ArticleOncogene2004
mtDNA mutations in tumors of the central nervous system reflect the neutral evolution of mtDNA in populations.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 48 citations in OpenAlex.
- 'AnbioRxiv : the preprint server for biology · 2026Article
- Somatic Mutations in Nuclear and Mitochondrial Genes of Mitochondrial Proteins in Primary and Recurrent Glioblastoma.International journal of molecular sciences · 2026Article
- The effect of somatic mutations in mitochondrial DNA on the survival of patients with primary brain tumors.Croatian medical journal · 2024Article
- D-Loop Mutations as Prognostic Markers in Glioblastoma-A Pilot Study.International journal of molecular sciences · 2024Article
- Domestic Animal Models of Central Nervous System Tumors: Focus on Meningiomas.Life (Basel, Switzerland) · 2023Review
- Mitochondrial DNA Alterations in Glioblastoma (GBM).International journal of molecular sciences · 2021Review
- High Tumor Mitochondrial DNA Content Correlates With an Improved Patient's Outcome in WHO Grade III Meningioma.Frontiers in oncology · 2020Article
- Next-generation sequencing identifies novel mitochondrial variants in pituitary adenomas.Journal of endocrinological investigation · 2019Article
- Detection of somatic mutations in the mitochondrial DNA control region D-loop in brain tumors: The first report in Malaysian patients.Oncology letters · 2017Article
- Phylogenetic and population-based approaches to mitogenome variation do not support association with male infertility.Journal of human genetics · 2017Article
- Mitochondrial DNA Mutations in Grade II and III Glioma Cell Lines Are Associated with Significant Mitochondrial Dysfunction and Higher Oxidative Stress.Frontiers in physiology · 2017Article
- Proteomic and Mitochondrial Genomic Analyses of Pediatric Brain Tumors.Molecular neurobiology · 2015Article
- Identification and functional prediction of mitochondrial complex III and IV mutations associated with glioblastoma.Neuro-oncology · 2015Article
- Inhibition of oxidative metabolism leads to p53 genetic inactivation and transformation in neural stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Mitochondrial DNA mutations and breast tumorigenesis.Biochimica et biophysica acta · 2013Review
- Mitochondrial DNA mutations in human tumor cells.Oncology letters · 2012Article
- The maintenance of mitochondrial genetic stability is crucial during the oncogenic process.Communicative & integrative biology · 2012Article
- Article
- Uncovering the profile of somatic mtDNA mutations in Chinese colorectal cancer patients.PloS one · 2011Article
- A reduced number of mtSNPs saturates mitochondrial DNA haplotype diversity of worldwide population groups.PloS one · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial DNA (mtDNA) instability has been observed in different types of cancer, including colorectal, breast, and gastric cancer. The relationship between the occurrence of such alteration and the nuclear microsatellite instability (nMI) status of the neoplastic cells remains controversial. In an attempt to clarify this issue, we sequenced the first and second mtDNA hypervariable regions, and typed the mitochondrial (CA)(n) dinucleotide polymorphism in 69 patients with primary tumors of the central nervous system (CNS), previously screened for nMI. Tumor samples showed 27 D-loop sequence changes (39.1%) compared to the corresponding blood samples. Microsatellite homoplasmic allele mutations were detected in four cases (5.8%). We did not find significant associations of the mtDNA instability status with clinicopathological parameters including sex, age, tumor size, and duration of clinical course. Neither did we find any association between mtDNA and nuclear instabilities, indicating that, at least in CNS tumors, they respond to different DNA repair mechanisms. We have also compiled the mtDNA instabilities previously reported by other authors for several types of tumors, comparing them to mtDNA polymorphisms in human populations. Most of the tumor-associated changes are common human polymorphisms and mutational hotspots. To explain the molecular behavior of mtDNA instability in tumors, we propose a model also common to other biological situations.
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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.