Mitochondria and Cancer Prevention Publisher



Taghizadehhesary F ; Akbari H
Source: Mitochondria and Cancer: From Basic Science to Clinical Applications - Understanding Pathogenesis, Therapy Resistance, and Disease Relapse Published:2026

Abstract

Cancer remains one of the leading causes of morbidity and mortality worldwide. Despite decades of research, the precise mechanisms driving cancer development are still not fully elucidated. Historically, cancer metabolism has been a major focus, with early theories, such as Otto Warburg’s hypothesis, suggesting that mitochondrial dysfunction plays a central role in cancer metabolism. This chapter introduces a novel hypothesis: that progressive mitochondrial dysfunction, leading to cellular energy depletion, is the primary trigger for genomic instability and cancer formation. Drawing inspiration from Avicenna’s ancient notion of disease as a consequence of energy depletion, we propose that altered mitochondrial function not only initiates malignant transformation but also orchestrates the subsequent stages of cancer evolution. This chapter explores how various carcinogens—including aging, tobacco, alcohol, obesity, poor diet, inadequate sleep, environmental toxins, and infectious agents—compromise mitochondrial health. A new model of carcinogenesis is outlined, encompassing preparation, proliferation, quiescence, regeneration, and annihilation phases, each linked to mitochondrial dynamics. Importantly, we argue that preserving mitochondrial health may serve as a powerful strategy to prevent cancer initiation and progression by maintaining genomic integrity and enhancing immune surveillance. While genetic predisposition sets an underlying susceptibility, lifestyle factors play a decisive role in shaping cancer risk. By presenting an integrative, mitochondria-centered framework, this chapter aims to offer fresh insights into cancer prevention and inspire future research into therapeutic strategies targeting mitochondrial resilience. © 2026 Elsevier Inc. All rights reserved.