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Potential culprits of cancer: What are oncogenes and how do they affect our health?
In today's medical field, cancer research continues to attract the attention of scientists, among which the role of oncogenes is particularly noteworthy. These genes are not only crucial to the formation of tumors, but also affect the methods and effects of treatment. What exactly are oncogenes? And how do they play a key role in our health?
An oncogene is a gene that has the potential to cause cancer. In tumor cells, these genes are often mutated or highly expressed, causing cells that should have died to survive and continue to proliferate.
Normally, normal cells undergo a pre-programmed rapid cell death program called apoptosis if their key functions are altered. However, when oncogenes in these cells are activated, this rule is violated, causing the cells to survive and proliferate without limit. These oncogenes originally originate from proto-oncogenes, which are normal genes that are mainly involved in the inhibition of cell growth, proliferation and apoptosis.
When these normal cell growth-promoting genes are upregulated through mutation (gain-of-function mutations), they predispose cells to become cancerous and are called oncogenes. Studies using most oncogenes have shown that the development of cancer often requires the combined action of multiple oncogenes and mutated apoptosis or tumor suppressor genes.
Since the 1970s, dozens of oncogenes have been identified and associated with human cancer. Many cancer drugs target proteins encoded by oncogenes.
The diversity of oncogene characteristics leads to the multiple effects of their protein products in various complex regulatory pathways within cells. Proto-oncogenes are usually normal genes that encourage cell growth and division. When they are upregulated and activated, they become oncogenes.
Oncogenes can be activated in a variety of ways, including gene mutation, chromosome rearrangement, and gene duplication. Genetic mutations can cause a person's genetic code to change when cells divide, leading to the persistent activation of cancer-causing genes. Through chromosomal rearrangement, the DNA sequence of a gene may also change when a cell divides. This change may place a gene near a signal switch that originally functions, causing it to malfunction. Gene duplication can cause a cell to have multiple copies of a gene, resulting in overproduction of a particular protein.
Future advances that PMolecular will study are the discovery of small molecule inhibitors that specifically target different oncoproteins and in-depth analysis of how oncogenes perturb normal physiological signals to cause different cancer types and developmental syndromes.
To meet these challenges, scientists are bridging the gap between clinical needs and translation into practice. With the development of precision medicine strategies for cancer, various oncogenes are also considered as prognostic markers. For example, N-myc amplification has been identified as an independent predictor of poor outcome in childhood neuroblastoma, making therapeutic interventions targeting this population increasingly important.
From a historical perspective, the existence of oncogenes was predicted by German biologist Theodor Boveri in his 1914 book The Problem of the Origin of Malignant Tumors. As time went on, the term was rediscovered by scientists at the National Cancer Institute in 1970, and in the following decades, the discovery of oncogenes provided new perspectives for cancer diagnosis and treatment.
The regulatory effects of oncogenes on signal transduction networks in tumor cells make them important therapeutic targets, especially during tumorigenesis and progression.
Although there is no unified classification standard for oncogenes, they are broadly divided into multiple categories, including growth factors, receptor tyrosine kinases, etc. Through these classifications, the medical community hopes to be able to develop targeted therapies more effectively and improve treatment outcomes.
With the in-depth study of oncogenes, future cancer treatments may be more personalized according to the genetic characteristics of individual patients. However, in this process, should we think about whether the progress in genetic research and treatment development can really change our understanding and treatment of cancer?
