Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reduced expression of E-cadherin, a cell-cell adhesion molecule, was frequently observed in several types of human carcinomas, and the protein plays a role as an invasion suppressor in vitro. In an attempt to evaluate the significance of E-cadherin gene in non-small cell lung cancer (NSCLC), we undertook the immunohistochemical and molecule structural analyses of E-cadherin gene in 40 resection specimens of NSCLC and the corresponding paracarcinoma controls. E-cadherin expression was explored by immunohistochemistry with a monoclonal antibody, and the E-cadherin gene was studied by polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP). The analysis represented in this study demonstrated clear reduction in the expression of E-cadherin proteins in the cancer tissues. However, only in one amplicon were aberrant bands detected, which was a single polymorphic site (codon 692; exon 13), and no somatic mutation was found. These results indicated that defected E-cadherin expression might play a role in the development of malignant phenotype in NSCLC, even though the genetic mutation of E-cadherin gene is not involved in the pathogenesis of NSCLC and does not appear to be direct cause for the reduced expression of E-cadherin gene.
Lung Cancer 2002 Aug
PMID:Defected expression of E-cadherin in non-small cell lung cancer. 1214 Jan 37

Metastatic papillary adenocarcinomas of the ovary are rare compared to primary ovarian papillary serous carcinomas. We report a case of pulmonary papillary adenocarcinoma metastatic to the ovary and show how this tumor can be differentiated immunohistochemically from an ovarian primary. Paraffin blocks of the ovarian tumor were analyzed for carcinoembryonic antigen, CA 125, surfactant, E-cadherin, N-cadherin, and vimentin. These markers are useful in differentiating epithelial tumors of lung versus ovarian origin. The papillary tumor showed expression of carcinoembryonic antigen, surfactant, and E-cadherin, but was negative for CA 125, N-cadherin, and vimentin. These findings support a lung carcinoma metastatic to the ovary.
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PMID:Immunohistochemical confirmation of pulmonary papillary adenocarcinoma metastatic to ovaries. 1220 61

Immunoreactivity for fascin, an actin-bundling protein related to cell motility, has been reported in breast, ovary, pancreas, skin, and non-small cell carcinomas, and associated with more advanced disease stage and poorer prognosis. Data on pulmonary neuroendocrine (NE) tumors, however, are lacking. We evaluated the expression of fascin by immunohistochemistry--using two different monoclonal antibodies--in surgical specimens of pulmonary NE tumors of all the diverse histological types from 128 consecutive patients recruited between 1987 and 2001, and investigated its relationship with the presence of lymph node metastases. Overall, fascin immunoreactivity was detected in 5% of 38 typical carcinoids (TC), 35% of 23 atypical carcinoids (AC), 83% of 40 large-cell neuroendocrine carcinomas (LCNEC), and 100% of 27 small-cell lung carcinomas (SCLC) (P<0.001), Normal NE cells or hyperplastic NE tumorlets were consistently unreactive. No statistically significant differences in fascin immunoreactivity were found between the two antibodies. In TC and AC but not high-grade NE tumors, fascin immunoreactivity closely correlated with the occurrence of lymph node metastases, the pN class and the number of involved lymph nodes (P<0.001). It was also significantly associated with an increased proliferative activity (Ki-67 labeling index >5%) (P=0.020), and with either down-regulation or altered subcellular compartmentalization of E-cadherin (P<0.001) and CD99 (P=0.030), two cell adhesion complexes in pulmonary NE tumors. At multivariate analysis, only fascin emerged as an independent predictor of lymph node metastases in this tumor group (HR 30.28; 95% confidence intervals: 1.59-574.49; P=0.023). This study indicates that fascin immunoreactivity may identify subsets of pulmonary carcinoid patients with different metastatic potential to regional lymph nodes. Targeting the fascin pathway could be a novel therapeutic strategy of pulmonary carcinoids.
Lung Cancer 2003 Nov
PMID:Independent value of fascin immunoreactivity for predicting lymph node metastases in typical and atypical pulmonary carcinoids. 1456 88

This study was conducted to clarify the relationship between E-cadherin expression on tumor and lymph node metastasis as well as its prognostic roles in resected non-small-cell lung cancer. Two hundred forty-nine patients, who underwent surgical resection (stage I-IIIA), were examined. Paraffin-embedded sections of the primary tumors in all cases and of the metastatic lymph nodes in stage IIIA disease were stained with a monoclonal antibody against E-cadherin. Decreased expression of E-cadherin correlated with pathologic stage, tumor size, lymph node metastasis, and histological grade. The 5-year survival rate of E-cadherin-negative patients with stage IIIA disease was significantly lower than that of E-cadherin-positive patients. Multivariate analysis in stage IIIA disease indicated that E-cadherin was an independent prognostic factor. In the patients with clinical N0 tumors, the frequency of pathological N2 tumors was significantly higher in cases where the primary tumor was recognized as E-cadherin expression negative than in cases where the primary tumor was recognized as positive. Decreased E-cadherin expression showed correlation with presence of lymph node metastasis in resected non-small-cell lung cancer and with the prognosis of patients with stage IIIA disease.
Clin Lung Cancer 2001 Nov
PMID:Expression of E-cadherin and lymph node metastasis in resected non-small-cell lung cancer. 1465 29

