Recognizing Cancer via Somatic and Organic Evolution

TL;DR

This paper proposes a novel cancer hypothesis based on somatic evolution, suggesting that cancer cells are mutated cells with high fitness that damage their microenvironment, leading to new therapeutic strategies focused on microenvironment improvement.

Contribution

It introduces a new cancer cell hypothesis linking somatic evolution to invasion and metastasis, and proposes microenvironment-based therapy as an alternative to traditional treatments.

Findings

Cancer cells are mutated cells with high fitness that damage the microenvironment.

Normal cells have the highest fitness in healthy microenvironments due to evolution.

Improving microenvironment can lower cancer cell fitness and halt tumor growth.

Abstract

The fitness of somatic cells of metazoan, the ability of proliferation and survival, depends on microenvironment. In somatic evolution, a mutated cell in a tissue clonally expands abnormally because of its high fitness as normal cells in a corresponding microenvironment. In this study, we propose the cancer cell hypothesis that cancer cells are the mutated cells with two characteristics: clonal expansion and damaging the microenvironment through the behaviours such as producing more poison in metabolism than normal cells. This model provides an explanation for the nature of invasion and metastasis, which are still controversial. In addition, we theoretically reasoned out that normal cells have almost the highest fitness in healthy microenvironments as a result of long-term organic evolution. This inspires a new kind of therapy of cancer, which improving microenvironment to make cancer cells lower in fitness than normal cells and then halt the growth of tumours. This general therapy relies on a mechanism differing from chemotherapy and targeted therapy.