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Background: Platinum drug resistance is an important problem in lung cancer chemotherapy. In this study, we examined lung-resistance protein (LRP) gene expression in vivo and in vitro in relation to platinum drug exposure., Materials and Methods: The expression levels of the LRP gene were assessed by the reverse transcription polymerase chain reaction, in 80 autopsy samples (40 lung tumors and 40 corresponding normal lung tissues), two lung cancer cell lines and in peripheral mononuclear cells collected from 8 lung cancer patients before and after platinum drug administration., Results: The LRP gene expression levels of autopsy specimens exposed antemortem to platinum drugs were not significantly different to those of specimens without platinum drug exposure, for both lung tumors and normal lung tissues. Our results also demonstrate that LRP gene expression was not induced by platinum drugs either in vitro or in vivo., Conclusions: The present results indicate that LRP gene expression is not associated with platinum drug exposure in lung cancer.

Background: Radiologically undetected intrapulmonary solitary nodules are sometimes found in the resected lung. When the main tumor is a well-differentiated (w/d) adenocarcinoma, especially a bronchioloalveolar carcinoma (BAC), it can be difficult to determine morphologically whether the intrapulmonary nodules are atypical adenomatous hyperplasia (AAH) or intrapulmonary metastasis (PM). The authors evaluated the accuracy of the differential diagnosis of these two lesions from the prognostic point of view., Methods: A retrospective study was conducted of 1360 lung carcinoma patients who had undergone surgical resection. Differential diagnosis was made between AAH and PM based on the conventional histologic specimens. Their clinicopathologic features were also studied. Survival rates were compared between these two groups., Results: AAH was found in 137 patients (10%) with resected lung carcinoma. The 5-year survival rates were 72.9% in Stage I, 60.6% in Stage II, 27.1% in Stage IIIA, 0% in Stage IIIB, and 0% in Stage IV. They were not significantly different from the figures for all patients in the corresponding pathologic stages. Seventy-six cases were diagnosed as w/d adenocarcinoma associated with AAH, whereas PM was found in 46 cases of w/d adenocarcinoma. The 5-year survival rates of AAH and PM differed significantly: 64.6% and 35.5%, respectively (P 0.0004). When a comparison was made between cases of pT1-2, N0 w/d adenocarcinoma, most of which were BAC, with PM (n = 22) and those with AAH (n = 52), the latter had significantly better survival (P = 0.0086)., Conclusions: The prognosis of resected lung carcinoma was not affected by association with AAH. The significant difference in prognosis between AAH and PM in w/d adenocarcinoma, especially in BAC, indicates that their morphologic distinction was correctly made by conventional pathologic examination in most cases.

Atypical adenomatous hyperplasia (AAH) of the lung has been regarded as a precancerous lesion of lung adenocarcinoma, but the biologic significance of this lesion is still not well understood. In this study, DNA histogram patterns and nuclear size were examined, using an image cytometer. We studied 14 cases of Type II pneumocyte hyperplasia (HP), 7 cases of adenomatous hyperplasia with slight or no nuclear atypia (AH), 21 cases of AAH, and 26 cases of adenocarcinoma. The difference in mean nuclear sizes between the HP (32.08 microns2) and the AH (32.86 microns2) was not significant but between the AH, the AAH (38.52 microns2), and the well-differentiated adenocarcinomas with mild nuclear atypia (51.12 microns2), statistically significant differences were observed (P < 0.05). Seven (33%) of the 21 cases of AAH and 22 (85%) of the 26 cases of adenocarcinoma showed aneuploid histogram patterns. The difference in the incidence of aneuploid pattern between AAH and adenocarcinomas was statistically significant (P < 0.01). All of the cases of HP and AH were diploid. Two of the seven aneuploid cases of AAH showed hyperdiploid DNA histogram patterns, and the remaining five showed polyploid histogram patterns with diploid and hyperdiploid stemlines. In these five cases, the small-sized nuclei showed a diploid stemline and the large-sized nuclei showed a hyperdiploid stemline. Our data indicated that AAH can be distinguished from HP, AH, or adenocarcinoma by morphometric analysis and that some cases of AAH that display aneuploid histogram patterns are precancerous lesions that may lead to adenocarcinoma.