Similar to many other cancers, lung cancer is initiated by either the activation of oncogenes or the inactivation of tumor suppressor genes. Carcinogens cause mutations in these genes that induce the development of cancer. Mutations in the K-ras proto-oncogene contribute to roughly 10–30% of lung adenocarcinomas. Nearly 4% of non-small-cell lung carcinomas involve an EML4-ALK tyrosine kinase fusion gene. Epigenetic changes such as alteration of DNA methylation, histone tail modification, or microRNA regulation may result in the inactivation of tumor suppressor genes. Importantly, cancer cells develop resistance to oxidative stress, which enables them to withstand and exacerbate inflammatory conditions that inhibit the activity of the immune system against the tumor. The epidermal growth factor receptor (EGFR) regulates cell proliferation, apoptosis, angiogenesis, and tumor invasion. Mutations and amplification of EGFR are common in NSCLC, and they provide the basis for treatment with EGFR inhibitors. Her2/neu is affected less frequently. Other genes that are often mutated or amplified include c-MET, NKX2-1, LKB1, PIK3CA, and BRAF. The cell lines of origin are not fully understood. The mechanism may involve the abnormal activation of stem cells. In the proximal airways, stem cells that express keratin 5 are more likely to be affected, typically leading to squamous-cell lung carcinoma. In the middle airways, implicated stem cells include club cells and neuroepithelial cells that express club-cell secretory protein. SCLC may originate from these cell lines or neuroendocrine cells, and it may express CD44. Metastasis of lung cancer requires transition from epithelial to mesenchymal cell type. This may occur through the activation of signaling pathways such as Akt/GSK3Beta, MEK-ERK, Fas, and Par6.
medical cause of Hemoptysis
symptom of Lung cancer
types of Lung cancer
medical cause of Hemothorax
medical cause of Bronchiectasis
medical cause of Chylothorax
medical cause of Bronchiolitis
symptom of Bronchiectasis