Home About us Contact
|
Home About us Contact | ||
|
|
||
Large Cell Carcinoma (large + cell_carcinoma)
Selected AbstractsHigh resolution analysis of non-small cell lung cancer cell lines by whole genome tiling path array CGHINTERNATIONAL JOURNAL OF CANCER, Issue 6 2006Cathie Garnis Abstract Chromosomal regions harboring tumor suppressors and oncogenes are often deleted or amplified. Array comparative genomic hybridization detects segmental DNA copy number alterations in tumor DNA relative to a normal control. The recent development of a bacterial artificial chromosome array, which spans the human genome in a tiling path manner with >32,000 clones, has facilitated whole genome profiling at an unprecedented resolution. Using this technology, we comprehensively describe and compare the genomes of 28 commonly used non-small cell lung carcinoma (NSCLC) cell models, derived from 18 adenocarcinomas (AC), 9 squamous cell carcinomas and 1 large cell carcinoma. Analysis at such resolution not only provided a detailed genomic alteration template for each of these model cell lines, but revealed novel regions of frequent duplication and deletion. Significantly, a detailed analysis of chromosome 7 identified 6 distinct regions of alterations across this chromosome, implicating the presence of multiple novel oncogene loci on this chromosome. As well, a comparison between the squamous and AC cells revealed alterations common to both subtypes, such as the loss of 3p and gain of 5p, in addition to multiple hotspots more frequently associated with only 1 subtype. Interestingly, chromosome 3q, which is known to be amplified in both subtypes, showed 2 distinct regions of alteration, 1 frequently altered in squamous and 1 more frequently altered in AC. In summary, our data demonstrate the unique information generated by high resolution analysis of NSCLC genomes and uncover the presence of genetic alterations prevalent in the different NSCLC subtypes. © 2005 Wiley-Liss, Inc. [source] Identification of occupational cancer risk in British Columbia: A population-based case,control study of 2,998 lung cancers by histopathological subtypeAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2009Amy C. MacArthur MHSc Abstract Background Few studies have investigated occupational lung cancer risk in relation to specific histopathological subtypes. Methods A case,control study was conducted to evaluate the relationship between lung cancer and occupation/industry of employment by histopathological subtype. A total of 2,998 male cases and 10,223 cancer controls, diagnosed between 1983 and 1990, were identified through the British Columbia Cancer Registry. Matched on age and year of diagnosis, conditional logistic regression analyses were performed for two different estimates of exposure with adjustment for potentially important confounding variables, including tobacco smoking, alcohol consumption, marital status, educational attainment, and questionnaire respondent. Results For all lung cancers, an excess risk was observed for workers in the primary metal (OR,=,1.31, 95% CI, 1.01,1.71), mining (OR,=,1.53, 95% CI, 1.20,1.96), machining (OR,=,1.33, 95% CI, 1.09,1.63), transport (OR,=,1.50, 95% CI, 1.08,2.07), utility (OR,=,1.60, 95% CI, 1.22,2.09), and protective services (OR,=,1.27, 95% CI, 1.05,1.55) industries. Associations with histopathological subtypes included an increased risk of squamous cell carcinoma in construction trades (OR,=,1.25, 95% CI, 1.06,1.48), adenocarcinoma for professional workers in medicine and health (OR,=,1.73, 95% CI, 1.18,2.53), small cell carcinoma in railway (OR,=,1.62, 95% CI, 1.06,2.49), and truck transport industries (OR,=,1.51, 95% CI, 1.00,2.28), and large cell carcinoma for employment in the primary metal industry (OR,=,2.35, 95% CI, 1.11,4.96). Conclusions Our results point to excess lung cancer risk for occupations involving exposure to metals, polyaromatic hydrocarbons and asbestos, as well as several new histopathologic-specific associations that merit further investigation. Am. J. Ind. Med. 52:221,232, 2009. © 2008 Wiley-Liss, Inc. [source] Cell type accuracy of transthoracic fine needle aspiration material in primary lung cancerRESPIROLOGY, Issue 2 2001Adnan Yilmaz Objective: The aim of this study was to evaluate the diagnostic accuracy of transthoracic fine needle aspiration (TFNA) materials in establishing the