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

Mismatch repair deficiency: a temozolomide resistance factor in medulloblastoma cell lines that is uncommon in primary medulloblastoma tumours

13 Sept 2012

Abstract excerpt

BACKGROUND: Tumours are responsive to temozolomide (TMZ) if they are deficient in O(6)-methylguanine-DNA methyltransferase (MGMT), and mismatch repair (MMR) proficient. METHODS: The effect of TMZ on medulloblastoma (MB) cell killing was analysed with clonogenic survival assays. Expression of DNA repair genes and enzymes was investigated using microarrays, western blot, and immunohistochemistry. DNA sequencing and...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Genetic factors in colorectal cancer
Share to Glioma Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 22976800
DOI: 10.1038/bjc.2012.403

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mismatch repair deficiency: a temozolomide resistance factor in medulloblastoma cell lines that is uncommon in primary medulloblastoma tumoursPMID 22976800Read ↗

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

Epigenetic preconditioning with decitabine sensitizes glioblastoma to temozolomide via induction of MLH1Semantic proximity Read ↗

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

Temozolomide: Mechanisms of Action, Repair and ResistanceSemantic proximity Read ↗

Temozolomide Resistance in Glioblastoma Cell Lines: Implication of MGMT, MMR, P-Glycoprotein and CD133 ExpressionSemantic proximity Read ↗

O6-methylguanine-DNA methyltransferase-deficient phenotype in human gliomas: frequency and time to tumor progression after alkylating agent-based chemotherapy.Semantic proximity Read ↗

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

O6-Methylguanine-DNA methyltransferase in pediatric primary brain tumors: relation to patient and tumor characteristics.Semantic proximity Read ↗

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

O<sup>6</sup>‐methylguanine DNA methyltransferase and p53 status predict temozolomide sensitivity in human malignant glioma cellsSemantic proximity Read ↗

Efficacy of protracted temozolomide dosing is limited in MGMT unmethylated GBM xenograft modelsSemantic proximity Read ↗

MSH6 haploinsufficiency at relapse contributes to the development of thiopurine resistance in pediatric B-lymphoblastic leukemia.Semantic proximity Read ↗

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