Mitochondria and Cancer Causation
Abstract
Mitochondria are integrated cellular organelles that couple nutrient oxidation to energy conservation and participate in biosynthesis, redox regulation, calcium handling, cell death, and intercellular signaling. Their contribution to cancer depends on cell lineage, genetic and epigenetic state, tissue environment, and disease stage. Mitochondrial alterations can promote malignant processes, restrict them, or arise as adaptations and consequences of disease. The mitochondria-first hypothesis assigns particular mitochondrial disturbances an initiating causal role, with a stronger interpretation proposing priority across cancer more generally. These interpretations require distinctions between mitochondrial participation, functional dependence, causal contribution to initiation, and universal necessity or sufficiency. Endosymbiotic ancestry and selection among mitochondrial genomes explain biological capacities and potential conflicts but do not establish the order of oncogenic events. Research on sleep, exercise, and diet identifies modifiable influences on cancer risk and outcomes, sometimes involving mitochondrial pathways. However, beneficial interventions acting through mitochondria do not retrospectively identify the cause of malignancy. Current evidence supports context-dependent mitochondrial contributions within interacting genetic, epigenetic, metabolic, immune, and tissue processes; it does not establish mitochondrial dysfunction as a generally necessary or sufficient initiating cause of cancer.
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BibTeX
@misc{silva2026mitochondria,
title = {{Mitochondria and Cancer Causation}},
author = {Sergio Da Silva},
howpublished = {Zenodo},
year = {2026},
month = oct,
doi = {10.5281/zenodo.23619411},
url = {https://zenodo.org/records/23619411},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - Mitochondria and Cancer Causation
AU - Sergio Da Silva
PY - 2026
DA - 2026/10/24
PB - Zenodo
DO - 10.5281/zenodo.23619411
UR - https://zenodo.org/records/23619411
AB - Mitochondria are integrated cellular organelles that couple nutrient oxidation to energy conservation and participate in biosynthesis, redox regulation, calcium handling, cell death, and intercellular signaling. Their contribution to cancer depends on cell lineage, genetic and epigenetic state, tissue environment, and disease stage. Mitochondrial alterations can promote malignant processes, restrict them, or arise as adaptations and consequences of disease. The mitochondria-first hypothesis assigns particular mitochondrial disturbances an initiating causal role, with a stronger interpretation proposing priority across cancer more generally. These interpretations require distinctions between mitochondrial participation, functional dependence, causal contribution to initiation, and universal necessity or sufficiency. Endosymbiotic ancestry and selection among mitochondrial genomes explain biological capacities and potential conflicts but do not establish the order of oncogenic events. Research on sleep, exercise, and diet identifies modifiable influences on cancer risk and outcomes, sometimes involving mitochondrial pathways. However, beneficial interventions acting through mitochondria do not retrospectively identify the cause of malignancy. Current evidence supports context-dependent mitochondrial contributions within interacting genetic, epigenetic, metabolic, immune, and tissue processes; it does not establish mitochondrial dysfunction as a generally necessary or sufficient initiating cause of cancer.
ER -