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  • DKFZ Publication Database  (7)
  • CANCER  (7)
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  • DKFZ Publication Database  (7)
  • 1
    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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  • 2
    Keywords: ENVIRONMENT ; CANCER ; GROWTH ; IN-VITRO ; tumor ; carcinoma ; IN-VIVO ; MODEL ; tumor growth ; SURGERY ; AIR ; animals ; BODY-WEIGHT ; METASTASIS ; IMPLANTATION ; PRESSURE ; CARBON-DIOXIDE ; helium ; INSUFFLATION ; laparoscopy ; RANDOMIZED TRIAL ; experimental studies ; experimental study ; hepatectomy ; insufflation gas
    Abstract: Background: After exposure of neoplastic tissue to helium, a significant reduction of tumor growth has been detected in experimental studies, both in vitro and in vivo. This tumor- suppressive effect of helium is controversly discussed in the literature. It was therefore the aim of this study to investigate the influence of pneumoperitoneum with CO2, room air, or helium in a tumor-bearing small animal model comparing laparoscopic partial hepatic resection for hepatocellular carcinoma with conventional open partial hepatectomy. Methods: One-hundred forty-eight male American Cancer Institute rats underwent partial hepatectomy for curative resection of previously induced hepatocellular carcinoma (Morris hepatoma 3924A). Resection was performed either in open laparotomy (n = 30) or laparoscopically under the employment of CO2 (n = 30), room air (n = 30), or helium (n = 30) for the pneumoperitoneum. Twenty-eight animals served as controls receiving anesthesia but no tumor resection. All animals were sacrificed on postoperative days 21, 35, or 56 for autopsy and evaluation of possible tumor recurrence and metastasis. Results: Significant reduction of postoperative tumor recurrence and metastasis was observed in the group of animals receiving laparoscopic tumor resection under helium insufflation compared to open surgery or laparoscopic resection with air pneumoperitoneum. Conclusions: The results of this study suggest a suppressive effect of helium pneumoperitoneum on postoperative tumor growth and metastatic spread. Furthermore, tumor exposure to room air appears to have a stimulative influence on tumor recurrence and metastasis compared to a pneumoperitoneum established with CO2
    Type of Publication: Journal article published
    PubMed ID: 12632132
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  • 3
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; radiotherapy ; SURVIVAL ; tumor ; TUMOR-CELLS ; AGENTS ; BLOOD ; CELL ; Germany ; THERAPY ; SAMPLE ; SAMPLES ; transcription ; PATIENT ; treatment ; bone marrow ; BONE-MARROW ; STAGE ; resistance ; colorectal cancer ; COLORECTAL-CANCER ; EFFICACY ; RATES ; chemotherapy ; CANCER-CELLS ; CANCER-PATIENTS ; CARCINOMAS ; CYTOKERATIN-20 ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; BINARY ; ELIMINATION ; neoadjuvant treatment
    Abstract: Objective: To compare the detection rates for rectal cancer cells in blood and bone marrow in patients with or without preoperative chemoradiation.Summary Background Data: Previous reports have postulated a resistance of disseminated tumor cells to antiproliferative agents because of tumor cell dormancy.Methods: Blood samples from 142 patients (pre, intra-, and postoperative samples) and bone marrow samples from 127 patients undergoing resection of rectal adenocarcinoma were analyzed for tumor cells using a cytokeratin (CK) 20-reverse transcription polymerase chain reaction. The results were stratified according to preoperative therapy.Results: In patients without preoperative chemoradiation, tumor cell detection in blood and bone marrow correlated to tumor stage (Cochran Armitage trend test, P 〈 0.05). Tumor cells were detected in 34 of 103 (33%) bone marrow and 65 of 117 (55.6%) blood samples of patients without neoadjuvant treatment versus in 4 of 24 (16.7%) bone marrow and in 10 of 25 (40%) blood samples of patients with neoadjuvant treatment. The tumor cell detection rate was significantly lower in the group having undergone chemoradiation (binary logistic regression analysis, P 〈 0.05). The overall and disease-free survival were significantly worse in patients with tumor cell detection in the bone marrow after neoadjuvant therapy.Conclusions: Preoperative chemoradiation is associated with a decreased detection rate of rectal cancer cells in blood and bone marrow. These findings may explain the observed clinical benefit of patients with rectal cancer receiving chemoradiation. This is the first study suggesting that detection of disseminated rectal cancer cells may be useful for assessing the efficacy of neoadjuvant therapy
