28 July 2011

Is a cancerous tumor an independent biological species?

Carcinogenesis as speciation
Kirill Stasevich, Compulenta

According to a group of scientists, the cause of cancer is large-scale chromosomal rearrangements, and not point mutations in several genes. Cancer cells eventually get their own, relatively stable karyotype, which makes it possible to call another cancer a new biological species.

The idea that cancer is not only a disease, but also a stage of speciation is far from new; such views were expressed, for example, by the evolutionary biologist Julian Huxley in 1956. The criterion of the new species for him was autonomy: as soon as a cell becomes independent of its environment, it can be considered, if not a new species, then at least confidently embarked on the path of speciation.

Cancer cells really have this ability: they do not obey the laws of the host organism and decide for themselves where, how and when to live and reproduce. Finally, there is an example of long-lived cancer cell lines like HeLa. Attempts were made to describe the development of cancer clones in terms of evolutionary theory, but in the case of malignant tumors, evolutionists faced one problem: the karyotype of cancer cells does not differ in constancy.

Peter Duesberg and his colleagues from the University of California at Berkeley in their article in the journal Cell Cycle (Is carcinogenesis a form of speciation?) describe carcinogenesis as one of the ways of speciation, based precisely on the instability of the karyotype of cancer cells. At the same time, Mr. Duesberg encroaches on the currently prevailing theory that explains malignant degeneration by multiple mutations that fall into some key genes. On the contrary, according to the researchers, the cause of carcinogenesis is chromosomal malfunctions: doubling, deletions, remounting of chromosomes when a piece of another is sewn to one, etc. These changes affect not even tens, but thousands of genes. As a result of such rearrangements, a new cell appears, which may well claim to be the ancestor of a new species.

One of the most well–known clinical consequences of chromosomal aberration is Down syndrome, when a person has a third copy of the 21st chromosome. This phenomenon is called aneuploidy, it is a change in the number of copies of one or more chromosomes, and not their entire set. Aneuploidy is characteristic of all cancer cells, it has been known for a long time, but, as the authors of the article emphasize, this is not a consequence, but a cause of cancer degeneration. In a cell, something goes wrong in the mechanisms of duplication and (or) division of chromosomes preceding cell division; as a result, one of the daughter cells may be the owner of an extra copy of the chromosome, and the second, on the contrary, does not receive copies of one or more chromosomes. Usually, for a cell, this is equivalent to a death sentence (only plants calmly tolerate large-scale rearrangements in the karyotype). But it may also happen that the chromosomal aberration will be "compatible with life", and decades later a stable, but different from the "normal" set of chromosomes will be fixed in the descendants of this cell.

Cancer cells have a rather unstable, mobile chromosome set, which distinguishes them from ordinary biological species. But at the same time, they do not need to worry about reproduction, which in all others primarily suffers from chromosomal rearrangements. A malignant cell divides mitotically, and as long as the genes controlling mitosis are not affected, it can afford significant changes in the karyotype. The researchers analyzed the karyotypes of several cancer cell lines within several generations. It turned out that within the same line, the set and structure of chromosomes in cells do not change, but at the same time they can differ greatly from the chromosomal set of a tumor of a different type or even from a tumor of the same cancer, but taken from another patient. The most outstanding example here is again the HeLa cell line, which was taken from the patient Henrietta Lacks in 1951: since then, this line has existed autonomously, outside the body and has a completely stable karyotype compared to the one it had in the first years of its existence.


Chromosomal set of normal (left) and cancer cells (picture of the authors of the study).

The individual karyotype, set and structure of chromosomes is the "identity card" of a biological species. So far, no species with the same karyotype have been found, it differs even in humans and chimpanzees, although the number of common genes between us and chimpanzees reaches 99%. The presence of its own karyotype makes it possible to attribute cancer cell lines to new species or at least to the initial stages of speciation. As a convenient analogy, they can be compared with parasitic organisms, especially since there are at least three types of tumors that can be transmitted as parasites – with the help of individual cancer cells from individual to individual (these include a facial tumor that destroys marsupial Tasmanian devils, transmissible venereal sarcoma of a dog and a similar type of cancer found in hamsters).

According to scientists, within the framework of such a hypothesis, it is possible to explain the long time interval separating the initial chromosomal rearrangement and the appearance of a full-fledged cancer: not every variation in the set of chromosomes can lead to the appearance of an independent, species-specific karyotype.

Such a view of things can greatly change the approach to cancer therapy. Indeed, in reality, very, very few drugs developed on the basis of the concept of cancer as a consequence of several point mutations have brought at least some benefit. However, the power of the scientific and pharmacological industry, which tirelessly produces such drugs, is such that one can hardly hope for an early "paradigm shift"...

Prepared based on the materials of the University of California at Berkeley: Are cancers newly evolved species?

Portal "Eternal youth" http://vechnayamolodost.ru28.07.2011


Found a typo? Select it and press ctrl + enter Print version