Lung cancer is a solid tumour originating from the bronchial epithelial cells. This chapter distinguishes between non–small-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC) because they have different natural histories and responses to therapy.
WHAT ARE THE CAUSES OF LUNG CANCER?
Lung carcinomas arise from normal bronchial epithelial cells that have acquired multiple genetic lesions and are capable of expressing a variety of phenotypes.
Activation of proto-oncogenes, inhibition or mutation of tumour suppressor genes, and production of autocrine growth factors contribute to cellular proliferation and malignant transformation. Molecular changes, such as overexpression of c-KIT in SCLC and epidermal growth factor receptor (EGFR) in NSCLC, also affect disease prognosis and response to therapy. Cigarette smoking is responsible for approximately 80% of lung cancer cases. Other risk factors are exposure to environmental respiratory carcinogens (e.g., asbestos, benzene, and arsenic), genetic risk factors, and history of other lung diseases (e.g., chronic obstructive pulmonary disease [COPD] and asthma).
The major cell types are SCLC (~15% of all lung cancers), adenocarcinoma (~50%), squamous cell carcinoma (<30%), and large cell carcinoma. The last three types are grouped together and referred to as NSCLC.
WHAT ARE THE SIGNS AND SYMPTOMS OF LUNG CANCER?
The most common initial signs and symptoms are coughs, dyspnea, chest pain, or discomfort, with or without hemoptysis. Many patients also exhibit systemic symptoms such as anorexia, weight loss, and fatigue.
Disseminated disease can cause neurologic deficits from CNS metastases, bone pain, or pathologic fractures secondary to bone metastases, or liver dysfunction from hepatic involvement.
Paraneoplastic syndromes may be the first sign of an underlying malignancy; examples include hypercalcemia, syndrome of inappropriate antidiuretic hormone secretion, and hypercoagulable state.
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