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 (

Although lung adenocarcinoma is a major cause of cancer death worldwide, details of its molecular carcinogenesis and stepwise progression are still unclear. To characterize the sequential progression from bronchioloalveolar adenocarcinoma of the lung (BAC, in situ carcinoma) to adenocarcinoma mixed subtype with BAC component, polymerase chain reaction-based cDNA suppression subtractive hybridization (SSH) was carried out using two representative cases of BAC (non-invasive tumors) and adenocarcinoma mixed subtype with BAC (invasive tumors). Through differential screening, virtual reverse northern hybridization and quantitative real-time reversetranscription-polymerase chain reaction (qRT-PCR) we selected five genes (TncRNA, OCIAD2, ANXA2, TMED4 and LGALS4) that were expressed at significantly higher levels in invasive adenocarcinoma mixed subtype with BAC than in BAC. After in situ hybridization and qRT-PCR analyses, we confirmed that only the OCIAD2 gene showed significantly higher expression in the tumor cells of invasive adenocarcinoma mixed subtype with BAC than in BAC (P = 0.026). We then carried out in situ hybridization of OCIAD2 in 56 adenocarcinoma mixed subtype with BAC component and assessed the correlation between OCIAD2 expression and clinicopathological features. In contrast to our expectation, the patients with OCIAD2 expression showed a better clinical outcome than those without OCIAD2 expression, and OCIAD2 expression showed an inverse correlation with lymphatic invasion, blood vessel invasion and lymph node metastasis. These results suggest that OCIAD2 begins to express at the progression from in situ to invasive carcinoma, and is associated with the favorable prognosis of adenocarcinoma mixed subtype with BAC component. (Cancer Sci 2007; 98: 50-57) L ung cancer is the most common fatal malignancy worldwide, including North America, Europe and Japan.(1) Its histology can be divided into four major subtypes: squamous cell carcinoma, adenocarcinoma, large cell carcinoma and small cell carcinoma. Among the major subtypes of non-small cell carcinomas (NSCLC), squamous cell carcinoma is directly attributable to cigarette smoking and its sequence of histological changes from dysplasia and in situ carcinoma to invasive carcinoma has been well established and accepted.(2) However, because of its histological and cytological heterogeneity, the sequential progression of adenocarcinoma has been very difficult to characterize on the basis of morphology.In 1999, the World Health Organization revised the histological classification of lung tumors, and bronchioloalveolar carcinoma (BAC) was added as one of the major histological subtypes of adenocarcinoma. Atypical adenomatous hyperplasia (AAH) was also newly added as a preinvasive lesion of adenocarcinoma.BAC is defined as adenocarcinoma that shows no invasive growth. Therefore, both AAH and BAC are thought to represent the very early stage of adenocarcinoma without invasion. Histologically, both entities show pure lepidic growth of existing alveolar structur...

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...

A semiconductor thin film with high carrier mobility was fabricated on a flexible film. During the solid-phase crystallization process of the densified amorphous Ge layer, the interfacial reaction with the GeO x underlayer is controlled by the GeO x thickness (0–300 nm) and the growth temperature (375–450 °C). The appropriate amount of oxygen diffusion from GeO x to Ge produces large Ge grains (up to 13 μm in diameter) with high crystal quality. The use of a high heat-resistant polyimide film allows postannealing at 500 °C and improves the hole mobility of Ge to 690 cm2 V–1 s–1 while maintaining flexibility. This hole mobility is higher than that of any other semiconductor thin films directly formed on insulators, including single-crystal Ge grown at high temperatures, and even higher than that of a Si wafer. The findings open up the possibility of incorporating high-speed transistors on flexible devices that surpass Si metal–oxide–semiconductor field-effect transistors.

BACKGROUND The regulation of programmed cell death, or apoptosis, is crucial for normal development and for the maintenance of homeostasis. It has been shown that the novel antiapoptotic protein Bax inhibitor‐1 (BI‐1) represents a new type of regulator of cell death pathways controlled by Bcl‐2 and Bax. METHODS Surgically resected lung specimens were obtained from 32 patients with peripheral adenocarcinomas, and BI‐1 gene expression was examined and compared with expression of the p53, bcl‐2 and Bax genes. RESULTS Fourteen of 32 tumors (43.8%) were positive for BI‐1 gene expression by in situ hybridization. BI‐1 gene expression in tumor specimens was significantly higher in adenocarcinomas with bronchioloalveolar carcinoma (BAC) and in adenocarcinomas of mixed subtypes with bronchioloalveolar spreading (14 of 17 tumors; 82.4%) than in carcinomas without it spreading. Patients who had BI‐1‐positive adenocarcinoma showed a relatively favorable prognosis compared with patients who had BI‐1‐negative adenocarcinoma. Eleven of 32 tumors (34.4%) were positive for the p53 protein, only 1 of 32 tumors (3.1%) was positive for the Bcl‐2 protein, and 26 of 32 tumors (81.3%) were positive for the Bax protein. Protein expressions of p53, Bcl‐2, and Bax, as detected by immunohistochemistry, were not associated with BI‐1 gene expression. CONCLUSIONS BI‐1 gene expression was restricted to tumor cells with lepidic growth and was a prognostic factor for peripheral‐type adenocarcinoma. It is believed that BI‐1 gene expression is conserved evolutionarily and may act as a key regulator of the apoptotic pathway in BAC. Cancer 2006. © 2005 American Cancer Society.