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Human Lung Carcinomas (human + lung_carcinoma)

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Medical Sciences100%

Terms modified by Human Lung Carcinomas

  • human lung carcinoma cell
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    Selected Abstracts

    Immunohistochemical expression of aminopeptidase N (CD13) in human lung squamous cell carcinomas, with special reference to Bestatin adjuvant therapy

    PATHOLOGY INTERNATIONAL, Issue 6 2006
    Eiji Ichimura
    Bestatin, a specific inhibitor of aminopeptidase N (CD13), has been reported to prolong survival time in patients with completely resected stage I lung squamous cell carcinoma. Considering the antitumor mechanism of Bestatin, it is interesting to know whether CD13 is expressed in human lung squamous cell carcinoma. The immunohistochemical expression of CD13 was examined in human lung carcinoma and the question of whether CD13 was immunohistochemically expressed in the interstitial tissue was investigated, mainly in the fibroblasts and blood vessels, surrounding the tumor nests of various kinds of non-small cell lung cancers, especially of squamous cell carcinomas. In Japanese squamous cell carcinoma of the lung, 38 (61.3%) out of 62 cancers were positively stained in the same manner on immunohistochemistry for CD13. The area of interstitial tissue positively stained for CD13 varied depending on the case. To confirm the cell nature of the interstitial tissue with CD13 positivity, double immunohistochemistry using CD34 and ,-smooth muscle actin was performed. Double immunohistochemistry showed that the majority of CD13-positive cells were slender fibroblastic cells around the blood vessels and some endothelial cells. [source]

    Isolation of coumarins and ferulate from the roots of Angelica purpuraefolia and the antitumor activity of khellactone

    PHYTOTHERAPY RESEARCH, Issue 5 2007
    Hyeong-Kyu Lee
    Abstract A new coumarin, hydroxylomatin (1), was isolated from the CHCl3 -soluble fraction of the roots of Angelica purpuraefolia, along with one ferulate (2) and three other known coumarins (3,5) including khellactone (3). The structure of hydroxylomatin (1) was determined to be 3,,,5,-dihydroxy-3,,4,-dihydroseselin (1) by spectroscopic means including 2D-NMR. The modified Mosher's method was used to determine the chiral center at C-1 of compound 2. Khellactone (3) is a major compound of the roots of A. purpuraefolia. This study also examined the antitumor activity of khellactone (3) using a LLC mouse lung carcinoma in the BDF-1 mice and a NCI-H460 human lung carcinoma in a human tumor xenograft model in nude mice. This compound (3) inhibited LLC tumor growth with a T/C (mean value of treated group/mean value of control group) value of 12.9% at a dose of 5 mg/kg and 33.2% at a dose of 10 mg/kg, respectively, in a dose-dependent manner. In addition, it suppressed the growth of NCI-H460 tumor cells, accounting for 81.4% at a dose of 10 mg/kg in nude mice. Copyright © 2007 John Wiley & Sons, Ltd. [source]

    Loss of Betaig-h3 protein is frequent in primary lung carcinoma and related to tumorigenic phenotype in lung cancer cells

    MOLECULAR CARCINOGENESIS, Issue 2 2006
    Yongliang Zhao
    Abstract Betaig-h3 as a secreted protein induced by transforming growth factor-, has been suggested to modulate cell adhesion and tumor formation. Although we have previously shown that downregulation of Betaig-h3 gene is involved in the cellular transformation of human bronchial epithelial cells induced by radiation, its regulation in primary human lung cancers is not clearly understood. In this study, Betaig-h3 expression was studied in 130 primary human lung carcinomas by immunohistochemistry. Betaig-h3 protein was absent or reduced by more than two-fold in 45 of 130 primary lung carcinomas relative to normal lung tissues examined. Recovery of Betaig-h3 expression in H522 lung cancer cells lacking endogenous Betaig-h3 protein significantly suppressed their in vitro cellular growth and in vivo tumorigenicity. In addition, parental H522 cancer cells are resistant to the etoposide induced apoptosis compared with normal human bronchial epithelial cells. However, recovery of Betaig-h3 expression in H522 cancer cells results in significantly higher sensitivity to apoptotic induction than parental tumor cells. IGFBP3 is upregulated in Betaigh3-transfected H522 cells that may mediate the apoptotic sensitivity and antitumor function of Betaig-h3 gene. These observations demonstrate that downregulation of Betaig-h3 gene is a frequent event and related to the tumor progression in human lung cancer. © 2005 Wiley-Liss, Inc. [source]