We performed a retrospective analysis of potential prognostic markers in 260 patients with surgically resected stage I and II non small-cell lung cancer (NSCLC) with a minimum 5-year follow-up. Cox proportional hazard models and Wilcoxon tests were employed to analyze the effect of patient characteristics on survival and disease-free survival (DFS). In the univariate analysis, the following were significant predictors of shorter overall survival: N-stage (N1 vs N0) (p<0.001); T-stage (T2 vs T1) (p<0.001); antigen A (loss vs presence) (p<0.01); cough (present vs absent) (p=0.01); bcl-2 expression (positive vs negative) (p=0.03); age (>63.5 vs <63.5) (p=0.03); mucin (positive vs negative) (p<0.03). The following were significant predictors of shorter DFS: N-stage (p<0.001); T-stage (p=0.001); loss of antigen A (p=0.01); mucin expression (p<0.01); cough (p=0.02); Ki-67 expression (p=0.02) and negative bcl-2 expression (p=0.03). Analysis of survival difference for histologic subtype, degree of differentiation, aneuploidy, %S-phase, codon 12 K-ras mutation, and immunohistochemistry staining for Lewisy, p53, Rb, microvessel count, HER2, E-cadherin and neuroendocrine markers did not reach statistical significance. In multivariate analysis, the following predicted for shorter overall survival: N-stage (p<0.01), antigen A (p=0.01), age (p<0.01), and bcl-2 (p=0.05); and for DFS, N-stage (p<0.01), antigen A (p<0.01), Ki-67 (p=0.03), mucin (p=0.04) and T-stage (p=0.05). Of all the clinical-pathological, proliferative, and biological markers studied, only a few carried independent prognostic significance.
Clin Lung Cancer 1999 Aug
PMID:Prognostic markers in resected stage I and II non small-cell lung cancer: an analysis of 260 patients with 5 year follow-up. 1472 52

Cadherins and their associated cytoplasmic proteins, catenins, are critical to the maintenance of normal tissue integrity and the suppression of cancer invasion. The cadherin profile in malignant mesothelioma (MM) is not well defined and the role of the cadherin-catenin system in the pathogenesis of MM remains to be determined. By means of Western blot analysis and immunohistochemistry the expression of E (epithelial)-, N (neural)-, P (placental)-cadherin, and alpha-, beta- and gamma-catenins was studied in nine human MM cell lines and five human mesothelial cell lines. Mesothelial cells consistently expressed only N-cadherin and alpha- and beta-catenins. All but one MM cell line were N-cadherin-positive and all of them were also positive for alpha- and beta-catenins. E-cadherin was found in six (66.7%) and gamma-catenin in seven (77.8%) MM cell lines. Five of these E-cadherin-positive lines co-expressed N-cadherin and the remaining one was also P-cadherin-positive. Double immunofluorescence staining revealed the plasma membrane co-localisation of both cadherin types in MM cell lines that co-expressed E- and N-cadherin or E- and P-cadherin, respectively. Immunoprecipitation showed complexes of beta-catenin with both cadherin types when co-expressed. The results point to upregulation of E-cadherin and gamma-catenin in most MM cases and demonstrate that cadherin expression is more heterogeneous and less mutually exclusive in MM compared with the mesothelium, although the biological significance of this finding remains unclear.
Lung Cancer 2004 Aug
PMID:Aberrant E-cadherin and gamma-catenin expression in malignant mesothelioma and its diagnostic and biological relevance. 1526 32

