Medically Reviewed By:
Last Updated on June 8, 2023 by Shabnam Sengupta
Lung cancer is a complex disease influenced by a combination of genetic and environmental factors. While smoking contributes to lung cancer, emerging evidence suggests that genetic variations play a role in determining an individual’s susceptibility to the disease. This article explores the genetic factors associated with lung cancer development, highlighting key gene mutations and their implications.
Can lung cancer be inherited?
The available evidence suggests that lung cancer is mostly not genetic. However, family history may increase the risk of lung cancer in both smokers and non-smokers. According to National Library of Medicine, the available evidence has shown that approximately 8% of lung cancer is inherited or has occurred due to heritable genetic factors. Some more studies have shown that a family history of lung disease is responsible to a certain extent for early-onset of the condition within the next generations. We need more studies to understand better how toxic genetic changes transfer to offspring that increase the risk of lung cancer.
What are some key genetic mutations associated with increased susceptibility to lung cancer?
Certain genetic mutations may have an increased susceptibility to lung cancer. One such mutation involves the EGFR gene, which regulates cell growth and division. Specific mutations like the exon 19 deletion and the L858R mutation in EGFR have been linked to a higher risk of developing non-small cell lung cancer (NSCLC). These mutations result in the overactivation of the EGFR protein, leading to uncontrolled cell growth and the formation of tumors. Testing for EGFR mutations is now a standard practice in NSCLC patients to guide targeted therapy.
Another genetic factor is the ALK gene, responsible for cell signaling and development. Rearrangements of the ALK gene, particularly fusion with the EML4 gene, have been identified in a subset of NSCLC patients. These rearrangements cause the constant activation of ALK signaling, promoting cancer cell growth and survival. ALK-targeted therapies, such as crizotinib, have shown significant effectiveness in treating ALK-positive NSCLC.
Additionally, several other genetic factors play a role in lung cancer development. KRAS mutations are frequently found in lung adenocarcinomas, especially in individuals with a history of smoking. These mutations activate KRAS signaling pathways, promoting tumor growth and resistance to certain therapies. Mutations in the TP53 gene, a tumor suppressor responsible for regulating cell division and DNA repair, are associated with an increased risk of developing lung cancer and poorer treatment outcomes. Mutations in the STK11 gene, often observed in individuals with familial adenomatous polyposis (FAP), are linked to a higher risk of developing lung cancer, particularly squamous cell carcinoma.
How does the interplay between genetic and environmental factors contribute to the development of lung cancer?
It’s important to note that genetic factors alone do not determine the development of lung cancer. Smoking, exposure to environmental pollutants (e.g., asbestos, radon), and other lifestyle factors interact with genetic predispositions, increasing the overall risk. Individuals with certain genetic mutations may be more susceptible to the carcinogens present in tobacco smoke or other environmental toxins, enhancing their likelihood of developing lung cancer.
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