Lung cancer can affect the airways or the air sacs deep within the lungs. Patients with cancerous growth in the lungs develop a number of symptoms of tumor growth, such as difficulty breathing, shortness of breath, persistent coughing and coughing up blood. Lung cancer development often relies on a number of factors, including environmental factors such as cigarette smoke, but may also be influenced by genetic mutations.
p53 Mutations
A common genetic influence on lung cancer are p53 mutations. Under normal conditions, p53 acts as a tumor suppressor gene--it helps to control cell division and prevents rapid cell proliferation. Cells also activate p53 in response to DNA damage, allowing the cell to repair any genetic mistakes before division. In lung cancer, p53 mutations prevent the activation of p53, allowing the cell to rapidly divide and accumulate genetic mutations and errors. A study published in the "Annals of Surgical Oncology" in 2010 indicates that p53 mutations usually develop early in lung cancers such as non-small cell lung cancer, and the mutations help drive future cancer development.
KRAS Mutations
Another common genetic influence on lung cancer development are mutations to the KRAS gene. Mutant KRAS is considered an oncogene--it helps drive cancer development. Under normal conditions, KRAS plays a role in the transmission of proliferative signals within the cell, with the activation of KRAS often promoting cell division. In lung cancer, mutations lead to a constantly active KRAS gene, so the cancer cell always receives signals to divide, and the cells eventually form a tumor. A study published in "The Proceedings of the American Thoracic Society" in 2009 notes that KRAS mutations are one of most common mutations in non-small cell lung cancer, and that lung cancers with KRAS mutations tend to prove aggressive and resistent to treatment.
EGFR Mutations
Mutations to the EGFR gene and protein can also influence lung cancer development. Under normal conditions, the EGFR protein, found at the cell surface, senses the presence of chemical signals outside the cell and becomes activated. The active EGFR then transmits a proliferative signal to the cell, triggering cell division. In cancer, EGFR mutations lead to an over-activation of EGFR, and the cell continually receives signals to divide, even in the absence of chemical signals outside the cell. A study published in "Science" in 2004 indicates that EGFR often proves an effective target for lung cancer treatment. The study reports that investigating EGFR mutations in patients can lead to sensitivity to EGFR-targeting cancer treatments, such as gefitinib.
References
- Annals of Surgical Oncology: Comparison of p53 and Epidermal Growth Factor Receptor Gene Status Between Primary Tumors and Lymph Node Metastases in Non-Small Cell Lung Cancers.
- The Proceedings of the American Thoracic Society: KRAS Mutations in Non--Small Cell Lung Cancer
- Science: EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy
