Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • lung cancer  (16)
  • Germany  (14)
  • smoking  (9)
Collection
Keywords
  • 1
    Keywords: CANCER ; EXPRESSION ; carcinoma ; CELL ; Germany ; human ; LUNG ; lung cancer ; LUNG-CANCER ; EXPOSURE ; RISK ; GENE ; PROTEIN ; METABOLISM ; TISSUE ; PATIENT ; RISK-FACTORS ; FREQUENCY ; polymorphism ; SUSCEPTIBILITY ; PROMOTER ; OVARIAN-CANCER ; WOMEN ; MEN ; risk factors ; smoking ; PROSTATE-CANCER ; cancer risk ; RISK FACTOR ; CYP3A4 ; LINKAGE DISEQUILIBRIUM ; CANCER-PATIENTS ; CARCINOMAS ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; ADENOCARCINOMAS ; CARRIERS ; case-control studies ; CLINICAL PRESENTATION ; CYP3A,genetic polymorphism,lung cancer susceptibility,small cell lung cancer,LightCycler ; EXPRESSED HUMAN CYTOCHROME-P450S ; GENETIC VARIANT ; HUMAN LIVER-MICROSOMES ; PROSTATE TUMORS ; PROTEIN LEVELS ; squamous cell carcinoma ; TOBACCO
    Abstract: CYP3A isozymes are involved in tobacco carcinogen- and steroid-metabolism, and are expressed in human lung tissue showing interindividual variation in expression and activity. The CYP3A4* 1 B allele has been associated with a two-fold higher promoter activity and with high-grade prostate cancers. The very frequent intron 3 polymorphism in the CYP3A5 gene (CYP3A5*3) results in decreased CYP3A5 protein levels. A case-control study was conducted in 801 Caucasian lung cancer patients that included 330 adenocarcinomas, 260 squamous cell carcinomas, 171 small cell lung cancers (SCLC) and 432 Caucasian hospital-based controls. CYP3A-genotyping was performed by capillary polymerase chain reaction followed by fluorescence-based melting curve analysis. A significantly increased SCLC risk for CYP3A4* 1B allele carriers [odds ratio (OR) 2.25, 95% confidence interval (CI) 1.11-4.55, P = 0.02] was found. After dividing cases and controls by gender, an increased lung cancer risk for CYP3A4* 1B carriers (OR 3.04, 95% CI 0.94-9.90, P= 0.06) for women but not for men (OR 1.00, 95% CI 0.56-1.81) was revealed. Heavier smoking men (greater than or equal to 20 pack-years) with the CYP3A4* 1 B allele had a significant OR for lung cancer of 3.42 (95% CI 1.65-7.14, P= 0.001) compared to * 1A/1* 1A carriers with lower tobacco exposure (〈 20 pack-years). For women, the respective OR was 8.00 (95% CI 2.12-30.30, P = 0.005). Genotype frequencies were generally in Hardy-Weinberg equilibrium, except for CYP3A5 where a greater than expected number of CYP3A5* 1 homozygotes was observed among cases (P = 0.006). In addition, we observed linkage disequilibrium of CYP3A4 and CYP3A5 (P 〈 0.00001), but a nonsignificantly increased lung cancer risk was only found for homozygous CYP3A5* 1 allele carriers (OR 5.24,95% CI 0.85-102.28, P = 0.14) but not for heterozygotes. To confirm our observation that the CYP3A4* 1B allele increases SCLC risk and modifies the smoking-related lung cancer risk in a gender-specific manner, further studies, including CYP3A haplotype analysis, will be necessary. Pharmacogenetics 13:607-618 (C) 2003 Lippincott Williams Wilkins
    Type of Publication: Journal article published
    PubMed ID: 14515059
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: CANCER ; EXPRESSION ; carcinoma ; CELL ; Germany ; LUNG ; COMMON ; lung cancer ; LUNG-CANCER ; EXPOSURE ; RISK ; GENE ; GENES ; HYBRIDIZATION ; DNA ; MECHANISM ; primary ; RISK-FACTORS ; mechanisms ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; NO ; AMPLIFICATION ; AGE ; DNA-REPAIR ; REPAIR ; CIGARETTE-SMOKING ; risk factors ; smoking ; PCR ; cancer risk ; DAMAGE ; RISK FACTOR ; REGION ; CARCINOGENS ; adenocarcinoma ; case-control studies ; squamous cell carcinoma ; INDIVIDUALS ; CANCER-RESEARCH ; SMOKERS ; NUCLEOTIDE EXCISION-REPAIR ; CELL CARCINOMA ; case control study ; case-control study ; REGRESSION ; OCCUPATIONAL-EXPOSURE ; CARCINOGEN ; HEAVY ; LUNG ADENOCARCINOMA ; PIGMENTOSUM GROUP-A
    Abstract: Polymorphisms of genes coding for DNA repair can affect lung cancer risk. A common single nucleotide (-4) G-to-A polymorphism was identified previously in the 5' untranslated region of the XPA gene. In a case-control study in European Caucasians, the influence of this polymorphism on primary lung cancer risk overall and according to histologic subtypes was investigated. Four hundred sixty-three lung cancer cases (including 204 adenocarcinoma and 212 squamous cell carcinoma) and 460 tumor-free hospital controls were investigated using PCR amplification and melting point analysis of sequence-specific hybridization probes. Odds ratios (OR) were calculated by multiple logistic regression analysis adjusting for age, gender, smoking habits, and occupational exposure and showed a slightly enhanced risk