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  • CELL CARCINOMA  (8)
  • ONCOLOGY  (6)
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  • 1
    Keywords: CANCER ; EXPRESSION ; tumor ; carcinoma ; Germany ; human ; DISEASE ; GENE ; MONOCLONAL-ANTIBODY ; PATIENT ; DONOR ; ANTIGEN ; SKIN ; BREAST-CANCER ; IMMUNE-RESPONSES ; antibodies ; CELL-LINE ; LINE ; TUMOR-ASSOCIATED ANTIGENS ; CYTOLYTIC T-LYMPHOCYTES ; SERUM ; CELL CARCINOMA ; renal cell carcinoma ; RE ; HUMAN-MELANOMA ; SEREX ; human renal cell carcinoma ; AUTOLOGOUS ANTIBODY ; cancer-testis antigen ; CDNA CLONING ; immunome ; SADA ; VALOSIN-CONTAINING PROTEIN
    Abstract: Serological analysis of cDNA expression libraries (SEREX) has proven to be a useful technique in the quest to elucidate the repertoire of immunogenic gene products in human cancer. We have applied the SEREX method to human renal cell carcinoma (RCC) in order to identify associated immunogenic gene products. cDNA expression libraries were prepared from a RCC tumor, a RCC cell line and human testis. The 3 libraries were screened with sera from 35 RCC patients and 15 healthy controls. Approximately 4.5 x 10(6) phage plaques were screened resulting in 234 positive clones, which corresponded to 74 different gene products. The seroreactivity toward 49 of these antigens was assessed. Seroreactivity to 21 (43%) of the antigens was similar in RCC patients and healthy controls, 9 antigens (18%) elicited antibodies more frequently and 19 antigens (39%) solely in RCC patients. In the reverse setting, reactivity of RCC patients' sera was tested against a panel of 44 previously identified "tumor-associated" antigens via the SADA (serum antibody detection array) method; 6 antigens reacted with RCC patients' and healthy donors' sera, 8 were reactive only with RCC patients' sera. From the 27 antigens identified by SEREX and SADA, which did not react with sera from healthy controls, 10 antigens reacted with a significant proportion of RCC patients' sera and 77% of RCC patients' sera reacted at least with one of these antigens. Sera from patients with nonmalignant renal diseases or an autoimmune disease did not react with these 10 antigens. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16331622
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  • 2
    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
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  • 3
    Keywords: APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; INHIBITOR ; carcinoma ; CELL ; Germany ; INHIBITION ; THERAPY ; LUNG-CANCER ; GENE ; PROTEIN ; SAMPLE ; SAMPLES ; TISSUE ; kidney ; FAMILY ; tumour ; ALPHA ; TARGET ; ISOFORM ; immunohistochemistry ; DIFFERENCE ; resistance ; CANCER-CELLS ; BETA ; STRATEGIES ; IMMUNOTHERAPY ; NORMAL TISSUE ; sensitivity ; OVEREXPRESSION ; CANCER-THERAPY ; protein expression ; TRANSCRIPTS ; CELL CARCINOMA ; renal cell carcinoma ; ONCOLOGY ; ADULT ; RE ; THERAPIES ; INCREASE ; cancer therapy ; REAL-TIME ; SURVIVIN ; NUCLEAR ; ML-IAP ; inhibitor of apoptosis ; apoptotic ; quantitative ; livin/ML-IAP ; APOPTOSIS PROTEIN ; CYTOPLASM ; tumour therapy ; Livin/ML-IAP/KIAP ; MELANOMA INHIBITOR
    Abstract: The antiapoptotic Livin/ML-IAP gene has recently gained much attention as a potential new target for cancer therapy. Reports indicating that livin is expressed almost exclusively in tumours, but not in the corresponding normal tissue, suggested that the targeted inhibition of livin may present a novel tumour-specific therapeutic strategy. Here, we compared the expression of livin in renal cell carcinoma and in non-tumorous adult kidney tissue by quantitative real-time reverse transcription-PCR, immunoblotting, and immunohistochemistry. We found that livin expression was significantly increased in tumours (P=0.0077), but was also clearly detectable in non-tumorous adult kidney. Transcripts encoding Livin isoforms alpha and beta were found in both renal cell carcinoma and normal tissue, without obvious qualitative differences. Livin protein in renal cell carcinoma samples exhibited cytoplasmic and/or nuclear staining. In non-tumorous kidney tissue, Livin protein expression was only detectable in specific cell types and restricted to the cytoplasm. Thus, whereas the relative overexpression of livin in renal cell carcinoma indicates that it may still represent a therapeutic target to increase the apoptotic sensitivity of kidney cancer cells, this strategy is likely to be not tumour-specific
