Mitochondrial defects in cancer
By J. Carew, Peng Huang. Molecular Cancer, 2002
613 citations recorded by the source corpus.
Mitochondria play important roles in cellular energy metabolism, free radical generation, and apoptosis. Defects in mitochondrial function have long been suspected to contribute to the development and progression of cancer. In this review article, we aim to provide a brief summary of our current understanding of mitochondrial genetics and biology, review the mtDNA alterations reported in various types of cancer, and offer some perspective as to the emergence of mtDNA mutations, their functional consequences in cancer development, and therapeutic implications.
Subfields: Cancer Research, Clinical Biochemistry, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/ff988ddfa6a75ee6bdfbde000d74cabea31d85a3
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In Cancer Research
In Clinical Biochemistry
In Molecular Biology
Citations in the corpus
- Glycolysis inhibition for anticancer treatment (2006, background): “Subsequent studies revealed that mitochondrial DNA (mtDNA) has high rates of mutations in cancer cells (for a review, see Carew and Huang, 2002; Singh, 2004; Taylor and Turnbull, 2005).”
- Succinate dehydrogenase and fumarate hydratase: linking mitochondrial dysfunction and cancer (2006, background): “This initial work was extended to a mammalian system, in which NIH3T3 mouse fibroblasts were transfected with a murine mutant of SDHC equivalent to the mev-1 mutant, and high levels of ROS accompanied by increased nuclear DNA mutagenesis were detected (Ishii et al., 2005).”
- Gene expression profiling of the tumor microenvironment during breast cancer progression (2009, background): “Given the importance of mitochondria in cancer [29,30], our novel finding suggests that the mitochondrial ribosome may be a potential therapeutic target and thus warrants further study.”
- Mitochondrial tumour suppressors: a genetic and biochemical update (2005, background): “Many tumours were shown to contain somatic mutations in mitochondrial DNA (mtDNA”
- Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, neutral): “…(mtDNA) is especially vulnerable because of its close proximity to the site of ROS generation, as well as its lack of introns and limited DNA repair. mtDNA mutations are frequently detected in cancer cells and are likely to result in mETC malfunction, further amplifying the generation of ROS (15).”
- ROS stress in cancer cells and therapeutic implications. (2004, background): “It is also known that mtDNA is more vulnerable to damage than nuclear DNA, and mtDNA mutations are frequently detected in cancer cells (Fliss et al., 2002; Augenlicht and Heerdt, 2001; Copeland et al., 2002; Carew and Huang, 2002; Carew et al., 2003; Kang and Hamasaki, 2003; Kumimoto et al., 2004).”