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  • tumor  (11)
  • 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: 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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  • 6
    Keywords: CANCER ; tumor ; carcinoma ; Germany ; CT ; imaging ; ACCURACY ; computed tomography ; PATIENT ; prognosis ; MR ; MRI ; SEQUENCE ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; US ; tomography ; CARCINOMAS ; COMPUTED-TOMOGRAPHY ; sensitivity ; volume rendering ; ANGIOGRAPHY ; GD-DTPA ; nuclear medicine ; RECONSTRUCTION ; MR imaging ; staging ; renal cell carcinoma ; EXTENSION ; SURGICAL-TREATMENT ; PROTOCOL ; 3D ; CELL-CARCINOMA ; RENAL-CELL-CARCINOMA ; surgical planning ; caval thrombus ; COMPUTERIZED-TOMOGRAPHY ; multidetector CT ; TSE ; TUMOR THROMBUS ; VEIN ; VENACAVOGRAPHY
    Abstract: Objective: To evaluate the accuracy of multidetector computed tomography (CT) and magnetic resonance imaging (MRI) in staging and estimating renal carcinomas with caval thrombus. Methods: Initially, 23 patients with suspected caval thrombi were admitted into this prospective study. Triphasic CT imaging was performed using a multidetector CT with a reconstructed slice thickness of 2 mm. 3D CT reconstructions were used to improve surgical planning. MRI protocol included: a transversal T1-weighted GE sequence with and without Gd-DTPA, a transversal T2-weighted respiratory-gated TSE, and a coronal T1-weighted GE sequence with Gd-DTPA and fat saturation. In addition, a multiphase 3D angiography was performed after Gd-DTPA injection. Patients were divided into 3 groups: caval thrombus below the insertion of the hepatic veins, within the intrahepatic vena cava, and intra-atrial extension. The results the tumor thrombus extension and staging results of 2 independent readers were correlated with surgical and histopathological staging. Results: Of the 23 patients admitted, CT and MR scans of 14/13 patients respectively were correlated with histopathological workup. CT thrombus detection sensitivity and specificity for both readers was 0.93 and 0.8 respectively. MRI sensitivity and specificity for both readers was 1.0/0.85 and 0.75. Readers I and II evaluated the uppermost extension of the cranial tumor thrombus by both CT and MRI. CT and MR accuracy was 78% and 72%, 88% and 76% respectively. Conclusion: In cases of a suspected tumor thrombus, MRI and multidetector CT imaging showed similar staging results. Consequently, these staging modalities can be used to assess the extension of the tumor thrombus
    Type of Publication: Journal article published
    PubMed ID: 15665685
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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: RECEPTOR ; CELLS ; EXPRESSION ; tumor ; carcinoma ; Germany ; LUNG-CANCER ; POPULATION ; TUMORS ; ACTIVATION ; STAGE ; DESIGN ; NUMBER ; NK cells ; PROGNOSTIC-SIGNIFICANCE ; T-LYMPHOCYTES ; RECEPTORS ; GENE-EXPRESSION ANALYSIS ; EFFECTOR ; CYTOTOXICITY ; renal cell carcinoma ; INFILTRATION ; RE ; COLORECTAL-CARCINOMA ; function ; NATURAL-KILLER ; ZETA-CHAIN
    Abstract: Purpose: Renal cell carcinoma harbors high numbers of infiltrating lymphocytes with apparent limited efficacy in tumor control. This study focused on the natural killer (NK) cells infiltrating renal cell carcinoma. Experimental Design: Tumor-infiltrating lymphocytes (TIL) were isolated from renal cell carcinoma and analyzed for NK cell frequency and phenotype (n = 34). NK cells were enriched and tested for effector function. Results: Two renal cell carcinoma subtypes were identified, one containing high (〉20% of the lymphocyte population, n = 14), the other low (〈20%, n = 20), NK cell numbers. NK cells of both groups were noncytolytic ex vivo but differed in CD16 and cytotoxic effector molecule expression as well as in their capacity to acquire cytotoxic activity: The majority of NK cells from tumors with high NK cell content (high NK-TIL) were CD16(bright), whereas few CD16(bright) NK cells were found in tumors with low NK cell frequencies (low NK-TIL). The CD16 dichotomy correlated with different capacities to develop cytotoxicity after short-term activation with interleukin-2 ex vivo: Low NK-TIL remained noncytolytic against K562 and unresponsive to signals via the activating receptor NKp46 despite expression of receptor and adaptor molecules. In contrast, high NK-TIL acquired cytotoxic function. As described for peripheral CD16(bright), NK cells, NK cells from high-NK tumors showed high per cell expression of granzyme A, granzyme B, and perforin. NK cells from low NK-TIL resembled CD16(neg/dim) peripheral NK cells with few cytotoxin(+) cells and lower expression of perforin. Conclusion: The extent of NK cell infiltration and the expression of markers (CD16 and cytotoxins) predict the functional capacity of NK cells infiltrating renal cell carcinoma and can be used to characterize subgroups of renal cell carcinoma