    Type of Publication: Journal article published
    PubMed ID: 17968430
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  • 4
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; CANCER CELLS ; EXPRESSION ; IN-VITRO ; SURVIVAL ; carcinoma ; PATHWAY ; PATHWAYS ; NF-KAPPA-B ; prognosis ; ASSOCIATION ; TUMOR PROGRESSION ; METASTASIS ; PROGNOSTIC FACTORS ; FAS LIGAND EXPRESSION ; APOPTOSIS-INDUCING LIGAND ; ONCOLOGY ; CD95-MEDIATED APOPTOSIS ; death receptor ; renal cell cancer ; (APO-1/FAS)-MEDIATED APOPTOSIS ; CD95 (Fas/APO1) ; DECOY RECEPTOR-3 ; FREQUENT LOSS
    Abstract: CD95 (Fas/APO1) is one of the best known members of the death receptor family which can either mediate apoptosis or activate tumor-promoting pathways. Using a tissue microarray we investigated the association between the expression of CD95 and prognosis in 617 patients with renal cell carcinomas (RCCs). CD95 was expressed in the vast majority of RCCs. High CD95 expression was associated with lymph node metastasis and correlated negatively with disease-specific survival. Multivariate Cox regression analysis confirmed CD95 expression as an independent prognostic factor. In conclusion, high CD95 expression is a negative independent prognostic factor in RCCs which could be used to identify high-risk patients with a poor clinical prognosis.
    Type of Publication: Journal article published
    PubMed ID: 21196076
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  • 5
    Keywords: CANCER ; EXPRESSION ; neoplasms ; DISEASE ; TUMORS ; ACTIVATION ; kidney ; MECHANISM ; prognosis ; cytogenetics ; FUSION ; FISH ; adenocarcinoma ; CELL CARCINOMA ; renal cell carcinoma ; MITF ; GENE FUSION ; MET ; SOFT PART SARCOMA ; TFE3 ; Xp11 ; XP11.2 TRANSLOCATION
    Abstract: Renal cell carcinomas associated with Xp11.2 translocations have recently been identified as a distinct biological entity. The translocation results in the fusion of the transcription factor TFE3 to one of several different fusion partners including PRCC, PSF, NONO, ASPL or CTLC with consecutive overexpression of the chimeric protein. As the true frequency of these neoplasms as well as the biological properties of TFE3 activation in renal cell carcinomas are largely unknown, we have examined TFE3 expression as well as the underlying genetic alterations in a large, hospital-based series of renal cell carcinomas with long-term follow-up information. Out of a total of 876 tumours, TFE3 translocations were detected in five cases (0.6%). Three additional cases were identified in a second series of cases comprising of renal cell carcinomas developing in patients before the age of 50. However, using immunohistochemistry, 9% of all renal cell carcinomas showed some degree of TFE3 reactivity. Interestingly, these cases were associated with high nuclear grade, greater tumour extent and metastatic disease as well as an unfavourable patient outcome on uni- and multivariate analysis. Fluorescence in situ hybridisation (FISH) revealed TFE3 amplifications as an additional, novel mechanism leading to increased TFE3 expression levels. In conclusion, our data show that Xp11 translocation renal cell carcinomas are uncommon tumours accounting for 〈1% of adult renal cell carcinomas and that the diagnosis of Xp11 translocation renal cell carcinomas needs to be verified using molecular techniques. In turn, TFE3 overexpressing tumours show an aggressive behaviour and Xp11 translocation is only one of several possible underlying genomic alterations.
