Cancer is a multifactorial disease
Last reviewed: 23.04.2024
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Scientists from the Institute of Biomedical Research in Barcelona (Spain), led by Travis Stacker and colleagues from the Sloan-Kettering Cancer Center in New York (USA), provided new information on the origin of malignant tumors. The results of their research are published in the journal Proceedings of the National Academy of Sciences (available publicly).
The authors of the paper believe that the primary appearance of a tumor, its type and aggressiveness depend on a specific combination of defects in several processes whose purpose is to preserve the integrity of cells, such as ways of restoring the normal structure of DNA or controlling the cell cycle (fission). As evidence of this, it was shown that mice with a high degree of chromosomal instability and a defective program of apoptosis (cell death) - these most expressive "black marks" of cancer - in fact rarely get cancer.
According to the researchers, whether a tumor is formed or not depends on, first, on that moment during the cell cycle, when the damage occurred, and secondly, on what particular component of the restoration system was affected, and finally on what else components of the system of self-destruction are weakened here and now. That is, most important is not one factor, not one breakdown (easily detected after the fact), but an unfortunate combination of several factors and defects.
The authors used mice carrying mutations in key genes responsible for the repair of damaged DNA. Then, these genes were combined with other mutations affecting either the course of apoptosis or the quality of control over the cell cycle, until the "unlucky" combination for mice was identified, the set of factors of which was sufficient to initiate oncogenesis.
During DNA replication in the dividing cell, there is a whole series of control points in which the correctness of the ongoing process of duplication is tested. If the cell detects errors at any point, the cell growth stops, and an extremely complex process of DNA repair is brought into play. If he also works with errors, and the cell accumulates more errors in the genome, the proteins of the last line of defense, such as the tumor suppressor p53, appear on the scene. Not exchanging for trifles, they immediately go on to activate the program of cell death or interrupt the cell cycle (the cell will grow old and die without leaving offspring). All this, as can be seen, is a very complex network of interacting proteins.
The study showed that genomic instability in itself is not a necessary and sufficient condition for the compulsory development of a tumor. The authors believe that it is necessary to study the different types of malignant neoplasms in more detail, trying to determine the key factors of the oncogenesis that has occurred, even if it is more difficult than to search for a needle in a haystack, as one single obvious factor, as it turns out now, is not enough.
Accurate identification of the components of "unlucky combinations" can turn modern diagnostics and therapy of oncological diseases.
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