In the field of cancer research, the transformation of "proto-oncogenes" into "oncogenes" is an important topic of discussion. How changes in these genes affect cell growth and division is a question that scientists today are trying to answer. When normal cells encounter mutations, genes that originally functioned to control cell proliferation and promote death unexpectedly transform into oncogenes that promote cancer growth.
Under normal conditions, proto-oncogenes are responsible for helping cells grow and divide, and their transformation into oncogenes usually involves mutation or overexpression.
Proto-oncogenes are forms of normal genes that are normally involved in cell growth and inhibiting apoptosis. Through various mutated forms, they may be "activated" to become oncogenes. The impact of such changes cannot be underestimated, as mutations in multiple oncogenes and tumor suppressor genes often need to cooperate for cancer to develop.
Activation of oncogenes can occur through several different mechanisms:
For example, the discovery of the Philadelphia chromosome is closely related to the formation of chronic myelogenous leukemia. This is a special chromosomal rearrangement that leads to the Bcr-Abl gene fusion, thereby producing a continuously active tyrosine kinase that promotes the development of tumor cells. proliferation.
Research on oncogenes can be traced back to the early 20th century. German biologist Theodore Bovelli predicted the existence of oncogenes in 1914, but the term was not renamed until 1969. In 1970, the first confirmed oncogene, SRC, was discovered in a chicken retrovirus. With the passage of time, more and more oncogenes have been identified, and research in this field is also frequently innovating.
Active oncogenes can affect a series of cell signaling pathways and promote abnormal cell proliferation. The role of these genes in cancer medicine is becoming increasingly clear, and many cancer treatment drugs are designed to target the proteins encoded by these genes.
Scientists often group cancer patients based on clinical characteristics to develop targeted treatments. If a patient has a high-risk genetic profile, he or she may need more aggressive treatment than other patients with benign disease. ”
N-myc amplification is considered an independent predictor of poor prognosis in childhood neuroblastoma. As long as N-myc amplification is detected in children at any stage, survival will be shortened, so intensive treatment is required.
Currently, research on oncogenes is not limited to the genetic level, but also involves the study of epigenetics. This shows that genes are not just markers of DNA sequences, but may be affected by environmental influences that change their expression patterns. With the advancement of science and technology, researchers hope to find specific inhibitors of oncogenes to reduce their harmful effects on cells.
The study of oncogenes not only helps to understand the mechanism of cancer, but also allows the development of treatments for specific types of cancer. Faced with the rapid progress in this field, we should think about: Will we be able to find an effective way to cure cancer in the future?