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

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

Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine - 1 May 2015

Feng Chenchen, Ding Guanxiong, Jiang Haowen, Ding Qiang, Wen Hui

Abstract excerpt

Renal clear cell carcinoma (ccRCC) is characterized by frequent mutation in SETD2, which has recently been shown to regulate mismatch repair (MMR). We aim to investigate the association between MMR machinery genes and SETD2 mutation in ccRCC. We exploited the Genomics of Drug Sensitivity in Cance...

Read the complete abstract on PubMed

Topics

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

Share to Adaptor Proteins, Signal Transducing
Share to Carcinoma, Renal Cell
Share to DNA Mismatch Repair

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Histone-Lysine N-Methyltransferase

Share to Kidney Neoplasms

Share to MutL Protein Homolog 1

Share to Phosphoinositide-3 Kinase Inhibitors

Share to Proto-Oncogene Proteins c-akt

Source

Identifiers

PMID: 25528216
DOI: 10.1007/s13277-014-2981-y

Genes

SETD2
MLH1
PMS2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-25528216-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of MLH1 confers resistance to PI3Kβ inhibitors in renal clear cell carcinoma with SETD2 mutation.PMID 25528216Read ↗

High selectivity of PI3Kβ inhibitors in SETD2-mutated renal clear cell carcinoma.Semantic proximity Read ↗

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

PI3Kβ inhibitor TGX221 selectively inhibits renal cell carcinoma cells with both VHL and SETD2 mutations and links multiple pathways.Semantic proximity Read ↗

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

PRMT1 is a critical dependency in clear cell renal cell carcinoma through its role in post-transcriptional regulation of DNA damage response genesSemantic proximity Read ↗

Expression and Mutation Patterns of PBRM1, BAP1 and SETD2 Mirror Specific Evolutionary Subtypes in Clear Cell Renal Cell CarcinomaSemantic proximity Read ↗

BAP1, PBRM1 and SETD2 in clear-cell renal cell carcinoma: molecular diagnostics and possible targets for personalized therapies.Semantic proximity Read ↗

Significance of PBRM1 mutation in disease progress and drug selection in clear cell renal cell carcinoma.Semantic proximity Read ↗

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

POLR2A Drives Tumor Cell Aggressive in Both VHL and PBRM1 Mutation Renal-Cell CarcinomaSemantic proximity Read ↗

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