    Type of Publication: Journal article published
    PubMed ID: 22037260
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  • 6
    Keywords: CELLS ; EXPRESSION ; GROWTH ; SURVIVAL ; tumor ; carcinoma ; CELL ; Germany ; MICE ; GENE-TRANSFER ; ACTIVATION ; INDUCTION ; T-CELL ; T-CELLS ; cytokines ; MHC ; VECTOR ; EFFICACY ; REQUIRES ; VACCINES ; PEPTIDES ; MONOCLONAL-ANTIBODIES ; MHC CLASS-I ; immune response ; IMMUNE-RESPONSE ; vaccination ; CANCER-IMMUNOTHERAPY ; REJECTION ; CYTOKINE ; CELL CARCINOMA ; renal cell carcinoma ; TUMOR-GROWTH ; DNA VACCINATION ; immunology ; regulatory T cells ; EXPANSION ; SALMONELLA-TYPHIMURIUM ; SUPPRESSOR-CELLS ; TIMES ; IMMUNE ; TRANSFECTED DENDRITIC CELLS
    Abstract: Efficient tumor vaccination frequently requires adjuvant. Concomitant induction of an autoimmune response is discussed as a means to strengthen a weak tumor Ag-specific response. We asked whether the efficacy of dendritic cell (DC) vaccination with the renal cell carcinoma Ags MAGE-A9 (MAGE9) and G250 could be strengthened by covaccination with the renal cell carcinoma autoantigen GOLGA4. BALB/c mice were vaccinated with DC loaded with MHC class I-binding peptides of MAGE9 or G250 or tumor lysate, which sufficed for rejection of low-dose RENCA-MAGE9 and RENCA-G250 tumor grafts, but only retarded tumor growth at 200 times the tumor dose at which 100% of animals will develop a tumor. Instead, 75-100% of mice prevaccinated concomitantly with Salmonella typhimurium transformed with GOLGA4 cDNA in a eukaryotic expression vector rejected 200 times the tumor dose at which 100% of animals will develop tumor. In a therapeutic setting, the survival rate increased from 20-40% by covaccination with S. typhimurium-GOLGA4. Autoantigen covaccination significantly strengthened tumor Ag-specific CD4(+) and CD8(+) T cell expansion, particularly in peptide-loaded DC-vaccinated mice. Covaccination was accompanied by an increase in inflammatory cytokines, boosted IL-12 and IFN-gamma expression, and promoted a high tumor Ag-specific CTL response. Concomitant autoantigen vaccination also supported CCR6, CXCR3, and CXCR4 upregulation and T cell recruitment into the tumor. It did not affect regulatory T cells, but slightly increased myeloid-derived suppressor cells. Thus, tumor cell eradication was efficiently strengthened by concomitant induction of an immune response against a tumor Ag and an autoantigen expressed by the tumor cell. Activation of autoantigen-specific Th cells strongly supports tumor-specific Th cells and thereby CTL activation. The Journal of Immunology, 2010, 185: 902-916
    Type of Publication: Journal article published
    PubMed ID: 20548033
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  • 7
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; proliferation ; tumor ; carcinoma ; CELL ; CELL-PROLIFERATION ; Germany ; human ; INHIBITION ; THERAPY ; HEPATOCELLULAR-CARCINOMA ; GENE ; RNA ; SAMPLE ; SAMPLES ; TISSUE ; LINES ; kidney ; primary ; CELL-LINES ; TARGET ; virus ; MALIGNANCIES ; resistance ; CARCINOMA CELLS ; PROSTATE-CANCER ; CELL-LINE ; CARCINOMA-CELLS ; HOMOLOG ; STRATEGIES ; METHYLTRANSFERASE ACTIVITY ; CANCER-THERAPY ; CELL CARCINOMA ; renal cell carcinoma ; MALIGNANCY ; ONCOLOGY ; ENHANCER ; ADULT ; RE ; INTERFERENCE ; RNA INTERFERENCE ; THERAPIES ; cancer therapy ; cell proliferation ; TUMOR TISSUE ; LEVEL ; RNAi ; USA ; tumor therapy ; RENAL-CELL ; GROUP PROTEIN EZH2 ; POLYCOMB REPRESSION ; HISTONE H3 ; AGGRESSIVE BREAST-CANCER ; enhancer of zeste homolog 2 (EZH2) ; ZESTE HOMOLOG-2