for all lung cancer cases as well as for squamous cell carcinoma and adenocarcinoma cases. Gene-environment interactions were analyzed with respect to smoking and occupational exposure. A nearly 3-fold increased risk for adenocarcinoma associated with the XPA AA genotype was observed for occupationally exposed individuals (OR, 2.95; 95% confidence interval, 1.42-6.14) and for heavy smokers (OR, 2.52; 95% confidence interval, 1.17-5.42). No genotype-dependent increase in OR was found for nonexposed individuals or those smoking 〈20 pack-years. The significant effect of the XPA polymorphism in heavy smokers and occupationally exposed individuals suggests an important gene-environment interaction for the XPA gene. The underlying mechanisms as to why AA homozygotes are predisposed to lung adenocarcinoma and which specific carcinogens are involved remains to be determined
    Type of Publication: Journal article published
    PubMed ID: 15598786
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: APOPTOSIS ; CELLS ; carcinoma ; Germany ; LUNG ; THERAPY ; TOOL ; TIME ; resistance ; INITIATION ; pancreas ; RE ; pancreatic ; rectum ; viability ; MOLECULAR ANALYSIS ; tumour specimen ; surgical resection ; rectum carcinoma
    Abstract: Surgical resected tumours are often stored for hours in the clinic upon transfer to the bench leading to apoptosis of tumour cells making them no longer suitable for molecular analysis and diagnostic procedures. The way out of this problem may be a new oxygen-enriched solution (OES). We tested this agent using surgical resections of carcinomas of lung, rectum and pancreas. Immediately after resection, one part of each individual tumour was stored in PBS and the other part in OES, and the content of viable or dead cells was determined by trypan blue exclusion and MTT-assay. We found that OES keeps tumour cells up to 3 days and longer more viable than PBS and reduces the percentage of dead cells without inducing therapy resistance and affecting the outcome of experimental procedures. Thus, storing freshly resected tumours in OES may save time for tumour transfer and initiation of experiments
    Type of Publication: Journal article published
    PubMed ID: 16596178
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; CELLS ; IN-VITRO ; tumor ; AGENTS ; carcinoma ; CELL ; Germany ; IN-VIVO ; INHIBITION ; THERAPY ; VITRO ; VIVO ; SAMPLES ; TUMORS ; TIME ; PATIENT ; INDUCTION ; cell cycle ; CELL-CYCLE ; CYCLE ; treatment ; PROGRESSION ; resistance ; INDUCED APOPTOSIS ; PLASMA ; prostate cancer ; PROSTATE-CANCER ; chemotherapy ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; DERIVATIVES ; HEPATOMA-CELLS ; EPITHELIAL-CELLS ; CARCINOMAS ; PHARMACOKINETICS ; AGENT ; SINGLE ; ONCOLOGY ; RE ; EX-VIVO ; SOLID TUMORS ; MEDIATED APOPTOSIS ; MOLECULAR-MECHANISMS ; LEVEL ; analysis ; methods ; PLASMA-LEVELS ; dexamethasone ; PROMOTION ; USA ; GLUCOCORTICOIDS ; prospective ; in vivo ; clinical study
    Abstract: Background: Glucocorticoids have been used widely in conjunction with cancer therapy due to their ability to induce apoptosis in hematological cells and to prevent nausea and emesis. However, recent data including ours, suggest induction of therapy resistance by glucocorticoids in solid tumors, although it is unclear whether this happens only in few carcinomas or is a more common cell type specific phenomenon. Material and Methods: We performed an overall statistical analysis of our new and recent data obtained with 157 tumor probes evaluated in vitro, ex vivo and in vivo. The effect of glucocorticoids on apoptosis, viability and cell cycle progression under diverse clinically important questions was examined. Results: New in vivo results demonstrate glucocorticoid - induced chemotherapy resistance in xenografted prostate cancer. In an overall statistical analysis we found glucocorticoid - induced resistance in 89% of 157 analysed tumor samples. Resistance is common for several cytotoxic treatments and for several glucocorticoid - derivatives and due to an inhibition of apoptosis, promotion of viability and cell cycle progression. Resistance occurred at clinically achievable peak plasma levels of patients under anti - emetic glucocorticoid therapy and below, lasted for a long time, after one single dose, but was reversible upon removal of glucocorticoids. Two nonsteroidal alternative anti - emetic agents did not counteract anticancer treatment and may be sufficient to replace gluco corticoids in cotreatment of carcinoma patients. Conclusion: These data demonstrate the need for prospective clinical studies as well as for detailed mechanistic studies of GC - induced cell - type specific pro - and anti - apoptotic signalling
