ArticleCommunicative & integrative biology2012
The maintenance of mitochondrial genetic stability is crucial during the oncogenic process.
Article in Communicative & integrative biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Cancerous time estimation for interpreting the evolution of lung adenocarcinoma.Briefings in bioinformatics · 2024Article
- Consideration of Ketogenic Metabolic Therapy as a Complementary or Alternative Approach for Managing Breast Cancer.Frontiers in nutrition · 2020Review
- Screening of hub genes and pathways in colorectal cancer with microarray technology.Pathology oncology research : POR · 2014Article
- The identification of mitochondrial DNA variants in glioblastoma multiforme.Acta neuropathologica communications · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main energetic resources of the cell are the mitochondria. As such, these organelles control a number of processes related to the life and death of the cell and also have a prominent function in the maintenance of tumor cells. In the last years, several authors have proposed an active role for mitochondria in tumorigenesis, more specifically concerning somatic mutations in mitochondrial DNA (mtDNA). Here, we wanted to evaluate this hypothesis based on the conclusions obtained in a model of gliomagenesis with elevated levels of ROS (reactive oxygen species), a toxic by-product of tumor metabolism. According to our findings, none of the mtDNA variants were found relevant to the tumoral process or suggest the involvement of mitochondria in tumorigenesis beyond the metabolic requirements of the tumoral cell. We conclude that there is not enough evidence to support the claim that mitochondrial instability holds any relevant role in the tumoral process.
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Registered trials
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