation and induces a neoplastic state characterized...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Bladder and Urothelial Cancer Treatments
Share to Epigenetics and DNA Methylation
Share to Ferroptosis and cancer prognosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36638328
DOI: 10.1158/0008-5472.can-22-1444

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

KDM6A Loss Triggers an Epigenetic Switch That Disrupts Urothelial Differentiation and Drives Cell Proliferation in Bladder CancerPMID 36638328Read ↗

Significance of KDM6A Mutation in Bladder Cancer Immune EscapeSemantic proximity Read ↗

Significance of KDM6A mutation in bladder cancer immune escape.Semantic proximity Read ↗

Significance of KDM6A Mutation in Bladder Cancer Immune EscapeSemantic proximity Read ↗

Kdm6a Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with p53 DysfunctionSemantic proximity Read ↗

Loss of UTX/KDM6A and the activation of FGFR3 converge to regulate differentiation gene-expression programs in bladder cancer.Semantic proximity Read ↗

Concurrent alterations in TERT, KDM6A, and the BRCA pathway in bladder cancer.Semantic proximity Read ↗

Loss of KDM6A-mediated genomic instability and metabolic reprogramming regulates response to therapeutic perturbations in bladder cancer.Semantic proximity Read ↗

Depletion of the m1A writer TRMT6/TRMT61A reduces proliferation and resistance against cellular stress in bladder cancerSemantic proximity Read ↗

Loss of KDM6A-mediated genomic instability and metabolic reprogramming differentially regulates responses to immune checkpoint therapy and chemotherapy in bladder cancerSemantic proximity Read ↗

Analysis of the role of mutations in the KMT 2D histone lysine methyltransferase in bladder cancerSemantic proximity Read ↗

Comprehensive integrative profiling of upper tract urothelial carcinomas.Semantic proximity Read ↗

The tumor-maintaining function of UTX/KDM6A in DNA replication and the PARP1-dependent repair pathwaySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.