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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

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Updated: Jul 12, 2026

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

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Mitochondrial mutations in cancer.

M Brandon¹, P Baldi, D C Wallace

¹Center for Molecular and Mitochondrial Medicine and Genetics (MAMMAG) and Institute for Genomics and Bioinformatics, University of California at Irvine, Irvine, CA 92697-3940, USA.

|August 8, 2006

Summary

Mitochondrial DNA mutations in tumors can either impair energy production, promoting cancer growth, or help tumors adapt to new environments. These findings suggest mitochondrial dysfunction is key to cancer development and may offer new treatment strategies.

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Area of Science:

Mitochondrial biology
Cancer research
Genetics

Background:

Solid tumors exhibit aerobic glycolysis, producing lactate and suggesting mitochondrial defects.
Mitochondria are crucial for cellular energy (OXPHOS), ROS generation, and apoptosis, using both nuclear and mitochondrial DNA (nDNA, mtDNA).
mtDNA, essential for OXPHOS, has a high mutation rate; severe mutations cause disease, while some polymorphisms aid environmental adaptation.

Purpose of the Study:

To investigate the role of mitochondrial DNA (mtDNA) mutations in cancer etiology.
To explore the dual nature of mtDNA mutations in tumor development and adaptation.
To identify potential new avenues for cancer diagnosis and treatment based on mitochondrial dysfunction.

Main Methods:

Analysis of tumor metabolism, specifically aerobic glycolysis and lactate production.
Review of known mutations in nuclear-encoded mitochondrial genes (e.g., fumarate hydratase, succinate dehydrogenase).
Examination of germline and somatic mtDNA mutations, including their prevalence in cancer and the general population.

Main Results:

Tumor cells utilize OXPHOS-derived ATP to drive glycolysis via induced hexokinase II.
Germline mtDNA mutations are linked to breast and endometrial cancers.
A significant percentage of tumor-specific somatic mtDNA mutations are also found in the general population, suggesting two classes: severe (inhibiting OXPHOS, promoting proliferation) and mild (aiding adaptation).

Conclusions:

Mitochondrial dysfunction is implicated in cancer etiology.
mtDNA mutations in tumors can be severe, promoting proliferation, or mild, facilitating adaptation.
Understanding these mtDNA mutations may lead to novel cancer diagnostic and therapeutic strategies.