    Abstract: The enhancer of zeste homolog 2 (EZH2) gene has been recently linked to human malignancies where it may serve as a new target for cancer therapy. Here, we analyzed EZH2 expression in primary renal cell carcinoma (RCC) specimens and in nontumorous tissue samples from adult kidney. EZH2 transcripts were detectable in all RCC specimens examined. Expression levels were significantly higher in tumor tissue (p 〈= 0.0001) than in samples from normal adult kidney. Moreover, inhibition of endogenous EZH2 expression in RCC cell lines by RNA interference (RNAi) led to reduced proliferation and increased apoptosis in RCC cells. These data show that EZH2 is overexpressed in RCC. Furthermore, they indicate that the EZH2 gene plays a role for both the proliferation and the apoptosis resistance of RCC cells. Targeted inhibition of EZH2 could therefore represent a novel strategy to improve the therapeutic response of RCC. (C) 2008 Wilely-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18623083
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  • 8
    Keywords: CANCER ; EXPRESSION ; proliferation ; SURVIVAL ; carcinoma ; DISEASE ; GENE ; microarray ; MARKER ; BREAST ; DOUBLE-BLIND ; CELL CARCINOMA ; PREDICT ; PHASE-III TRIAL ; GROUP PROTEIN EZH2 ; ENHANCER-OF-ZESTE-HOMOLOG-2 GENE ; METASTATIC PROSTATE-CANCER
    Abstract: Background: The enhancer of zeste homolog 2 (EZH2) gene exerts oncogene-like activities and its (over) expression has been linked to several human malignancies. Here, we studied a possible association between EZH2 expression and prognosis in patients with renal cell carcinoma (RCC). Methods: EZH2 protein expression in RCC specimens was analyzed by immunohistochemistry using a tissue microarray (TMA) containing RCC tumor tissue and corresponding normal tissue samples of 520 patients. For immunohistochemical assessment of EZH2 expression, nuclear staining quantity was evaluated using a semiquantitative score. The effect of EZH2 expression on cancer specific survival (CSS) was assessed by univariate and multivariate Cox regression analyses. Results: During follow-up, 147 patients (28%) had died of their disease, median follow-up of patients still alive was 6.0 years (range 0-16.1 years). EZH2 nuclear staining was present in tumor cores of 411 (79%) patients. A multivariate Cox regression analysis revealed that high nuclear EZH2 expression was an independent predictor of poor CSS (〉 25-50% vs. 0%: HR 2.72, p = 0.025) in patients suffering from non-metastatic RCC. Apart from high nuclear EZH2 expression, tumor stage and Fuhrman's grading emerged as significant prognostic markers. In metastatic disease, nuclear EZH2 expression and histopathological subtype were independent predictive parameters of poor CSS (EZH2: 1-5%: HR 2.63, p = 0.043, 〉 5-25%: HR 3.35, p = 0.013, 〉 25%-50%: HR 4.92, p = 0.003, all compared to 0%: HR 0.36, p = 0.025, respectively). Conclusions: This study defines EZH2 as a powerful independent unfavourable prognostic marker of CSS in patients with metastatic and non-metastatic RCC
    Type of Publication: Journal article published
    PubMed ID: 20920340
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  • 9
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; IN-VITRO ; SURVIVAL ; tumor ; carcinoma ; CELL ; Germany ; THERAPY ; INFORMATION ; DEATH ; DISEASE ; incidence ; MORTALITY ; microarray ; PROTEIN ; SAMPLE ; SAMPLES ; TISSUE ; TUMORS ; PATIENT ; LIGAND ; SERA ; prognosis ; T-CELL ; ASSOCIATION ; PERFORMANCE ; NEOPLASIA ; PROGRESSION ; immunohistochemistry ; METASTASIS ; SUPERFAMILY ; MULTIVARIATE ; CARCINOMAS ; NORMAL TISSUE ; gene amplification ; OVEREXPRESSION ; PROGNOSTIC FACTOR ; SERUM ; CELL CARCINOMA ; ELISA ; renal cell carcinoma ; ONCOLOGY ; REGRESSION ; THERAPIES ; MEDIATED APOPTOSIS ; PROGNOSTIC-FACTOR ; ADJUVANT THERAPY ; TUMOR TISSUE ; LEVEL ; analysis ; methods ; FAS LIGAND ; SERUM-LEVELS ; USA ; HIGH-GRADE ; PROGRESSION-FREE SURVIVAL ; PROBABILITY ; RENAL-CELL ; DCR3 ; lymph node metastasis ; PERFORMANCE STATUS
