Is there something fundamentally wrong with our conceptions of the nature of cancer or the orientation of cancer research? Are different biological principles required to understand the cellular phenomenon that is cancer, rather than the pathological principles that we have been applying for the last 100 years?

In this book, the author proposes a conceptual view of the nature of cancer that is fundamentally different from that currently considered to be correct. This view explains cancer not as a change driven by chromosomal aberrations or pathological forces, as it has been traditionally viewed, but as a change determined by basic principles of cell survival and evolution that have governed cellular life on Earth for millions of years. This concept unifies and explains the great diversity of abnormalities reported to take place within cancer cells into one single phenomenon called “atavistic metamorphosis,” and suggests a different approach to the treatment of cancer.

Atavistic metamorphosis proposes that cancer cells revert, evolutionarily, to their ancestral, independent status as single-celled organisms. That cancer cells metamorphose into that life form from a differentiated cell through a biological phenomenon known as “atavism” (a reversion to a past ancestral cell form). During atavistic transformation, cancer cells reacquire phenotypic properties of their ancestral precursor cells, the primitive prokaryotic bacteria-like and eukaryotic protist-like cells by reactivating evolutionary genetic information that has been conserved in the genome throughout the evolution of cells from single-celled, to multicellular organisms. An example of that phenomenon is the activation of the so called oncogenes, which are in many cases conserved homologous genes of those constitutively active in single-celled organisms. As independent, single-celled organisms, cancer cells have a life of their own and struggle inside the host for their own survival, where they feed, grow, reproduce, spread to surrounding tissues and distant organs, and kill the host as any other independent pathogenic single-celled organism (bacterial, protozoal or yeast cells) does.

This does not imply that cancer cells are bacteria, or protozoa, or yeasts. Instead, on the basis of the atavistic metamorphosis hypothesis, cancer cells are considered to be “chimeras.” This means that cancer cells express functional genetic and molecular elements of ancestral single-celled organisms (such as bacteria-like and protist-like organisms), in addition to expressing elements of their status as advanced animal cells. Thus, the phenotypic features of pathogenicity such as unlimited replicative potential; capacity for invasion, migration, and metastases; abilities to evade the host’s immune system, generate multidrug resistance; and abilities to live in hostile conditions are cellular traits reasserted from their hereditary past as primitive, independent single-celled organisms. At the same time, however, most of the cellular structure, molecular machinery and histocompatibility that allow them to live in the host, remain intimately connected with the biology of the human body in general and with the tissue of origin in particular. Their eradication requires the targeting of both components of the chimera.