The Conglomerate Theory of Oncogenesis extends the foundational principles of the Conglomerate Theory of Aging to cancer development. It proposes that many forms of oncogenesis result from the reactive species initiated, universal processes that we posit as simultaneously driving aging: transition metal bioaccumulation, advanced glycation end product (AGE) formation, advanced lipoxidation end product (ALE) formation, and metal-AGE/ALE hybrid complex formation. The theory postulates that these processes create autocatalytic, mutually re-enforcing feedback loops that accelerate cellular transformation and tumor progression through their gradual accumulation. Unlike aging, which manifests as systemic decline, cancer represents a localized acceleration of these molecular damage processes, creating tumor-promoting microenvironments that drive oncogenesis, metastasis, and therapeutic resistance. This unified framework provides mechanistic insights into cancer development and offers a research agenda for multi-targeted therapeutic strategies to address the upstream molecular drivers of oncogenesis.
Nicholaus Nelson-Goedert (2025) studied this question.