To better understand the relationship between specific chromosome changes found in human lung tumors and their phenotypic consequences a the tissue level, an in situ hybridization (ISH) procedure of chromosome 17 and immunohistochemistry of proliferating cell nuclear antigen (PCNA) were done. The deparaffinized sections were stained with pericentromeric probes for chromosome 17 and an immunohistochemical study of a monoclonal antibody against PCNA were performed. The numbers of chromosome signals were than compared with the positivity of PCNA expression. The mean numbers of chromosome were 1.62 in normal lymphocytes and 2.48 in lung cancer cells. Tumors showed a high mean positivity of PCNA of 43.4%. Mean PCNA expression was higher in squamous carcinomas than in adenocarcinomas (p < 0.05). A linear correlation between numbers of ISH signals and PCNA expression was not demonstrated, but there was a tendency of increasing PCNA positivity according to increasing numbers of ISH signals in adenocarcinomas of the lung and the tumor tissues which were over 50% positive PCNA expression. There was no linear correlation between numbers of ISH signals, PCNA positivity and tumor stages, and keratinization of squamous cell lung cancer. These results suggest that ISH will prove to bo an important tool for determining the underlying genetic basis for tissue phenotypic heterogeneity by allowing genetic determinations to be made on paraffin-embedded tissue sections where histologic architecture is preserved, and immunohistochemical nuclear staining with anti-PCNA on routinely processed tissue is a simple technique for the assessment of proliferation in non-small cell lung carcinoma.
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