    Type of Publication: Journal article published
    PubMed ID: 14501498
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  • 4
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; IONIZING-RADIATION ; radiotherapy ; COMBINATION ; Germany ; PATHWAY ; PATHWAYS ; PROTEIN ; MOLECULES ; SURGERY ; PATIENT ; ACTIVATION ; primary ; SEQUENCE ; MOLECULE ; CLEAVAGE ; FORM ; immunohistochemistry ; PATTERNS ; CELL-DEATH ; Western-blot ; colorectal cancer ; RATES ; RECURRENCE ; RT-PCR ; adenocarcinoma ; ADENOCARCINOMAS ; beta-catenin ; western blot ; GREECE ; C-MYC ; PATTERN ; ENHANCED EXPRESSION ; FOCAL CEREBRAL-ISCHEMIA ; mesorectal excision ; MYC-INDUCED APOPTOSIS ; neoadjuvant radiotherapy ; PREOPERATIVE RADIOTHERAPY ; RADIATION-INDUCED APOPTOSIS
    Abstract: Recent surgical concepts for primary rectal cancer include the combination of surgery and short-term neoadjuvant radiotherapy (STNR). This is usually given in a dose of 25 Gy over five days in order to reduce local recurrence rates. Clinical studies have shown that local recurrence is found in some patients despite STNR. We identified molecular patterns of the Wnt- and apoptosis pathways as well as expression of junction-associated molecules in rectal cancer specimens of patients who received STNR and in those who did not. Expression patterns were examined by immunohistochemistry and molecular techniques such as LightCycler RT-PCR and Western blot analysis in 25 sporadic rectal adenocacrinoma specimens derived from STNR-patients or non-pretreated donors, respectively. The molecular pattern in response to STNR was heterogeneous and was reflected by responders who show activation of apoptosis and cellular remodeling, whereas the group of non-responders from STNR did not show such reaction and was very similar to untreated controls. Enhanced expression of beta-catenin was generally mediated by STNR, but exclusively in the responder group impaired expression of c-Myc and junction-associated molecules as well as cleavage of poly-ADP-ribose polymerase and of the caspase substrate cytokeratin 19 were found. The molecular profile suggests that STNR interferes with Writ-signaling and c-Myc expression. STNR in its present form is not suitable to fully complete the sequence of apoptosis in all rectal adenocarcinomas
    Type of Publication: Journal article published
    PubMed ID: 15547689
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  • 5
    Keywords: CANCER ; CELLS ; EXPRESSION ; INVASION ; tumor ; TUMOR-CELLS ; CELL ; Germany ; human ; IN-VIVO ; VIVO ; SITE ; SITES ; PROTEIN ; cell line ; MOLECULES ; TUMORS ; PATIENT ; CONTRAST ; PHOSPHORYLATION ; treatment ; MOLECULE ; MOUSE ; NO ; STAGE ; TUMOR PROGRESSION ; METASTASIS ; REQUIRES ; NUDE-MICE ; CELL-LINE ; LINE ; MELANOMA ; EXTRACELLULAR-MATRIX ; ADHESION ; MAMMALIAN-CELLS ; MIGRATION ; INTEGRIN ALPHA(V)BETA(3) ; MALIGNANT-MELANOMA ; malignant melanoma ; DIFFERENTIAL EXPRESSION ; TUMOR CELLS ; MATRIX ; ONCOLOGY ; CAPACITY ; INCREASE ; extracellular matrix ; MELANOMA-CELLS ; analysis ; TUMOR-CELL ; USA ; function ; MEDIATED ADHESION ; correlation ; in vivo ; correlates ; 3-DIMENSIONAL COLLAGEN LATTICES ; L-plastin ; MATRIX METALLOPROTEINASE-2 MMP-2
