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)

We have identified a small proline-rich protein, spr1, which is a sensitive and specific marker for distinguishing squamous cancer from the other cell types of lung carcinoma. A rabbit antiserum against a 15-amino-acid peptide of the C-terminus of spr1 was prepared. The specificity of this antiserum was demonstrated in normal squamous tissues by Western blotting and immunohistochemical analysis. Expression of spr1 in 63 cases of formalin-fixed and paraffin-embedded human bronchogenic carcinoma was studied by immunohistochemical staining. For these 63 cases of bronchogenic carcinoma previously diagnosed by hematoxylin/eosin (H/E) staining, the number of spr1-positive cases/total number of H/E cases of each cell type of lung cancer were as follows: 20/20 of squamous carcinoma, 2/18 of adenocarcinoma, 4/14 of large-cell carcinoma, and 0/11 of small-cell lung carcinoma. Squamous differentiation evidenced by spr1 expression was substantiated by the presence of squamous features observed under transmission electron microscopy (TEM). We conclude that spr1 is a sensitive and specific marker for squamous bronchogenic carcinoma.
Lung Cancer 1998 Apr
PMID:A small proline-rich protein, spr1: specific marker for squamous lung carcinoma. 969 84

A small proline-rich protein, SPR1, is overexpressed in squamous metaplasia of bronchial epithelium. We studied the expression and regulation of SPR1 in a series of human bronchial epithelial cell lines representing a model of multistep bronchial carcinogenesis. These cell lines included a primary culture of tracheobronchial epithelial cells (HTBE), a papilloma virus-transformed tracheobronchial epithelial cell line (HBE1), a cell line selected from HBE1 by a tobacco carcinogen and a phorbol ester (HBE1-C), a simian virus-transformed bronchial epithelial cell line (BEAS-2B), and a lung carcinoma cell line (H460). Different tumorigenic potentials of these cell lines were indicated by graded levels of telomerase activity. Concomitant with squamous transformation, there was an increase in SPR1 expression in HTBE, HBE1, and HBE1-C that was reversible by vitamin A. With progression of tumorigenicity, there was a marked reduction in SPR1 expression in BEAS-2B and a total loss of expression in H460. In these latter cell lines representing advanced malignant transformation, there was a loss of up- and downregulation, respectively, by the phorbol ester and vitamin A. Transfection study with chimeric constructs of the SPR1 promoter and a reporter gene showed that the dysregulation of SPR1 expression in malignant transformation was a result of perturbation of the basal and enhancer elements of the first 162 nucleotides in the 5'-flanking promoter region of the SPR1 gene. These findings suggest an association of transcriptional dysregulation of the SPR1 gene with multistep bronchial carcinogenesis.
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PMID:Expression and regulation of a molecular marker, SPR1, in multistep bronchial carcinogenesis. 1061 70