Endometrial stromal sarcoma (ESS) of the uterus is a rare uterine malignancy that has not been characterized in detail. To characterize the phenotype of ESS of the uterus, we extracted RNA from ESS and the stroma of normal endometrium using a tissue microdissection system and compared the expression profiles in the two tissues. After suppression subtractive hybridization and differential screening, we detected the metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) gene as one of the major genes upregulated in ESS, and a full-length placental cDNA clone (

The heated cigarette (HC) generates mainstream smoke by vaporizing the components of the tobacco rod using a carbon heat source at the cigarette tip. Mainstream smoke of HC contains markedly less chemical constituents compared to combusted cigarettes. Mainstream smoke from HC was generated under Health Canada Intense regimen and its biological effects were compared to those of Reference (3R4F) cigarettes, using nose-only 5-week and 13-week inhalation studies. In the 13-week study, SD rats were necropsied following exposure to mainstream smoke from each cigarette at 200, 600 or 1000 µg wet total particulate matter/L for 1 h/day, 7 days/week or following a 13-week recovery period. Histopathological changes in the respiratory tract were significantly lesser in HC groups; e.g. respiratory epithelial hyperplasia in the nasal cavity and accumulation of pigmented macrophages in alveoli. After a 13-week recovery, the lesions were completely or partially regressed, except for accumulation of pigmented macrophages in alveoli, in both HC and 3R4F groups. In the 5-week study, SD rats were necropsied following exposure to mainstream smoke of either cigarette at 600 or 1000 µg/L for 1 h, two times/day (with 30 min interval), 7 days/week or following a 4-week recovery period. Bronchoalveolar lavage fluid (BALF) analysis of neutrophil percentages and enzyme levels like γ-GT, ALP and LDH indicated that pulmonary inflammation was significantly less in HC groups compared to 3R4F groups. In conclusion, HC demonstrated significantly lower biological effects compared to 3R4F, based on the BALF parameters and histopathology.

Atypical adenomatous hyperplasia (AAH) is classified as a precancerous lesion of lung adenocarcinoma. We established an immortalized AAH cell line (PL16T) and a human non-neoplastic bronchial epithelial cell line (PL16B) from the same patient by transfection with the gene for SV40 large T antigen. The expression profile of PL16T was compared with that of PL16B by the suppression subtractive hybridization method. From 704 selectively hybridized clones, we finally selected 25 fragments of mRNA that showed transcription levels more than three times higher in PL16T than in PL16B. Thirteen (52%) and eight (32%) of them encoded tumor-associated calcium signal transducer 2 (TACSTD2) and S100 calcium binding protein A2 (S100A2), respectively. The high transcription of TACSTD2 and S100A2 in PL16T was confirmed by in situ hybridization. In normal lung tissue, both TACSTD2 and S100A2 were expressed at very low levels, but seven and five of 14 AAH were positive for TACSTD2 and S100A2, respectively However, studies of its molecular carcinogenesis are still limited, and the 5-year survival rate for patients with advanced lung carcinoma is less than 30%. However, with advances in radiological diagnostic techniques, many early adenocarcinoma lesions originating in the peripheral lung can be detected by multidetector computed tomography (CT) and thin-slice CT techniques. Lesions showing ground glass opacity on CT examination correspond to precancerous lesions and in situ adenocarcinoma of the peripheral lung. To study the molecular carcinogenesis of lung adenocarcinoma, we believe it is critical to analyze lesions showing ground glass opacity on CT examination.Atypical adenomatous hyperplasia (AAH) and bronchioloalveolar carcinoma (BAC) are diagnostic criteria included in the World Health Organization (WHO) classification (3rd edition) as precancerous lesions and in situ lesions of peripheral-type adenocarcinoma.(2) They show a pure bronchioloalveolar (lepidic) growth pattern that replaces the original alveolar pneumocytes. Most cases of AAH and BAC are composed of non-mucinous tumor cells mimicking type II pneumocytes, and show ground glass opacity on CT examination.(3) However, most cases of advanced adenocarcinoma of the peripheral lung are adenocarcinoma of mixed subtype, containing more than two of BAC, acinar subtype, papillary subtype and other components.Noguchi et al. proposed a new histological classification of small adenocarcinoma of the lung.(4) They divided adenocarcinoma into two groups. One is adenocarcinoma showing growth that replaces the original alveolar structure, and the other is adenocarcinoma that shows expansive and destructive growth of the alveolar structure. The former group is the major histology of peripheral adenocarcinoma, and is further divided three types: type A, localized bronchioloalveolar carcinoma (LBAC); type B, LBAC with alveolar collapse; and type C, LBAC with a focus of fibrotic lesion, including active fibroblastic proliferation. The latter group is further divided into three types: t...

Female C57BL/6 mice were exposed to mainstream cigarette smoke at 600 μg WTPM/L, 4 h/day and 5 days/week for up to 52 weeks. At 26, 52 and 65 weeks (52 weeks of exposure plus 13 weeks of no exposure), lungs were assessed for inflammation, function, histopathology and morphometry. Structural changes were observed and accompanied by altered lung function at 26 and 52 weeks (e.g. increase of static compliance and hysteresis, and decrease of elastance). Lung morphometry quantified significant increase in airspace enlargement at 52 weeks. Chronic smoke exposure induced inflammation in respiratory organs, e.g. mixed inflammatory cell infiltrates, perivascular lymphocyte infiltrates and pigmented alveolar macrophages in the lungs. Minimal or mild alveolar emphysema was diagnosed in 70% by 26 weeks or 80% by 52 weeks. After 13 weeks of recovery, most biochemical, histopathological and morphometrical alterations were restored, while emphysema was observed to persist at 18% incidence by 65 weeks. In conclusion, the employed exposure conditions induced emphysematous changes in the lungs, accompanied by altered lung function and morphological/histopathological changes. Following the 13 weeks of no exposure, morphological changes persisted, although some functional/biochemical alterations regressed.

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