Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Squamous dysplasia in the bronchi has been long recognized as a precursor of lung carcinoma, particularly squamous carcinoma. Atypical adenomatous hyperplasia (AAH) has been recently implicated as a precursor to adenocarcinoma. Bronchiolar neuroendocrine cell hyperplasia has also been suggested as a precursor to some pulmonary carcinoid tumors. The atypical adenomatous hyperplasia-adenocarcinoma sequence has been likened to the adenoma-carcinoma sequence in the large intestine. AAH is commonly multifocal, and may explain multicentricity that is observed with some adenocarcinomas. AAH has been shown to have immunohistochemical, morphometric, flow cytometric and genetic abnormalities overlapping with adenocarcinoma. Bronchiolar neuroendocrine cell hyperplasia (carcinoid tumorlets) is classically associated with inflammatory lesions in the airways, but may also be multifocal and bilateral. In the latter setting, lesions may attain a size greater than 0.5 cm and be (arbitrarily) classified as carcinoid tumors.
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PMID:Precursors to pulmonary neoplasia. 985 53

Pulmonary epithelium is known to undergo a preneoplastic process prior to the development of lung carcinoma. Squamous dysplasia and atypical adenomatous hyperplasia have been identified and classified as preinvasive lesions of squamous cell carcinoma and peripheral pulmonary adenocarcinoma, respectively. However, these commonly recognized preinvasive lesions do not completely explain the development of all histological types of lung carcinoma. By examining 114 resection lung specimens, we concluded that there are four histological patterns of bronchial epithelial dysplasia based on morphological features (basal cell dysplasia, columnar cell dysplasia, bronchial epithelial dysplasia with transitional differentiation, and squamous dysplasia). The histological patterns were further characterized by immunohistochemistry. Basal cell dysplasia was focally positive for cytokeratin (CK) 17 and 10/13; columnar cell dysplasia was generally positive for CK7, 8, and 18; bronchial epithelial dysplasia with transitional differentiation had a heterogeneous immunoprofile, while squamous dysplasia was positive for CK10/13 and focally positive for CK17. Various degrees of abnormal expression of p53 and Ki-67 were found in the different types of bronchial epithelial dysplasia. The cases were divided into three groups based on degree and extent of bronchial epithelial dysplasia. By Crosstabs McNemar test, the Mann-Whitney U-test (for two independent groups), the Kruskal-Wallis one-way nonparametric ANOVA (for >2 independent groups) and Spearman correlation analysis, the degree and extent of bronchial epithelial dysplasia was shown to be positively correlated with the incidence of bronchogenic carcinoma and multifocal primary lung carcinoma (P<0.05). These findings indicated the following: (1) bronchial epithelium can develop various patterns of dysplasia with abnormal/ambiguous cell differentiation and abnormal expressions of p53 and Ki-67. Thus, these bronchial epithelial dysplastic lesions may represent a preneoplastic process. (2) The degree of bronchial epithelial dysplasia may significantly predispose individuals to bronchogenic carcinoma and multifocal primary lung carcinoma.
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PMID:Histological types and significance of bronchial epithelial dysplasia. 1641 91