Note in Science page
Created Jul 28 11, Updated Jul 28 11 17:11
Carcinogenesis: a form of speciation? go to comments

A new (or revived) theory / view on cancer

In a Cell Cycle journal article, researchers propose that cancer formation is akin to the evolution of a new species and that carcinogenesis is fulled by aneuploidy – losses or gains of chromosomes – [and other chromosomal damages] altering the expression and stability of the whole genome. Aneuploidy itself could be caused by carcinogens, certain replication errors (c.f. mitotic catastrophe) [and genome destabilizing mutations].
The Proponents of the classic mutation theory claim that aneuploidy is the consequence of cancer, here the researchers argue that it is the cause.

Spectral karyotyping of highly aneuploid (69 chromosomes!) human cell line UMSCC 81 ©

Driven by their inherent genetic instability, aneuploid cells evolve random karyotypes automatically. Most of these cell die, but a very small minority acquires reproductive autonomy and immortality [with enrichment in proto-oncogenes and tumor suppressor genes mutations]. Selection for reproductive survival stabilizes new cancer cells against the inherent instability of aneuploidy within specific margins of variation.
Genetic divergence, selection, then stabilization of a new karyotype: this looks like a speciation process.

In few words: Aneuploidy is not a wasteful side effect of being an immortal cancer cell harboring few cancer causing mutations, but the “root” of the cancer: messing the whole genome, and providing a pool of unstable = fast evolving parasitic cells – representing new species – ready to evolve against/around most treatments.
n.b. All cancer cells are aneuploid!
n.b. Some tumors are transmissible + with a distinct karyotype = they literally represent autonomous parasitic species! c.f. transmissible cancer wikipedia article

[but few mutations might induce/favor aneuploidy, so the classical “mutation theory” might be kind of right! just not starting with tumor suppressor gene / proto-oncogene mutations]

Cell Cycle paper: Is carcinogenesis a form of speciation? article article

“I think Duesberg is correct by criticizing mutation theory, which sustains a billion-dollar drug industry focused on blocking these mutations,” said Vincent, a medical oncologist. “Yet very, very few cancers have been cured by targeted drug therapy, and even if a drug helps a patient survive six or nine more months, cancer cells often find a way around it.”

[yes, but maybe there is only a finite number of “ways” a cell can be immortal and invasive, so blocking several – actual and potential – key mutations at the same time could some day keep most cancers at bay?]

because the disrupted chromosomes of newly evolved cancers are visible in a microscope, it may be possible to detect cancers earlier

[it’s known since ages isn’t it?... but ‘looks like it’s not that easy to put a tiny microscope inside our bodies to visit each cell ;-)] article

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