ArticleOncogene2000
Chromosomal instability and p53 inactivation are required for genesis of glioblastoma but not for colorectal cancer in patients with germline mismatch repair gene mutation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Molecular Pathogenesis of Glioblastoma in Adults and Future Perspectives: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Unconventional guardians of the brain: MAIT cells as emerging players in glioblastoma immunity.Frontiers in immunology · 2026Review
- Mismatch repair-deficient glioma with spatially distinct IDH-mutant and IDH-wild type components arising in the setting of Lynch syndrome.Cold Spring Harbor molecular case studies · 2023Article
- Sporadic and Lynch syndrome-associated mismatch repair-deficient brain tumors.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Multiple Faces of the Glioblastoma Microenvironment.International journal of molecular sciences · 2022Review
- CD9- and CD81-positive extracellular vesicles provide a marker to monitor glioblastoma cell response to photon-based and proton-based radiotherapy.Frontiers in oncology · 2022Article
- Lipid-Based Nanocarriers for The Treatment of Glioblastoma.Advanced nanobiomed research · 2021Article
- Role of Asparagine Endopeptidase in Mediating Wild-Type p53 Inactivation of Glioblastoma.Journal of the National Cancer Institute · 2020Article
- The Process and Regulatory Components of Inflammation in Brain Oncogenesis.Biomolecules · 2017Review
- Aberrant signaling pathways in glioma.Cancers · 2011Article
- Article
- Cerebral primitive neuroectodermal tumor in an adult with a heterozygous MSH2 mutation.Nature reviews. Clinical oncology · 2009Article
- Frequent loss of heterozygosity encompassing the hMLH1 locus in low grade astrocytic tumors.Journal of neuro-oncology · 2007Article
- Lack of EGF receptor contributes to drug sensitivity of human germline cells.British journal of cancer · 2005Article
- Molecular pathogenesis of astrocytic tumours.Journal of neuro-oncology · 2004Review
- Genome characteristics of primary carcinomas, local recurrences, carcinomatoses, and liver metastases from colorectal cancer patients.Molecular cancer · 2004Article
- Early-onset colorectal cancer with stable microsatellite DNA and near-diploid chromosomes.Oncogene · 2001Article
- Evidence of chromosomal instability in prostate cancer determined by spectral karyotyping (SKY) and interphase fish analysis.Neoplasia (New York, N.Y.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously reported high-frequency microsatellite instability (MSI-H) and germ-line mismatch repair gene mutation in patients with unusually young onset of high-grade glioma. Some of these patients developed metachronous MSI-H colorectal cancer and conformed to the diagnosis of Turcot's syndrome. Frameshift mutation of TGFbetaRII was present in all the colorectal carcinomas but not in brain tumours. We further characterized the genetic pathways of tumour evolution in these metachronous gliomas and colorectal carcinomas. All MSI-H glioblastomas had inactivation of both alleles of the p53 gene and showed over-expression of the p53 protein while none of the colorectal carcinomas had p53 mutation or protein over-expression. Flow cytometry and comparative genomic hybridization revealed that all glioblastomas were chromosomal unstable with aneuploid DNA content, and with a variable number of chromosomal arm aberrations. In contrast, the colorectal carcinomas had diploid or near-diploid DNA content with few chromosomal arm aberrations. The pattern of chromosomal aberrations in the two organs was different. Loss of 9p was consistently observed in all glioblastomas but not in colorectal carcinomas. Epidermal growth factor receptor amplification was absent in all glioblastomas and colorectal carcinomas. Our results suggest that both the frequency of p53 mutation and its effects differ greatly in the two organs. Following loss of mismatch repair function, p53 inactivation and chromosomal instability are not necessary for development of colorectal carcinoma, but are required for genesis of glioblastoma. Oncogene (2000) 19, 4079 - 4083.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.