    Nkx2.1 transcription factor in lung cells and a transforming growth factor-,1 heterozygous mouse model of lung carcinogenesis,

    MOLECULAR CARCINOGENESIS, Issue 4 2004
    Yang Kang
    Abstract The Nkx2.1 homeobox gene and transforming growth factor-,1 (TGF-,1) are essential for organogenesis and differentiation of the mouse lung. NKX2.1 is a marker of human lung carcinomas, but it is not known whether this gene participates in early tumorigenesis. Addition of TGF-,1 to TGF-,1-responsive nontumorigenic mouse lung cells cotransfected with a NKX2.1Luc luciferase reporter and either a Sp1 or Sp3 plasmid showed a significant increase or decrease, respectively, in NKX2.1Luc transcription. Cotransfection of Sp3 and dominant-negative TGF-, type II receptor plasmids negated the effect of Sp1. Cotransfected Sp1 plasmid with either dominant-negative Smad2 or Smad3 or Smad4 plasmids significantly decreased NKX2.1Luc transcription. Electrophoretic mobility shift assays revealed binding of Sp1 and Smad4 to the NKX2.1 promoter. With a TGF-,1 heterozygous mouse model, Nkx2.1 mRNA and protein in lungs of TGF-,1 heterozygous mice were significantly lower compared to wildtype (WT) littermates. Competitive reverse transcription (RT)-polymerase chain reaction (PCR) and immunostaining showed that Nkx2.1 mRNA and protein decreased significantly in adenomas and adenocarcinomas compared to normal lung tissue. Our in vitro data showed that regulation of Nkx2.1 by TGF-,1 occurs through TGF-, type II receptor and Smad signaling, with Sp1 and Sp3 in lung cells. Our in vivo data showed reduced Nkx2.1 in lungs of TGF-,1 heterozygous mice compared to WT mice, that is detectable in adenomas, and that is further reduced in carcinogenesis, and that correlates with reduction of Sp1, Sp3, and Smads in lung adenocarcinomas. Our findings suggest that reduced Nkx2.1 and TGF-,1 signaling components may contribute to tumorigenesis in the lungs of TGF-,1 heterozygous mice. Published 2004 Wiley-Liss, Inc. [source]

    Immunohistochemical analysis of CYP2A13 in various types of human lung cancers

    CANCER SCIENCE, Issue 4 2010
    Tatsuki Fukami
    Human CYP2A13, which is expressed in the respiratory tract, is the most efficient enzyme for the metabolic activation of tobacco-specific nitrosamines such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The relevance of CYP2A13 in carcinogenicity and toxicity in the respiratory tract has been suggested, but the expression of CYP2A13 protein in lung cancer tissues remains to be determined. We first prepared a mouse monoclonal antibody against human CYP2A13. The antibody showed no cross reactivity with the other CYP isoforms including CYP2A6. Using the specific antibody, we performed immunohistochemical analysis for human lung carcinomas. In adenocarcinomas (n = 15), all specimens were positive for the staining and five samples showed strong staining. In squamous cell carcinomas (n = 15) and large cell carcinomas (n = 15), each 14 samples were positive for the staining and two and three samples showed strong staining, respectively. In small cell carcinoma samples (n = 15), eight samples were negative for the staining and five samples showed weak or moderate staining. In conclusion, we first found that the expression of CYP2A13 was markedly increased in non-small cell lung carcinomas. The high expression might be associated with the tumor development and progression in non-small cell lung carcinomas. (Cancer Sci 2010; 101: 1024,1028) [source]