Slowly progressive adenocarcinoma of the lung: report of a case.

A case report of a slowly progressive adenocarcinoma of the lung, followed by computed tomography is herein discussed. The patient was a 76-year-old woman, who was operated on about four years after a small lung nodule on her left upper lobe was discovered. The tumor was suspected to be either well differentiated adenocarcinoma or atypical adenomatous hyperplasia (AAH) by the findings of chest computed tomography before the operation, and the resected specimen demonstrated well differentiated adenocarcinoma, without lymph node metastasis. This case demonstrates the possibility that some adenocarcinomas with particular histology are slowly progressive, and also there might be the option of lobectomy or segmentectomy for treating such tumors.

Expression status of E-cadherin and alpha-, beta-, and gamma-catenins in thymoma.

BACKGROUND: A loss or dysfunction of E-cadherin or catenins, which maintain tissue integrity, is associated with an invasive phenotype of various solid tumors. Therefore, we analyzed the expression of E-cadherin and alpha-catenin, beta-catenin, and gamma-catenin in thymoma tissue specimens to investigate its clinical significance. METHODS: The expressions of E-cadherin and alpha-catenin, beta-catenin, and gamma-catenin in thymoma tissues were evaluated in 21 patients, including 9 epithelial predominant type, 5 lymphocytic predominant type, and 7 mixed type patients based on an immunohistochemical analysis using monoclonal antibodies, and the relationship between the expression status and clinicopathologic features was investigated. RESULTS: Reduced expressions were observed in 11 patients (52%) for E-cadherin, 10 (45%) for alpha-catenin, 6 (27%) for beta-catenin, and 10 (45%) for gamma-catenin. Such an expression status (reduced or preserved) of the molecules closely correlated with each other. The expression of E-cadherin was well preserved in 5 of 5 patients with lymphocyte predominant type whereas E-cadherin was reduced in 11 of 17 patients with other histologic subtypes. All of the 9 cortex type thymomas (B1 to 3) showed preserved expression of beta-catenin. There was no significant relationship among the expressions of the molecules and the Masaoka stage classification (I versus others). CONCLUSIONS: The status of expressions for these molecules may affect the degree of lymphoid infiltration while not affecting the degree of invasiveness in thymoma.

Micrometastasis in the bone marrow of patients with lung cancer associated with a reduced expression of E-cadherin and beta-catenin: risk assessment by immunohistochemistry.

BACKGROUND: The presence of disseminated tumor cells in bone marrow is considered to be a premetastatic state, which is called micrometastasis. To evaluate the relationship between micrometastasis and cellular adhesion molecules in the primary lesion, E-cadherin and beta-catenin were immunohistochemically investigated. Methods. Fifty-eight patients with non-small cell lung cancer who underwent a complete resection were entered into this study. Tumor cells in bone marrow aspirates were detected by immunohistochemistry using cytokeratin (CK) 18. Immunohistochemical studies of E-cadherin and beta-catenin were performed in the corresponding primary tumor. RESULTS: CK-positive cells were detected in the bone marrow aspirates from 27 of 58 patients. A reduced expression of the E-cadherin and beta-catenin was found in 16 (27.6%) and in 22 (37.9%) of 58 patients, respectively. In 26 cases with a reduced expression of E-cadherin and/or beta-catenin, 16 cases had CK-positive cells, whereas 11 of 32 cases with normal expression of both factors had CK-positive cells (P=.0392). The patients with micrometastasis demonstrated an earlier recurrence (P =.0642) and a significantly poorer survival (P =.0437) than those without such cells. CONCLUSIONS: Micrometastasis in the bone marrow might be a significant predictor of poor prognosis, and a reduced expression of E-cadherin and beta-catenin are important determinants for the metastatic capability of individual cancer cells.