LUN is a novel RING finger protein that is highly expressed in the lung and might be a transcriptional regulator of E-cadherin [J. Biol. Chem. 276 (2001) 14004]. It might be possible that LUN plays important roles in the development and progression of lung cancer through regulating expression of E-cadherin, but no clinical study on LUN expression has been reported. In the present study, we quantitatively examined gene expression of the LUN in surgical specimens resected from non-small cell lung cancer (NSCLC) patients. In normal lung tissues, the LUN gene expression was down-regulated in smokers (the mean LUN/GAPDH ratios, 0.222 for non-smokers and 0.144 for smokers; P = 0.030). In addition, the mean LUN/GAPDH ratio in lung cancer tissues was significantly lower than that in normal lung tissues (0.072 versus 0.162; P < 0.001). In addition, the LUN gene expression was slightly down-regulated along with progression of primary tumors, and strongly down-regulated along with nodal metastases (the mean LUN/GAPDH ratios, 0.091 for pN0, 0.073 for pN1, and 0.034 for pN2 diseases; P = 0.001). These results suggested that LUN might play important roles in inhibition of nodal metastases as well as in suppression of smoking-related oncogenesis in NSCLC.
Lung Cancer 2004 Oct
PMID:Expression of LUN gene that encodes a novel RING finger protein is correlated with development and progression of non-small cell lung cancer. 1536 29

Surgical material from 157 patients with lung carcinoma was studied. Immunohistochemical detection of the following oncomarkers was performed: Ki67, p53, CD34, CAS, Topoisomerase II alfa, nm23 protein, E-cadherin. The existence of association between proliferation, tumour cell apoptosis and formation of vessels in the tumour stroma is established. Angiogenesis correlated with proliferative activity of tumour cells this resulting from the effect of growth factors secreted by cells of both tumours and stroma. Angiogenesis in lung carcinoma may also be stimulated by mitogenetic factors accumulating in tumour tissue due to the "uncompleted" apoptosis. Low nm23 and E-cadherin expression is found in lung carcinoma with regional lymphogenic metastases indicating probably cancer metastases.
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PMID:[Correlation of proliferation, apoptosis, angiogenesis and metastasizing in various histogenetic types of pulmonary cancer (an immunohistochemical investigation)]. 1564 65

E-cadherin, a calcium-dependent cell-cell adhesion molecule, functions as maintenance of epithelial integrity. nm23, encoded by non-metastatic 23 gene, plays a key role in differentiation of many kinds of epithelium. Loss or dysfunction of E-cadherin and nm23 was frequently identified in many types of human cancers and is considered to correlate with invasive/metastatic phenotype. We previously reported that defective expression of E-cadherin might play a role in the development of the malignant phenotype in non-small cell lung cancer (NSCLC) [Q.Y. Fei, H.T. Zhang, X.F. Chen, et al., Defected expression of Ecadherin in non-small cell lung cancer, Lung Cancer 37 (2002) 147-152]. In an attempt to evaluate the significance of E-cadherin and nm23 in human non-small cell lung cancer, we performed mRNA expression and genetic structure analyses of the E-cadherin and nm23 genes in 54 NSCLCs and 46 normal lung tissues. The mRNA expression was determined by semi-quantitative RT-PCR, and genetic structure was examined through PCR-SSCP followed by sequencing. Although no mutation of the E-cadherin and nm23 genes was detected, the results obtained in the present study showed that reduction of E-cadherin and nm23 mRNA expression remarkably correlated with low histological differentiation, increasing stage as well as lymph node metastases (P<0.05). These data provide us with support for the idea that dysfunction of E-cadherin and nm23 has a role in progression of NSCLC and that the examination of E-cadherin and nm23 expression can provide experimental evidence for clinical treatment.
Lung Cancer 2005 Apr
PMID:Expression of E-cadherin and nm23 is associated with the clinicopathological factors of human non-small cell lung cancer in China. 1577 72

Inactivation of the cadherin-mediated cell-cell adhesion system is believed to play a role in the initial steps of cancer invasion and metastasis. Expression of E-cadherin and its intracytoplasmic binding molecules (alpha-catenin, beta-catenin, and plakoglobin) was examined immunohistochemically in 84 cases of intrabronchial precancerous lesions (bronchial squamous metaplasia (BSM) without atypia, BSM with atypia, dysplasia), and 21 cases of carcinoma in situ, and 4 cases of microinvasion to the bronchial wall, and 32 cases of stage I well differentiated squamous cell carcinoma (squamous cell carcinoma) to investigate the association between expression of E-cadherin and/or catenins and cancer progression. Reduced expression of E-cadherin and/or catenins was closely correlated with an atypical grade of dysplasia in the basal layer (p<0.05). In particular, downregulation of E-cadherin and/or catenins was associated with an atypical grade of BSM with atypia in intrabronchial lesions (p<0.01). We conclude that downregulation of alpha-catenin and/or beta-catenin, which may reflect dysfunction of the cadherin-mediated cell-cell adhesion system, is an important marker for atypical grade during carcinogenesis of the bronchial epithelium.
Lung Cancer 2005 Jun
PMID:Frequent loss of E-cadherin and/or catenins in intrabronchial lesions during carcinogenesis of the bronchial epithelium. 1589


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