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The majority of lung malignancies is represented by lung carcinoma, while sarcomas and lymphomas constitute less than 0.5% of this series. Less than 5% of lung cancers are benign or low-grade tumors. A further distinction must be made between primary neoplasms and secondary neoplasms; in fact, while the former originate from the lung structures, the latter are represented by metastases of neoplasms originating in other organs such as, for example, the kidney, liver, breast and prostate.
Cigarette smoking is considered the main causative agent for the development of lung cancer. According to one study using statistical projections, it is responsible for about 90% of fatal lung cancers in developed countries.
In particular, again according to a study, in the USA cigarette smoking is responsible for the development of 87% of cases of lung cancer with an incidence that increases considerably if the first exposures occur within the age of 25.
Cigarette smoke contains about 60 known carcinogens, including radioisotopes from radon decay, benzopyrene and some nitrosamines. Furthermore, the nicotine present is able to depress the immune response, decreasing the surveillance and killing capacity of the neoplastic cells by T lymphocytes and NK lymphocytes.
Radon is an odorless and colorless gas, generated by the decay processes of radium, itself a product of the decay of uranium, widely present in the earth's crust (granite and minerals used for the construction of houses).
Radon is a volatile and radioactive element, capable of inducing mutations in DNA and therefore representing a concrete risk of neoplasia: recent research (2006) has promoted radon as the second risk factor for the development of fatal lung cancer .
Asbestos, in addition to being implicated in the pathogenesis of asbestosis and pleural mesothelioma, shows a synergistic role with tobacco smoke for the development of lung cancer. Although definitive data are not yet present, exposure to smog and atmospheric pollution (products of the combustion of petroleum derivatives and products of processes involving the use of particular metals such as nickel and chromium) are implicated in the pathogenesis of deadly lung cancer.
The aetiological elements analyzed lead to DNA mutations that trigger a set of modifications that have as a final result an intense proliferation of the epithelium, with aberrations of the lung tissue architecture. Over time and with the prolongation of exposure, all these modifications constitute the ground on which the neoplasm originates and moves.
From these considerations it can be deduced that microscopic, macroscopic and molecular alterations are associated with the neoplastic disorder, which evolve coherently in time and space. While the latter will be discussed in the section Biological-molecular events, the first two correspond to visible alterations that support the clinical-pathological picture.
It must therefore always be considered that, simultaneously with the visible neoplastic disorder, a synchronous and evolutionary molecular substrate moves capable of influencing the clinical history and prognosis of the tumor, conferring properties of invasiveness, metastasis or resistance to chemo-radiotherapy.
