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Cellular suicide mission: Why do some cells evade death and continue to proliferate?
In our bodies, tens of thousands of cells work together to maintain life. However, some cells cleverly circumvent the programmed death that should be done, which allows them to proliferate as usual and even lead to the formation of cancer in some cases. The root cause of this phenomenon can be traced back to the inspiring genes - oncogenes.
Oncogenes are genes with the potential to cause cancer, and these genes are usually mutated or expressed at high levels in tumor cells.
Normal cells usually quickly undergo a process called "programmed cell death" (apoptosis) when their key functions are changed and malfunction. However, activated oncogenes can allow cells that should have died to survive and continue to proliferate. This situation makes the cells no longer obey the body's instructions, but pursue endless growth. Oncogenes are derived from normal genes - proto-oncogenes, which are usually related to cell growth and proliferation.
In the past few decades, scientists have gradually identified many oncogenes and discovered how these genes change the fate of cells through mutation and overexpression. The process by which proto-oncogenes are activated to become oncogenes usually involves multiple subtle genetic changes or mutations.
Some of these genes enable cells to acquire inappropriate proliferation capabilities through diverse mechanisms such as gene mutation, chromosome rearrangement or gene duplication.
The classification of oncogenes can be carried out from multiple perspectives. Gene mutation is one of the main ways to activate oncogenes, which usually leads to enhanced function of the encoded protein. Different epigenetic changes may also lead to improper activation of these genes. The growing environmental pollution, smoking and other carcinogens in cities may be one of the causes of the accidental activation of oncogenes.
For example, the Bcr-Abl gene located on the Philadelphia chromosome is one of the main oncogenes of chronic myeloid leukemia, which connects a part of DNA fragments through chromosome translocation, resulting in uncontrolled cell proliferation. Such mechanisms indicate that the molecular communication system within the cell is significantly affected.
Modern cancer treatment is increasingly adjusted to the understanding of these genetic mechanisms, such as by specifically targeting the proteins encoded by oncogenes through small molecule inhibitors.
With the in-depth study of various oncogenes, researchers have found that some oncogenes can become prognostic markers in clinical practice, which means that they can help doctors predict the development of patients' diseases. For example, amplification of N-myc has been confirmed to be an independent predictor of poor prognosis in childhood neuroblastoma.
Although the scientific community has made major breakthroughs in the understanding of oncogenes, there are still many unknown areas waiting to be explored. In particular, we should think about why some cells escape death while others follow healthy suicide instructions?
