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

Novel MSH6 mutations in treatment-naïve glioblastoma and anaplastic oligodendroglioma contribute to temozolomide resistance independently of MGMT promoter methylation.

Clinical cancer research : an official journal of the American Association for Cancer Research - 15 Sept 2014

Nguyen Stephanie A, Stechishin Owen D M, Luchman H Artee, Lun Xueqing Q, Senger Donna L, Robbins Stephen M, Cairncross J Gregory, Weiss Samuel

Abstract excerpt

PURPOSE: The current standard of care for glioblastoma (GBM) involves a combination of surgery, radiotherapy, and temozolomide chemotherapy, but this regimen fails to achieve long-term tumor control. Resistance to temozolomide is largely mediated by expression of the DNA repair enzyme MGMT; however, emerging evidence suggests that inactivation of MSH6 and other mismatch repair proteins plays an important role in...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Agents, Alkylating
Share to Dacarbazine

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to DNA Modification Methylases

Share to DNA Repair Enzymes

Share to Glioblastoma

Share to Oligodendroglioma

Share to Temozolomide

Share to Xenograft Model Antitumor Assays

Source

Identifiers

PMID: 25078279
DOI: 10.1158/1078-0432.CCR-13-1856

Genes

MSH6
MGMT

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Novel MSH6 mutations in treatment-naïve glioblastoma and anaplastic oligodendroglioma contribute to temozolomide resistance independently of MGMT promoter methylation.PMID 25078279Read ↗

MSH6 mutations arise in glioblastomas during temozolomide therapy and mediate temozolomide resistance.Semantic proximity Read ↗

Loss of the mismatch repair protein MSH6 in human glioblastomas is associated with tumor progression during temozolomide treatment.Semantic proximity Read ↗

A hypermutation phenotype and somatic MSH6 mutations in recurrent human malignant gliomas after alkylator chemotherapy.Semantic proximity Read ↗

A high frequency of MSH6 G268A polymorphism and survival association in glioblastoma.Semantic proximity Read ↗

ABT-888 restores sensitivity in temozolomide resistant glioma cells and xenograftsSemantic proximity Read ↗

Mismatch Repair Deficiency Does Not Mediate Clinical Resistance to Temozolomide in Malignant GliomaSemantic proximity Read ↗

Mechanisms of Resistance to Current Glioblastoma TherapiesSemantic proximity Read ↗

Restoration of Temozolomide Sensitivity by PARP Inhibitors in Mismatch Repair Deficient Glioblastoma is Independent of Base Excision RepairSemantic proximity Read ↗

The Temozolomide Mutational Signature: Mechanisms, Clinical Implications, and Therapeutic Opportunities in Primary Brain Tumor Management.Semantic proximity Read ↗

Mismatch repair proteins play a role in ATR activation upon temozolomide treatment in MGMT-methylated glioblastomaSemantic proximity Read ↗

Alkylpurine–DNA–N-glycosylase confers resistance to temozolomide in xenograft models of glioblastoma multiforme and is associated with poor survival in patientsSemantic proximity Read ↗

Hypermutagenesis in untreated adult gliomas due to inherited mismatch mutationsSemantic proximity Read ↗

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