    Abstract: The leukocyte specific actin-binding protein L-plastin is aberrantly expressed in several nonhematopoetic malignant tumors. However, little is known about the functional consequences of L-plastin expression. Here, we investigated the function of L-plastin in human malignant melanoma cells. Knock-down of endogenous L-plastin by siRNA treatment reduced migration of the melanoma cell line IF6. However, in melanoma patients, no correlation existed between L-plastin expression and tumor stages. This implied that additional factors such as phosphorylation of L-plastin may influence its function in tumor cells. To investigate this further, EGFP-tagged wild-type L-plastin (wt-LPL-EGFP) and a mutated, nonphosphorylatable L-plastin protein (5A7A-LPL-EGFP), were expressed in the L-plastin negative melanoma cell line MV3. Biochemical analysis revealed that wt-LPL-EGFP is phosphorylated in MV3 cells while 5A7A-LPL-EGFP is not. Although both wt-LPL-EGFP and 5A7A-LPL-EGFP were targeted to, and promote the formation of, vinculin-containing adhesion sites, static adhesion to either Matrigel or isolated extracellular matrix molecules was neither influenced by expression of wt-LPL-EGFP nor by expression of 5A7A-LPL-EGFP when compared with EGFP expressing control cells. In contrast, haptotactic, but not chemotactic, migration of melanoma cells towards either Matrigel or isolated extracellular matrix molecules was similarly enhanced, if either 5A7A-LPL-EGFP or wt-LPL-EGFP were expressed in MV3 cells. Interestingly, only cells expressing the phosphorylatable wt-LPL-EGFP protein showed enhanced invasion into Matrigel. In line with these findings the in vivo metastatic capacity of mouse B16 melanoma cells correlates with expression and phosphorylation of L-plastin. These data show that an increase in melanoma cell invasiveness requires not only expression but also phosphorylation of L-plastin. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17290393
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  • 6
    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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  • 7
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; IN-VITRO ; SURVIVAL ; tumor ; carcinoma ; CELL ; Germany ; THERAPY ; DEATH ; microarray ; SAMPLES ; MONOCLONAL-ANTIBODY ; SURGERY ; PATIENT ; NF-KAPPA-B ; LIGAND ; prognosis ; ASSOCIATION ; immunohistochemistry ; METASTASIS ; PROGNOSTIC-FACTORS ; CARCINOMA-CELLS ; TRAIL ; DEATH RECEPTORS ; CYTOTOXICITY ; APOPTOSIS-INDUCING LIGAND ; THERAPIES ; MEDIATED APOPTOSIS ; ENHANCEMENT ; development ; therapeutic ; DEATH LIGAND
    Abstract: Purpose: The death ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its receptors (TRAIL-R) are involved in immune surveillance and tumor development. Here, we studied a possible association between the expression of TRAIL/TRAIL-Rs and the prognosis in patients with renal cell carcinomas (RCC). Experimental Design: A tissue microarray containing RCC tumor tissue samples and corresponding normal tissue samples from 838 patients was generated. Expression of TRAIL and TRAIL-Rs was examined by immunohistochemistry and the effect of TRAIL and TRAIL-R expression on disease-specific survival was assessed. Results: High TRAIL-R2 expression levels were associated with high-grade RCCs (P 〈 0.001) and correlated negatively with disease-specific survival (P = 0.01). Similarly, high TRAIL expression was associated with a shorter disease-specific survival (P = 0.01). In contrast, low TRAIL-R4 expression was associated with high-stage RCCs (P 〈 0.001) as well as with the incidence of distant metastasis (P = 0.03) and correlated negatively with disease-specific survival (P = 0.02). In patients without distant metastasis, multivariate Cox regression analyses revealed that TRAIL-R2 and TRAIL are independent prognostic factors for cancer-specific survival (in addition to tumor extent, regional lymph node metastasis, grade of malignancy, and type of surgery). Conclusion: High TRAIL-R2, high TRAIL, and low TRAIL-R4 expression levels are associated with a worse disease-specific survival in patients with RCCs. Therefore, the assessment of TRAIL/TRAIL-R expression offers valuable prognostic information that could be used to select patients for adjuvant therapy studies. Moreover, our findings are of relevance for a potential experimental therapeutic administration of TRAIL-R agonists in patients with RCCs
    Type of Publication: Journal article published
    PubMed ID: 19147771
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