lung tumor

Etiology and Pathogenesis
Molecular basis

The accumulation of genetic abnormalities that result in transformation of benign bronchial epithelium into neoplastic tissue. The sequence of molecular changes is  not random but follows a predictable sequence that parallels the histologic progression toward cancer. Thus, inactivation of the putative tumor suppressor genes located on chromosome 3p is a very early event, whereas ?53 mutation or activation of the KRAS oncogene occur relatively late.
Cigarette smoking is strong  cacogenic factor.
The clinical evidence is largely composed of the documentation of progressive morphologic alterations in the lining epithelium of the respiratory tract in habitual cigarette smokers. These sequential changes have been best documented for squamous cell carcinomas, but they may also be present in other histologic subtypes. In essence, there is a linear correlation between the intensity of exposure to cigarette smoke and the appearance of ever more worrisome epithelial changes .
Major histologic subtypes of lung cancer, sequamous and small-cell carcinomas show the strongest association with tobacco exposure.
Asbestos workers; and workers exposed to dustus containing arsenic, chromium, uranium, nickel, vinyl chloride, and mustard gas.
The four major histologic types of carcinomas of the lung are squamous cell carcinoma, adenocarcinoma, small-cell carcinoma, and large-cell carcinoma.

Morphology
Squamous cell carcinomas are more common in men than in women and are closely correlated with a smoking history; they tend to arise centrally in major bronchi and eventually spread to local hilar nodes.
Large lesions may undergo central necrosis, giving rise to cavitation.
Squamous cell carcinomas are often preceded for years by squamous metaplasia or dysplasia  in the bronchial epithelium, which then transforms to carcinoma in situ.
When a well defined tumor mass begins to obstruct the lumen of a major bronchus, often producing distal atelectasis and infection.
Histologically, these tumors range from well-differentiated squamous cell neolasms showing keratin pearls and intercellular bridge to  poorly differentiated neoplasms having only minimal residual squamous cell features.
Adenocarinomas may occur as central lesions like the squamous cell variant but are usually more peripherally located, many arising in relation to peripheral lung scars ("scar carcinomas"). The etiologic basic for this association is not clear, although the current thinking is that the scarring probably occurred secondary to the tumor, rather than being contributory. Adenocarinomas are the most common type of lung cancer in woman and nonsmokers. In general, adenocarcinomas grow slowly and form smaller massage than do the other subtypes, but the tend to metastasize widely at an early stage. Histologically, they assume a variety of forms, including acinar (gland forming), papillary, and solid types.