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New mechanism of gene mutation inhibiting carcinogenesis of colorectal cancer!

publish:2021-07-14 10:08:13   views :979
unknown unknown publish:2021-07-14 10:08:13  
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For patients with ulcerative colitis (UC), chronic inflammation is often accompanied by periodic tissue damage and repair process, and eventually leads to the occurrence of colorectal cancer.


However, in the process of "damage repair" cycle, there is no clear answer to what kind of changes have taken place in the cellular structure of tissues, and how these changes lead to the occurrence of cancer.


Two articles published online today in nature, from different perspectives, analyzed the characteristics of cell mutation and tissue remodeling in intestinal tissues of patients with ulcerative colitis at different stages of development from chronic inflammation to cancer, and then revealed the key genes in the development of enteritis and colorectal cancer.


Research background


Somatic evolution refers to the process in which the number of somatic mutations is increasing and the degree of mutation is accumulating during the occurrence and development of cancer.


We know that most tissues in the human body maintain "steady-state balance" through continuous self-renewal. In the process of self-renewal, somatic cells inevitably produce gene mutation 2.


In recent years, the breakthrough of sequencing technology enables us to identify gene mutation types in normal tissues at the single cell level.


However, it is worth noting that these mutated genes are highly similar to the genes that drive tumor production.


Genetic studies have also shown that somatic cell evolution enables cells to produce the ability of "spontaneous self-renewal", thus contributing to the generation of tumors. These results emphasize the importance of somatic cell evolution in carcinogenesis.


Learning from Darwin's "natural selection theory", somatic mutation may be affected by the surrounding environment at the same time. However, there is no experimental evidence to confirm this hypothesis.

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