    Type of Publication: Journal article published
    PubMed ID: 17224649
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: CANCER ; tumor ; carcinoma ; Germany ; LUNG ; neoplasms ; SYSTEM ; SYSTEMS ; TUMORS ; SURGERY ; PATIENT ; kidney ; EXPERIENCE ; RADIOFREQUENCY ABLATION ; RESECTION ; FEASIBILITY ; RADIO-FREQUENCY ABLATION ; THERMAL ABLATION ; surgical resection ; CANDIDATES ; INITIAL-EXPERIENCE ; PULMONARY METASTASES
    Abstract: Background. Radiofrequency ablation (RFA) has received high interest in the treatment of primary and secondary lung neoplasms. Clinical experience continues to accumulate; however, the biologic effects after ablation remain poorly understood. This study evaluated the safety and feasibility of RFA in an open thoracotomy setting and investigated the early histopathologic changes after RFA. Methods. The study enrolled 18 subjects with multiple pulmonary metastases from a solid primary tumor. RFA was performed at an open thoracotomy setting, followed by wedge resection of the ablated tumor. Results. No intraoperative complications during the RFA procedure occurred. Immunostaining revealed a complete ablation in 7 patients (39%). The grade of ablation was greater than 90% in 9 patients (50%), and less than 90% in 2 (11%). No correlation was found between the grade of ablation and the applied energy and the diameter of the lesion. Conclusions. Intraoperative RFA in an open thoracotomy setting appears to be a safe and feasible technique. Tumor devitalization sufficient for local control was achieved in 89% in our series. Ablation was incomplete in 11%, subject to the methods used in this study. This result appears to be inferior to metastasectomy by surgical resection
    Type of Publication: Journal article published
    PubMed ID: 19161742
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: APOPTOSIS ; CANCER ; carcinoma ; CELL ; LUNG ; MODEL ; PATHWAY ; PATHWAYS ; lung cancer ; LUNG-CANCER ; RISK ; GENE ; GENES ; METABOLISM ; CARCINOGENESIS ; ASSOCIATION ; SUSCEPTIBILITY ; VARIANTS ; AGE ; DNA-REPAIR ; smoking ; ADHESION ; CELL-ADHESION ; inflammation ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; VARIANT ; CANDIDATE GENES ; METHYLENETETRAHYDROFOLATE REDUCTASE ; INCREASED RISK ; SQUAMOUS-CELL ; CHINESE POPULATION ; XUAN-WEI ; METHYLENE-TETRAHYDROFOLATE REDUCTASE ; GENE POLYMORPHISMS ; Genetic ; CENTRAL-EUROPE ; SEQUENCE VARIANTS
    Abstract: Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case-control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 x 10(-4)). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89-0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85-0.95), P = 1 x 10(-4)]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations
    Type of Publication: Journal article published
    PubMed ID: 20106900
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: CANCER ; EXPRESSION ; carcinoma ; lung cancer ; LUNG-CANCER ; SYSTEM ; TISSUE ; prognosis ; T-CELLS ; PROGRESSION ; LYMPHOCYTES ; PERIPHERAL-BLOOD ; microenvironment ; lymph nodes ; TRANSCRIPTION FACTOR FOXP3 ; tumor microenvironment ; NK-CELLS ; Foxp3(+) Tregs
    Abstract: INTRODUCTION: : Regulatory T cells (Tregs) can play a key role in suppressing T-cell-mediated immunity in patients with cancer. In this study, the immune cell composition of the lung tissue and draining lymph nodes from patients with non-small cell lung cancer was analyzed. METHODS: : Samples (solid tumor, tumor border, and tumor-free lung tissue, as well as intrapulmonal N1 and mediastinal N2 lymph nodes) from 30 patients subjected to curative resection were analyzed by immunohistochemistry and flow cytometry. RESULTS: : Immunohistochemistry showed the presence of Foxp3 Tregs in tumor-infiltrated lung tissue, scattered Tregs in tumor-free lung samples, and a large number of these cells in metastatic lymph nodes. Using flow cytometry, we observed a significant enhancement of CD4 T cells and Foxp3 Tregs in the tumor center of adenocarcinoma samples, when compared with tumor-free lung tissues and tumor periphery. This enrichment was associated with a drastic decrease in natural killer cell amounts. Metastatic lymph nodes also showed higher Treg numbers than tumor-free ones in patients with lung adenocarcinomas. In contrast, patients with squamous cell carcinomas displayed less profound accumulation of Tregs. CONCLUSION: : Accumulation of Tregs in the center of lung tumors and in metastatic lymph nodes in combination with a decrease in the natural killer cell numbers suggests a critical role of Treg in the formation of immunosuppressive tumor microenvironment. Therefore, lung cancer immunotherapy may be improved by a specific Treg elimination or suppression.
