BACKGROUND Telomerase activity in precancerous conditions of lung adenocarcinomas has not been well studied. This study is designed to investigate the role of telomerase in premalignant lesions of urethane-induced mouse lung adenocarcinoma. METHODS We harvested A/J mouse lung tissues at 3, 6, 9, 12, 28, 41, and 48 weeks after intraperitoneal urethane treatment, and classified each lesion in terms of histologic findings. We examined telomerase activity using a modified version of the telomeric repeat amplification protocol assay using both gel-based and enzyme linked immunosorbent assay methods. An immunohistochemical analysis of proliferating cell nuclear antigen (PCNA) was performed. RESULTS In urethane-induced mouse lung tissues, it was sequentially developed from hyperplasia, adenoma, and eventually to adenocarcinoma. Telomerase activity began to show a positive level in tissues with no histologically visible nodule after urethane administration. It revealed a statistically significant increase in hyperplasia compared to the "control" lung tissue (p<0.05), which was proportionally elevated relative to adenoma and adenocarcinoma. There was a direct correlation between telomerase activity and the PCNA labeling index (p<0.05). CONCLUSIONS The elevation of telomerase activity in normal-appearing lung lesions is thought to be a possible marker of early detection of pulmonary adenocarcinoma.
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Non-invasive quantification of cell-free DNA mutations in plasma during lung tumor progression in mice Soo-Jin Kim, Eunhee Kim, Kyung-Taek Rim Cancer Biomarkers.2017; 20(4): 477. CrossRef
A rare case of mesothelial/monocytic incidental cardiac excrescences (cardiac MICE) is described in the aspect of pathological interest. This cardiac lesion is pathologically characterized by exuberant proliferation of mixed mesothelia and monocytes and might be misdiagnosed as metastatic carcinoma, rhabdomyosarcoma, and histiocytoid hemangioma, if the disease is not in the minds of pathologists. The reactive nodular hyperplasia due to irritation to mesothelia by various causes is a most prevailing pathogenetic mechanism. About 20 cases have been reported in the worldwide literature.
A 67-year-old female patient presented with cough and dyspnea for 2 months, without any history of previous cardiac operation. 2D echocardiography of the heart revealed moderate amount of pericardial effusion with posterior wall thickening. Under the impression of metastatic malignancy, pericardiostomy was performed. Grossly, the tissue was dark hemorrhagic and friable and the histologic sections revealed the solid tumor-like proliferation of round to polygonal histiocytic cells admixed with small cuboidal mesothelial cells which formed strips and tubular arrays. They were found within the fibrinous network and there were scattered empty vacuolar spaces.
Immunohistochemical staining confirmed their biphasic nature with the CD68 positivity of the histiocytes and the cytokeratin positivity of the cuboidal cells. Factor VIII positivity was not detected in any cell components. The lesion was considered the monocytic and mesothelial proliferation of reactive nature, so-called cardiac MICE in the pericardial cavity. We report a typical case of so-called MICE first in the Korean literature.
BACKGROUND The aim of this study was to investigate the hepatic pathology of HBx transgenic mice. METHODS The gross and histological examinations were done in 125 HBx transgenic mice and 34 non-transgenic littermates. RESULTS The incidence of a hepatic tumor was in-creased in the HBx transgenic mice older than 7 months and the overall incidence of a hepatic tumor was 62.2% (51/82) in the 13-18 months group of the HBx transgenic mice. The size of the hepatic tumor was 2.06+/-.92 mm in the 7-12 months group and 4.94+/-.05 mm in the 13-18 months group of HBx transgenic mice. All hepatic tumors were hepatocellular carcinomas and the histological patterns of hepatocellular carcinoma were either solid (84.2%, 48/57) or trabecular (15.8%, 9/57).
Dysplastic changes in the hepatocytes were evident in 59.2% (74/125) of the HBx transgenic mice. There was lymphocyte infiltration, necrosis, fatty metamorphosis in both the dysplastic and tumor areas of the HBx transgenic mice.
Vascular ectasia was identified in the tumor area of the HBx transgenic mice. CONCLUSIONS The pathological findings of the HBx transgenic mice were dysplastic changes in the hepatocytes and development of a hepatocellular carcinoma associated with lymphocyte infiltration, necrosis, fatty metamorphosis in the dysplastic area and tumor area of the HBx transgenic mice.