    Type of Publication: Journal article published
    PubMed ID: 16467081
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  • 9
    Keywords: APOPTOSIS ; CANCER ; CELLS ; GROWTH ; radiotherapy ; tumor ; AGENTS ; carcinoma ; Germany ; human ; THERAPY ; DISEASE ; EXPOSURE ; TUMORS ; LINES ; TIME ; PATIENT ; BREAST ; resistance ; PROSTATE-CANCER ; CELL-LINE ; chemotherapy ; LINE ; BLADDER-CANCER ; BENIGN ; CISPLATIN ; CANCER-THERAPY ; paclitaxel ; LEUKEMIA-CELLS ; renal cell carcinoma ; GEMCITABINE ; RE ; cancer therapy ; dexamethasone ; GLUCOCORTICOID-INDUCED APOPTOSIS ; NAUSEA ; corticosteroids ; GLUCOCORTICOIDS ; LOSSES ; GAMMA-IRRADIATION ; CANCERS ; 5-FU ; bladder carcinoma ; testicular carcinoma
    Abstract: Purpose: Glucocorticoids such as dexamethasone are widely used for medication of urological diseases, e.g., as cotreatment of advanced prostate cancer, to improve appetite, weight loss, fatigue, relieve bone pain, diminish ureteric obstruction, to reduce the production of adrenal androgens, as an antiemetic in patients undergoing chemo- and/or radiotherapy together with serving as "standard" therapy arm in randomized studies. While the potent pro-apoptotic properties and the supportive effects of glucocorticoids to tumor therapy in lymphoid cells are well studied, the impact to growth of prostate and other urological carcinomas is unknown. Methods: We isolated cells from surgical resections of 21 prostate tumors and measured apoptosis and viability in these primary cells and 17 established cell lines from human prostate, bladder, renal cell and testicular carcinomas. Results: We found that dexamethasone induces resistance regarding exposure to several cytotoxic agents such as taxol, gemcitabine, cisplatin, 5-FU and gamma-irradiation in 86% of the freshly isolated prostate tumors and in 100% of the established urological cell lines. No difference in dexamethasone-mediated protection was found in normal, benign and malignant prostate tumors. Conclusions: These data show for the first time that dexamethasone induced therapy resistance in urological carcinomas is not the exception but a more common phenomenon and implicate that glucocorticoids may have two faces in cancer therapy, a beneficial and a dangerous one
    Type of Publication: Journal article published
    PubMed ID: 16294015
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  • 10
    Keywords: APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; IRRADIATION ; tumor ; TUMOR-CELLS ; AGENTS ; carcinoma ; CELL ; Germany ; INHIBITION ; LUNG-CANCER ; GENE ; GENE-EXPRESSION ; PROTEIN ; RNA ; SAMPLES ; DRUG ; cell line ; TISSUE ; LINES ; BIOLOGY ; CELL-LINES ; gene expression ; resistance ; CELL-LINE ; LINE ; CANCER-CELLS ; PROGNOSTIC-SIGNIFICANCE ; cell lines ; TUMOR CELLS ; ETOPOSIDE ; AGENT ; DEFICIENCY ; RE ; INTERFERENCE ; RNA INTERFERENCE ; INCREASE ; TUMOR TISSUE ; SURVIVIN ; TUMOR-CELL ; CHEMOTHERAPEUTIC DRUGS ; DRUGS ; CANCERS ; SPECIMENS ; apoptosis regulation ; IAP ; inhibitor of apoptosis proteins ; livin/ML-IAP ; MELANOMAS ; renal cell cancer
    Abstract: Cancer cells are typically characterized by apoptosis deficiency. In order to investigate a possible role for the anti-apoptotic livin gene in renal cell cancer (RCC), we analyzed its expression in tumor tissue samples and in RCC-derived cell lines. In addition, we studied the contribution of livin to the apoptotic resistance of RCC cells by RNA interference (RNAi). Livin gene expression was detected in a significant portion of RCC tumor tissue specimens (13/14, 92.9%) and tumor-derived cell lines (12/15, 80.0%). Moreover, targeted inhibition of livin by RNAi markedly sensitized RCC cells towards proapoptotic stimuli, such as UV irradiation or the chemotherapeutic drugs etoposide, 5-fluorouracil, and vinblastine. These effects were specific for livin expressing tumor cells. We conclude that livin can contribute significantly to the apoptosis resistance of RCC cells. Targeted inhibition of livin could represent a novel therapeutic strategy to increase the sensitivity of renal cancers towards pro-apoptotic agents
    Type of Publication: Journal article published
    PubMed ID: 17437058
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