    Type of Publication: Journal article published
    PubMed ID: 21258248
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: RECEPTOR ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; carcinoma ; FACTOR RECEPTOR ; Germany ; human ; THERAPY ; TYROSINE KINASE ; microarray ; TISSUE ; treatment ; antibodies ; antibody ; STAGE ; immunohistochemistry ; MALIGNANCIES ; microarrays ; NUMBER ; COLORECTAL-CANCER ; CARCINOMAS ; SQUAMOUS-CELL CARCINOMAS ; TARGETS ; gene amplification ; COX-2 ; EPIDERMAL-GROWTH-FACTOR ; INHIBITORS ; MALIGNANCY ; thymus ; EGFR ; CYCLOOXYGENASE-2 ; LEVEL ; SUBTYPES ; tissue microarray ; EPITHELIAL TUMORS ; CYCLOOXYGENASE-2 INHIBITORS ; correlation ; PROSTAGLANDIN-E SYNTHASE ; VARIETIES ; epidermal growth factor ; epidermal growth factor receptor ; GROWTH-FACTOR-RECEPTOR ; PRIMARY MALIGNANCIES ; thymoma ; E-2 PRODUCTION ; mPGES ; thymic carcinoma
    Abstract: The treatment of advanced stage thymomas and thymic carcinomas is a multimodal therapy. New therapeutic targets are currently under investigation, including the epidermal growth factor receptor (EGFR) as well as KIT. A number of studies have shown protumorigenic potential of Cyclooxygenase-2 (COX-2) in a variety of human malignancies, but so far it is unknown whether COX-2 is expressed in primary malignancies of the thymus. Using tissue microarrays, the expression of COX-2, microsomal-PGES-1 and -PGES-2 (mPGES-1 and mPGES-2), as well as EGFR was evaluated in different subtypes of thymoma and thymic carcinomas. COX-2 was expressed in all subtypes as determined by immunohistochemistry. Some cases of type B2 and thymic carcinomas had COX-2 staining levels classified as mild to moderate. However, when measuring the optical color intensity, no significant differences could be detected. Concerning the expression levels, a weak correlation between the expression of COX-2, mPGES-1 and mPGES-2 as well as EGFR was found. Furthermore, additional cases of thymomas and thymic carcinomas were analyzed by COX-2 Western immunoblot analysis and were compared to normal thymi. The analysis showed that thymomas and thymic carcinomas had a significantly stronger COX-2 expression than that of the normal thymi (p 〈 0.04). In summary, COX-2 is expressed in all subtypes of thymomas and thymic carcinomas and thus represents, in addition to EGFR and KIT, a potential therapeutic target. Further studies are needed in order to determine whether a combined therapy using COX-2 inhibitors in addition to the evolving anti-EGFR antibody therapy may be considered as a treatment option. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16823844
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: APOPTOSIS ; CANCER ; tumor ; carcinoma ; CELL ; Germany ; LUNG ; lung cancer ; LUNG-CANCER ; SYSTEM ; EXPOSURE ; RISK ; GENE ; GENES ; PATIENT ; RISK-FACTORS ; cell cycle ; CELL-CYCLE ; CYCLE ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; BREAST-CANCER ; risk factors ; smoking ; p53 ; cancer risk ; MUTATIONS ; TRANSFORMATION ; SQUAMOUS-CELL CARCINOMA ; adenocarcinoma ; case-control studies ; squamous cell carcinoma ; GASTRIC-CANCER ; DNA repair ; DNA-REPAIR GENES ; molecular epidemiology ; ONCOLOGY ; case-control study ; REGRESSION ; RE ; TUMOR-SUPPRESSOR ; VARIANT ; INCREASE ; CARCINOGEN ; case control studies ; analysis ; SUPPRESSOR ; GENOTYPE ; adenocarcinoma of the lung ; HISTOLOGY ; RISK-FACTOR ; CANCER-RISK ; PROLINE ; SQUAMOUS-CELL ; INCREASES ; cell cycle control ; CODON-72 ; P53 POLYMORPHISM
