Despite the fact that scientists have been researching the nature of cancer for many decades, they are still quite poorly understood. Even regarding the cause of their occurrence, debate continues in the scientific community. According to the main version, cancer occurs due to cell mutations. However, there are cases where a tumor appears without any changes in the DNA. Of course, it can be assumed that in these cases the changes simply could not be found. However, a recent study by an international group of scientists suggests that cancer can indeed occur without mutations.
Causes of cancer
Mutations in DNA that lead to cancer occur for various reasons. For example, this can be facilitated by external mutagens – products with harmful food additives, for example, deli meats, tobacco smoke, polluted air, etc. Mutations are also caused by oxidizing molecules, which are a byproduct of intracellular processes. Sometimes errors in DNA occur on their own during cell division.
It must be said that mutations associated with cancer can occur in different parts of the genome, both coding proteins and service RNAs, and non-coding ones. They also differ in their action – some contribute to the formation of a tumor, while others influence it after it has formed. But, in any case, as a result of mutations, the cell ceases to perform its function and begins to divide uncontrollably.
But how exactly do these mutations cause a healthy cell to turn cancerous? The answer is quite simple – they change the activity of genes. This suggests that there are other mechanisms that change gene activity without any changes in the DNA sequence.
How epigenetics affects gene activity
It has long been known that the activity of genes can be influenced by the epigenome – it is capable of both stimulating the work of a particular gene and suppressing it, without affecting the genetic sequence. Moreover, epigenetic changes can remain with a person throughout his life.
The epigenome modifies histone proteins in the cell, which affect the accessibility or inaccessibility of certain regions of the genome to other proteins that read genetic information. Simply put, they can hide part of the genome from reading proteins. Sometimes histones “package” certain parts of the genome into a “genetic archive,” hiding it throughout almost the entire life of the cell.
Epigenetic modification, that is, variation in the number and structure of histone proteins, can either promote or inhibit the transcription of certain genes. Epigenetic modification of histones occurs due to chemical methyl marks that are attached to them. However, the attachment of tags is not carried out by itself, but with the help of other Polycomb proteins. That is, without them, histones cannot receive methyl marks. But only methylated histones can package one or another section of DNA.
Why cancer occurs without mutation
Since polycomb proteins are the same in different organisms, for example, mammals and insects, scientists conducted an experiment with fruit fly larvae. During the study, they reduced the amount of some polycomb proteins. The result of this was the growth of tumors. That is, the larval cells lost their specialization and began to divide too quickly.
At a time when there was little of this protein in the cells, scientists noticed that the activity of some genes increased, which is not surprising. But the most interesting thing is that after the level of polycomb protein in the cells returned to normal, the tumors did not go away. At the same time, scientists noticed that after protein levels were normalized, gene activity decreased again, but not all. Some remained active.
As a result of further research, scientists discovered a chain of molecular signals that led to the constant activity of some proteins. These proteins are necessary for stem cells to maintain their stem state. In addition, they stimulate tissue regeneration and adjust metabolism in a certain way.
When “stem” proteins remain active all the time, malignant degeneration of cells occurs. Thus, an epigenetic anomaly, associated even with a temporary decrease in polycomb regulatory proteins, puts “stem” proteins into a mode of self-sustaining stimulation. Therefore, even when the “epigenetic brake” begins to work again, the “stem proteins” still continue to be active, thereby provoking tumor growth.
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All this suggests that cancer can arise without any mutations, solely due to certain failures in protein modification. Note that understanding the causes of tumor development and the processes that are associated with it is of great importance, as it will allow scientists to understand why different tumors not only develop differently, but also respond differently to treatment. For example, it is known that some tumors without mutations are able to resist chemotherapy and metastasize, but to this day it is not known how to effectively resist this.
It must be said that science also does not know many other points related to cancer. For example, scientists to this day do not know why fatal exhaustion occurs in cancer. We recently talked about the possible reason for this phenomenon, which can be found here.