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Traditionally, lung cancer has been stratified histologically as squamous/epidermoid, adenocarcinoma, and small/large cell lung cancers. Our current ability to profile cancers at the molecular level appears to have both prognostic and therapeutic value.
The most important distinction is between small cell and non–small cell carcinoma because of fundamental differences in tumor biology and clinical behavior ( Table 83.1 ). Patients with small cell lung cancer are classified as having either limited or extensive disease. Limited means that all known disease is confined to one hemithorax and regional lymph nodes, including mediastinal, contralateral hilar, and ipsilateral supraclavicular nodes. Extensive describes disease beyond these limits, including brain, bone marrow, and intraabdominal metastases.
Type | Incidence | Comments |
---|---|---|
Non–small cell carcinomas | 80% | |
Adenocarcinoma | 40% | Has increased in nonsmokers |
Squamous cell carcinoma | 40% | Referred to as epidermoid, is associated histologically with keratin pearls, and is promoted by smoking and other inhaled irritants |
Large cell carcinoma | 15% | |
Bronchoalveolar carcinoma | 5% | Single nodule, multiple nodules, or nonresolving infiltrate on chest radiography |
Small cell carcinoma | 20% | Very poor prognosis |
With small cell or neuroendocrine carcinoma, the small cell type is usually extensive at presentation, and 5-year survival is 5%. Neuroendocrine carcinoma, which is well differentiated, is known as atypical carcinoid and has a good prognosis but is not benign.
Yes. A family history of lung cancer probably increases the risk of getting lung cancer. Furthermore, a large array of important biomarkers that influence prognosis have been identified in lung cancer cells and lung cancer tissue.
Past:
Light microscopic evidence of vascular invasion
Lymphatic invasion
Cellular pleomorphism and mitotic figures
Present:
Proto-oncogenes, growth factors, growth factor receptors
Insulin-like growth factor
Epidermal growth factor receptor (EGFR)
K- ras mutation (cell growth regulation)
C- myc overexpression (cell growth)
bcl -2 underexpression (loss of apoptosis regulation)
Loss of tumor suppressor genes
p53
Retinoblastoma (RB gene)
Chromosomal allele loss
Fragile histidine triad gene
Retinoic acid receptor a
Overactivation of angiogenesis
Platelet-derived growth factor
Vascular endothelial-derived growth factor
Future:
Gene therapy directed at those listed in present
Antiangiogenesis therapy
Immunopotentiation
Adoptive immunotherapy: Isolation, expansion, and reinfusion of tumor-infiltrating lymphocytes
Nonspecific immunostimulation
Tumor vaccines
No single marker yet has a clear meaning with respect to prognosis in a given patient
Ninety percent of patients have a smoking history
Chemicals (aromatic hydrocarbons, vinyl chloride)
Radiation (radon gas and uranium)
Asbestos
Metals (chromium, nickel, lead, and arsenic)
Environmental factors (air pollution, coal tar, petroleum products)
EGFR-activating mutations are associated with increased frequency of stage IV disease and decreased overall survival.
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