    Abstract: Alterations in cell cycle regulation and apoptosis leading to malignant transformation could be caused by common genetic variants in tumor suppressor genes. The effects of the TP53 polymorphism Arg72Pro on lung cancer risk have been investigated in numerous studies with, however, conflicting results. In many studies, important risk modifiers such as smoking or tumor histology were not taken into account. We therefore investigated the combined effects of polymorphisms in TP53 (Arg72Pro) and p21/CDKN1A (Ser31Arg) and smoking on lung cancer risk. Our case-control study consisted of 405 patients with lung cancer, mainly squamous-cell carcinoma (185) and adenocarcinoma (177) and 404 unmatched tumor-free hospital controls. Multivariate regression analysis showed a moderate but statistically significant risk of lung cancer overall. and especially of squamous-cell carcinoma (OR, 1.65; CI, 1.10-2.47) for TP53 72Pro allele carriers. The risk was markedly increased in heavy smokers (〉 20 pack-years) with squamous-cell carcinoma (OR, 2.80 in patients homozygous for 72Pro; CI, 1.19-6.58), but not in tight smokers (〈= 20 pack-years). The results for the p21 Ser31Arg polymorphism suggested that 31Ser is a moderate-risk allele for squamous-cell carcinoma. Analysis of the combined effects of the two polymorphisms revealed a higher OR for TP53 72Pro carriers homozygous for p21 31Ser than for 72Pro carriers in general; this effect being most pronounced in heavy smokers with squamous-cell carcinoma (OR, 3.84; CI, 1.46-10.1). Our data indicate that the TP53 Arg72Pro polymorphism increases the risk for squamous-cell carcinoma mainly in heavy smokers. The observed interaction with smoking is biologically plausible as, for the 72Pro p53 variant, decreased apoptosis and extended G1 cell cycle arrest is reported after carcinogen exposure. Nevertheless, confirmation by further molecular and epidemiological studies is warranted. (c) 2006 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17059853
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: CANCER ; IN-VITRO ; INHIBITOR ; proliferation ; tumor ; carcinoma ; CELL ; Germany ; human ; VITRO ; SYSTEM ; TOOL ; DISEASE ; CLONES ; DRUG ; TUMORS ; COMPLEX ; INDEX ; primary ; CONTRAST ; CELL-LINES ; culture ; TARGET ; COMPARATIVE GENOMIC HYBRIDIZATION ; MALIGNANCIES ; CELL-LINE ; ABERRATIONS ; FISH ; CARCINOMAS ; sensitivity ; TARGETS ; BEHAVIOR ; CHROMOSOMAL IMBALANCES ; molecular ; ONCOLOGY ; UPDATE ; analysis ; TESTS ; EPITHELIAL TUMORS ; USA ; TOOLS ; thymoma ; thymic carcinoma ; HISTOLOGIC CLASSIFICATION ; permanent cell lines
    Abstract: Thymomas and thymic carcinomas are peculiar epithelial tumors of the anterior mediastinum. They may show aggressive clinical behavior and are a paradigm for the interaction between the tumor and the immune system. So far, adequate functional studies enabling a better understanding of this malignancy have not been performed, since human thymoma/thymic carcinoma cell lines have not been available. Here, the authors describe the establishment, characterization and functional analyses of epithelial cell lines from a Type B1-thymoma and a poorly differentiated thymic carcinoma. By Fluorescence-activated cell sorting (FACS) analyses, both cell lines were aneuploid. The aneuploid cell fraction of the thymic carcinoma cell line was characterized by a high proliferation index of 55.9%, in contrast to a lower proliferation rate of the aneuploid cell fraction of the thymoma (19.7%). Array-based comparative genomic hybridization (aCGH) and conventional cytogenctic analysis of the thymoma revealed only minor imbalances whereas the thymic carcinoma was characterized by a complex karyotype in the hyperdiploid range that was readily defined with multicolor FISH (mFISH). Application of a selective COX-2 inhibitor reduced cell viability in both cell lines in a dose-dependent manner. In conclusion, these first cell lines of a thymoma and a CD5-positive thymic carcinoma are useful tools for further in vitro studies of cellular, molecular and genetic aspects of the disease and for functional tests to evaluate new therapeutic targets. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18360827
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...