The pathophysiology of lung cancer development is complicated and incompletely understood. The genes influenced in the pathogenesis of the cancer generate proteins involved in cell development and differentiation, apoptosis, tumor progression, cell cycle processes, angiogenesis, and immune regulation. Exposing these mechanisms ought to translate into novel means of risk stratification, early detection, prevention, and therapy.
The cancers are in general divided into small cell (SCLC) and non-small cell lung cancer (NSCLC).
Small cell lung cancer responds to radiotherapy and chemotherapy, and for that reason the treatment is extremely different from the other types. Malignant tumors arise most generally in response to repetitive carcinogenic stimuli, inflammation, or irritation. The mucosal lining is the most susceptible to injury, particularly at locations of bronchial bifurcation. The slow alteration of normal mucosal cells into malignant cells is a complex course.
Non-small cell lung cancer accounts for about 85% of all cancers of lung. It is divided further into squamous cell carcinoma, adenocarcinoma, and large cell carcinoma histologies. All of them share identical treatment methods and prognoses but have different histologic and clinical characteristics.
Cigarette smoking is accounts for about 30% of all cancer deaths. Particularly for Case of cancer of lung, smoking is high risk to expand the disease. It is about 85% of the Cases of cancer of lung in men and 75% in women caused by smoking. There are approximately 38 million former cigarette smokers and roughly 50 million smokers in the United States nowadays.
To explain about how mechanisms pathophysiology of cancers of lung course occurred, perhaps it will be more than one book.
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