specific cell type in primary lung cancer, and to study the influence of several factors on this accuracy. Methodology: The present study included 129 patients [(12 females, 117 males; mean age 54.6 years (range 25,75)] who underwent thoracotomy. The initial diagnosis was obtained by means of TFNA biopsy in all patients. Transthoracic fine needle aspiration was performed by 22-gauge Chiba needle with fluoroscopy guide in 93 patients and with computed tomography guide in 36 cases. Results: The overall concordance was 73.6% (Kappa = 0.52). The worst agreement was obtained for the large cell carcinoma (40%; Kappa = 0.48). The likelihood of a correct diagnosis using the TFNA specimens was 6.2-fold higher for well-differentiated tumours than for poorly differentiated tumours (P < 0.005). The stage of tumour and diameter of the lesion had no effect on cell agreement. Cell agreement was higher in central lesions than peripheral lesions, but the difference was not statistically significant (P = 0.097). This difference was more significant between patients with central and peripheral epidermoid carcinoma (P = 0.057). Conclusion: In our opinion, cell typing by TFNA may lead to incorrect results in the presence of poor differentiation, mixed tumours and peripheral epidermoid carcinomas. [source] Genetic alterations in early-stage pulmonary large cell neuroendocrine carcinomaCANCER, Issue 6 2004Kenzo Hiroshima M.D. Abstract BACKGROUND Small cell lung carcinoma (SCLC) and pulmonary large cell neuroendocrine carcinoma (LCNEC) are high-grade malignant neuroendocrine tumors. Histologic differentiation between SCLC and LCNEC is difficult in some cases and to the authors' knowledge, genetic alterations associated with LCNEC have not been identified. Therefore, the authors studied genetic alterations found in LCNEC and compared them with those of SCLC and classic large cell carcinoma (CLCC). METHODS Twenty-two patients with UICC TNM Stage I LCNEC, 12 patients with Stage I CLCC, and 11 patients with SCLC with limited disease were studied. All tumors were resected completely. Loss of heterozygosity (LOH) of the tumor cells was detected using fluorescent primers. Methylation status of the p16 gene and expression of the p53 protein, retinoblastoma protein, and p16 protein were evaluated immunohistochemically. RESULTS LOH at TP53 and 13q14 was observed in most patients. The prevalence of LOH at D3S1295, D3S1234, and D5S407 was significantly higher in patients with LCNEC and SCLC than in patients with CLCC. The prevalence of LOH at D5S422 was higher in patients with CLCC and in patients with SCLC than in patients with LCNEC. Expression of the p16 protein was observed more frequently in SCLC than in CLCC or LCNEC. Hypermethylation of the p16 gene was observed more frequently in LCNEC than in SCLC. Patients with allelic losses at D3S1234 and D10S1686 had poorer prognoses compared with patients without allelic losses at these sites. CONCLUSIONS Genetic alterations of LCNEC were akin to those of SCLC. However, allelic losses at 5q and abnormalities in the p16 gene may differentiate LCNEC from SCLC. Cancer 2004. © 2004 American Cancer Society. [source] Reproducibility of Diagnosis and Its Influence on the Distribution of Lung Cancer by Histologic Type in Osaka, JapanCANCER SCIENCE, Issue 1 2000Seiichiro Yamamoto The histologic types of lung cancer cases diagnosed in 1979,1980 (n=799) and 1987 (n=587) were independently reviewed by two pathologists in order to investigate the reproducibility of the diagnosis of the histologic type when the WHO classification (1981) was used. The specimens from 354 surgical cases and biopsy or cytology specimens from 1032 non-surgical cases were reviewed. The inter-observer agreement was 87.9% (k=0.79) for surgical cases and 81.4% (k=0.72) for non-surgical cases. When compared to the original diagnosis, the agreement was 86.8% (k=0.78) for surgical and 86.4% (k=0.79) for non-surgical cases in 1979,1980 and the agreement was 92.8% (k=0.87) for surgical and 89.1% (k=0.83) for non-surgical cases in 1987. By histologic type, no difference in the agreement was observed except for large cell carcinoma. The distribution of histologic types after the review differed only slightly (less than 6%) from the original distribution. This suggests that in Osaka, Japan, the diagnosis based on the WHO classification (1981) had only a limited