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

SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer.

Cancer research - 15 Nov 2023

Zhou Xinyi, Sekino Yohei, Li Hong-Tao, Fu Guanghou, Yang Zhi, Zhao Shuqing, Gujar Hemant, Zu Xiongbing, Weisenberger Daniel J, Gill Inderbir S, Tulpule Varsha, D'souza Anishka, Quinn David I, Han Bo, Liang Gangning

Abstract excerpt

SETD2 deficiency alters the epigenetic landscape by causing depletion of H3K36me3 and plays an important role in diverse forms of cancer, most notably in aggressive and metastatic clear-cell renal cell carcinomas (ccRCC). Development of an effective treatment scheme targeting SETD2-compromised cancer is urgently needed. Considering that SETD2 is involved in DNA methylation and DNA repair, a combination treatment...

Read the complete abstract on PubMed

Topics

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

Share to Carcinoma, Renal Cell
Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Methylation

Share to Histone-Lysine N-Methyltransferase

Share to Kidney Neoplasms

Share to Poly(ADP-ribose) Polymerase Inhibitors

Source

Open in PubMed Open full text

Identifiers

PMID: 37695044
DOI: 10.1158/0008-5472.CAN-23-0401
PMCID: PMC10843145

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SETD2 Deficiency Confers Sensitivity to Dual Inhibition of DNA Methylation and PARP in Kidney Cancer.PMID 37695044Read ↗

Loss of MLH1 confers resistance to PI3Kβ inhibitors in renal clear cell carcinoma with SETD2 mutation.Semantic proximity Read ↗

Loss of SETD2, but not H3K36me3, correlates with aggressive clinicopathological features of clear cell renal cell carcinoma patients.Semantic proximity Read ↗

SETD2: an epigenetic modifier with tumor suppressor functionality.Semantic proximity Read ↗

SETD2 loss-of-function promotes renal cancer branched evolution through replication stress and impaired DNA repair.Semantic proximity Read ↗

Loss of histone H3 lysine 36 trimethylation is associated with an increased risk of renal cell carcinoma-specific death.Semantic proximity Read ↗

SETting the Stage for Cancer Development: SETD2 and the Consequences of Lost Methylation.Semantic proximity Read ↗

SETD2 deficiency impairs β-catenin destruction complex to facilitate renal cell carcinoma formationSemantic proximity Read ↗

Kidney cancer: SETD2 affects DNA replication.Semantic proximity Read ↗

SETD2 Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell CarcinomaSemantic proximity Read ↗

[Research progress on the expression and carcinogenic mechanisms of SETD2 in malignant tumors].Semantic proximity Read ↗

Decreased Expression of SETD2 Predicts Unfavorable Prognosis in Patients With Nonmetastatic Clear-Cell Renal Cell Carcinoma.Semantic proximity Read ↗

SETD2 loss in renal epithelial cells drives epithelial‐to‐mesenchymal transition in a TGF ‐β‐independent mannerSemantic proximity Read ↗

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