    Abstract: Background: Decoy receptor 3 (DcR3) is a soluble protein that binds to and inactivates the death ligand CD95L. Here, we studied a possible association between DcR3 expression and prognosis in patients with renal cell carcinomas (RCCs). Methods: A tissue microarray containing RCC tumor tissue samples and corresponding normal tissue samples was generated. Decoy receptor 3 expression in tumors of 560 patients was examined by immunohistochemistry. The effect of DcR3 expression on disease-specific survival and progression-free survival was assessed using univariate analysis and multivariate Cox regression analysis. Decoy receptor 3 serum levels were determined by ELISA. Findings: High DcR3 expression was associated with high-grade (P = .005) and high-stage (P = .048) RCCs. The incidence of distant metastasis (P = .03) and lymph node metastasis (P = .002) was significantly higher in the group with high DcR3 expression. Decoy receptor 3 expression correlated negatively with disease-specific survival (P 〈 .001) and progression-free survival (P 〈 .001) in univariate analyses. A multivariate Cox regression analysis retained DcR3 expression as an independent prognostic factor that outperformed the Karnofsky performance status. In patients with high-stage RCCs expressing DcR3, the 2-year survival probability was 25%, whereas in patients with DcR3-negative tumors, the survival probability was 65% (P 〈 .001). Moreover, DcR3 serum levels were significantly higher in patients with high-stage localized disease (P = .007) and metastatic disease ( P = .001). Interpretation: DcR3 expression is an independent prognostic factor of RCC progression and mortality. Therefore, the assessment of DcR3 expression levels offers valuable prognostic information that could be used to select patients for adjuvant therapy studies
    Type of Publication: Journal article published
    PubMed ID: 18813347
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  • 10
    Keywords: CANCER ; tumor ; carcinoma ; CELL ; Germany ; MODEL ; PERFUSION ; imaging ; DIFFERENTIATION ; TUMORS ; SURGERY ; PATIENT ; IMPACT ; CONTRAST ; MRI ; SEQUENCE ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; NUMBER ; tomography ; CARCINOMAS ; CONTRAST-ENHANCED MRI ; CELL CARCINOMA ; renal cell carcinoma ; ONCOLOGY ; dynamic contrast enhanced MRI ; SUBTYPES ; dCE MRI ; PHARMACOKINETIC PARAMETERS ; NEPHRON-SPARING SURGERY ; FUNCTIONAL ASSESSMENT ; grading ; AREA ; CELL CARCINOMAS
    Abstract: In this study, we investigated whether assessment of the tumor perfusion by dynamic contrast-enhanced magnetic resonance imaging (DCE MRI) enables to estimate the morphologic grading of renal cell carcinomas. A total of 21 patients with suspected renal cell cancer were examined using a Gadobutrol-enhanced, dynamic saturation-recovery, turbo-fast, low-angle shot sequence. Tumor perfusion and the tissue-blood ratio within the entire tumor and the most highly vascularized part of the tumor were calculated according to the model of Miles. Immediately after examination, patients underwent surgery, and the results from imaging were compared with the morphological analysis of the histologic grading. Fourteen patients had G2 tumors, and seven patients had G3 tumors. Significantly higher perfusion values (p 〈 0.05) were obtained in G3 tumors than in G2 tumors when the entire tumor area was considered (1.59 +/- 0.44 (ml/g/min) vs. 1.08 +/- 0.38 (ml/g/min)) or its most highly vascularized part (2.14 + 0.89 (ml/g/min) vs. 1.40 + 0.49 (ml/g/min)). By contrast, the tissue-blood ratios did not differ significantly between the two groups. In conclusion, unlike tissue-blood ratio, surrogate parameters of the tumor perfusion determined by DCE MRI seem to allow an estimation of the grading of renal cell carcinoma. However, further studies with high case numbers and including patients with G1 tumors are required to evaluate the full potential and clinical impact. (C) 2009 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19540690
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