Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • TUMORS  (7)
  • 1
    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 ...
  • 2
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: EXPRESSION ; SURVIVAL ; TUMORS ; DNA ; INFECTION ; SKIN ; virus ; PREVALENCE ; FEATURES ; MCV ; ABUNDANCE
    Abstract: The majority of Merkel cell carcinomas (MCCs) are associated with the recently identified Merkel cell polyomavirus (MCV). However, as it is still unclear to which extent the presence of MCV impacts tumor characteristics or clinical outcome, we correlated the MCV status of tumor lesions obtained from 174 MCC patients including 38 MCC patients from Australia and 138 MCC patients from Germany with clinical characteristics, histomorphology, immunohistochemistry, and course of the disease. MCV DNA was present in 86% of MCCs and, in contrast to previous reports, no significant difference in MCV prevalence was present between Australian and German MCC cases. When patients were stratified according to their MCV status, only tumor localization (P = 0.001), gender (P = 0.024), and co-morbidity, i.e., frequency of patients with previous skin tumors (P = 0.024), were significantly different factors. In contrast, year of birth and diagnosis, age at diagnosis, or histological type and features representing the oncogenic phenotype such as mitotic rate or expression of p16, p53, RB1, and Ki67 were not significantly different between MCV-positive and MCV-negative MCCs. MCV status also did not influence recurrence-free, overall, and MCC-specific survival significantly. In summary, although MCV-positive and MCV-negative MCCs may have different etiologies, these tumors have comparable clinical behaviors and prognosis
    Type of Publication: Journal article published
    PubMed ID: 21562568
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...