influence on the distribution of histologic types, and is not a major reason for the changing trends in lung cancer incidence by histologic type. [source] HER-2/neu overexpression in patients with radically resected nonsmall cell lung carcinomaCANCER, Issue 10 2002Impact on long-term survival Abstract BACKGROUND Using immunohistochemistry, the authors prospectively investigated the expression of HER-2/neu protein in radically resected specimens of nonsmall cell lung carcinoma (NSCLC) and evaluated its impact on long-term prognosis. METHODS Between January 1991 and February 1992, surgical specimens from 130 consecutive patients who underwent radical resection for NSCLC (60 squamous cell carcinoma, 48 adenocarcinoma cases, and 22 large cell carcinomas) and that were staged (according to the TNM staging system) pathologically as Stage I (41 cases [ 32%]), Stage II (37 cases [28%]), and Stage IIIA (52 cases [40%]) were investigated for the expression of HER-2/neu using an avidin-biotin complex immunohistochemical technique. A semiquantitative four-stage grading system was used (0%, 1,5%, 6,20%, and > 20% positive cells) and an average number of 1500 cells/section was considered. Data were correlated with clinical and pathologic variables. RESULTS Normal bronchial tissue was found to be completely negative for HER-2/ neu expression whereas 21 of the 130 tumor specimens (16%) were positive (range 1,> 20%). HER-2/neu positivity did not appear to differ significantly among pathologic stages and histotypes. Using a predetermined cutoff value of 5% positive cells, 15 tumor specimens (12%) were found to be above this value. The median survival time (85 weeks vs. 179 weeks) and overall survival rate were significantly lower in patients with > 5% HER-2/neu -positive tumors (hazard ratio for the group with > 5% positive cells: 2.94, 95% confidence interval, 1.62,5.34; P < 0.0004). On multivariate analysis, HER-2/ neu and extent of tumor emerged as independent factors for disease-related mortality. CONCLUSIONS In NSCLC, the negative impact of HER-2/neu overexpression on survival was maintained in the long-term follow-up of radically resected patients. HER-2/neu overexpression may be a valuable prognostic factor as well as a potential target for biologic therapies. Cancer 2002;94:2669,74. © 2002 American Cancer Society. DOI 10.1002/cncr.10531 [source] Immunohistochemical analysis of CYP2A13 in various types of human lung cancersCANCER SCIENCE, Issue 4 2010Tatsuki 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] Human Tissue Distribution of TA02, Which is Homologous with a New Type of Aspartic Proteinase, Napsin ACANCER SCIENCE, Issue 10 2000Takashi Hirano The N-terminal amino acid sequence of TA02 (molecular weight 35.0 kDa, isoelectric point 5.29), which is associated with primary lung adenocarcinoma, was determined and a fragment peptide was used to generate mouse monoclonal antibodies (mAbs) against TA02. The amino acid sequence suggested that TA02 might be homologous with napsin A, a new type of aspartic proteinase. In this context, we confirmed the expression of napsin A in primary lung adenocarcinoma using reversetranscription polymerare chain reaction (RT-PCR) and showed that the TA02 mAbs reacted with glutathione-S-transferase (GST)-napsin A fusion protein. We concluded that TA02 is the same molecule as napsin A, and showed immunohistochemically that it is distributed mainly in type II pneumocytes, alveolar macrophages, renal tubules and exocrine glands and ducts in the pancreas. In particular, type II pneumocytes and alveolar macrophages showed high expression of TA02 among human normal tissues. In primary lung adenocarcinoma, 47 out of 58 (81.0%) primary lesions were positive. All well-differentiated adenocarcinomas except those of goblet cell type showed high expression of TA02. In addition, two out of seven (28.6%) large cell carcinomas showed low expression of TA02. The other histopathological types of primary lung cancer did not express TA02 at all. A few cases of renal cell cancer, pancreatic cancer, breast cancer, thyroid cancer, colon cancer and ovarian cancer showed low expression, but the staining patterns were completely different from that of primary lung adenocarcinoma, which showed a granular staining pattern. Our novel mAbs should be valuable for immunochemical detection of TA02/napsin A. [source] | ||||||||||