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[Oncogenes and anti-oncogenes in lung cancer]
P Demoly1, J L Pujol, P Godard
1Clinique des Maladies respiratoires, Hôpital Arnaud de Villeneuve, Montpellier.
Abstract:
In all normal cells, two type of genes, oncogenes and anti-oncogenes, are expressed and control cell proliferation and differentiation. Cell growth is stimulated by oncogenes and inhibited by anti-oncogenes. Cancerization involves loss of control due to defective gene expression either by overexpression of a normal protein (loss of quantitative control) or expression of an abnormal protein (loss of qualitative control). Several oncogenes have been identified. They include three oncogenes, c-myc, N-myc and L-myc, known to be overexpressed in small-cell carcinomas of the lung. Point mutations of the oncogene K-ras is found in 15 to 30% of adenoma carcinomas, especially in smokers. Loss of anti-oncogene function has also been described in processes leading to lung cancer. Chromosome abnormalities, for example the 3p14-23 deletion described in 1982, are found in 100% of small-cell carcinomas and in 50% of non-small-cell carcinomas. This deletion is never found in normal tissue. The gene involved has not yet been cloned. Other mutations or deletions include the RB gene, necessary for neuroendocrine differentiation, and the p53 gene which has undergone mutation in 50% of the non-small-cell carcinomas and 70% of the small-cell carcinomas. These acquired mutations are strongly associated with tobacco smoking. Oncogenes and anti-oncogenes play an important role in the complex step-wise process leading to cancerization. As tumour characterization becomes more precise and precancerous states better controlled, future treatments may relief on inhibiting tumoural growth by using drugs which would substitute for the lost effect of anti-oncogenes or inhibit activation of an oncogene. But at the present time, it is still difficult to define criteria predicting high risk of postoperative relapse or resistance and further studies investigating the correlation between genetic abnormalities and clinical staging and survival curves are required.
Insights
Cancer arises from genetic control loss, involving oncogenes and anti-oncogenes. Understanding these genetic mutations, particularly in lung cancer, is crucial for future targeted therapies.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Context:
- Normal cells regulate proliferation and differentiation via oncogenes and anti-oncogenes.
- Cancerization results from a loss of this genetic control, through gene overexpression or abnormal protein expression.
Purpose:
- To review the roles of oncogenes and anti-oncogenes in cancer development, with a focus on lung cancer.
- To highlight specific genetic alterations associated with lung cancer, including oncogene mutations and anti-oncogene deletions.
Summary:
- Overexpression of c-myc, N-myc, and L-myc oncogenes is observed in small-cell lung carcinomas.
- Point mutations in the K-ras oncogene are common in lung adenocarcinomas, especially in smokers.
- Loss of anti-oncogene function, including 3p14-23 deletions and mutations in RB and p53 genes, is prevalent in lung cancers and linked to smoking.
Impact:
- Genetic abnormalities in oncogenes and anti-oncogenes are fundamental to the multi-step process of cancerization.
- Precise tumor characterization and better control of precancerous states may lead to novel treatments targeting oncogene activation or substituting anti-oncogene function.
- Further research is needed to correlate genetic alterations with clinical staging and survival to predict treatment response and postoperative relapse risk.