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  • DKFZ Publication Database  (26)
  • CELL  (22)
  • immunohistochemistry  (13)
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  • DKFZ Publication Database  (26)
Keywords
  • 1
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; tumor ; CELL ; Germany ; human ; COHORT ; PROTEIN ; PROTEINS ; cell line ; TISSUE ; TUMORS ; LINES ; PATIENT ; FAMILY ; CARCINOGENESIS ; TISSUES ; CELL-LINES ; LESIONS ; PROGRESSION ; immunohistochemistry ; CELL-LINE ; LINE ; LOCALIZATION ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; ADENOCARCINOMAS ; pathology ; OVEREXPRESSION ; cell lines ; pancreatic cancer ; protein expression ; chemoresistance ; SUBCELLULAR-LOCALIZATION ; SUBSET ; pancreas ; PANCREATIC-CANCER ; FAMILIES ; DUCTAL ADENOCARCINOMA ; polymerase chain reaction ; TUMOR TISSUE ; LEVEL ; analysis ; methods ; pancreatic ; RARE ; SURVIVAL-DATA ; Reverse Transcriptase Polymerase Chain Reaction
    Abstract: AIMS: To determine the role of two antiapoptotic proteins of the IAP family, cIAP1 and cIAP2, in human pancreatic carcinogenesis. METHODS: mRNA levels were measured in pancreatic tissues and pancreatic cancer cell lines by quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR). Protein expression was assessed in pancreatic cancer cell lines by immunoblotting and in pancreatic tissues by immunohistochemistry and correlated with pathological and survival data. RESULTS: cIAP1 expression was constantly high in non-neoplastic pancreatic tissues, in PanIN lesions, as well as in a subset of primary and metastatic pancreatic ductal adenocarcinomas (PDAC), and a preferential cytoplasmatic localization was observed in the tumor tissues. cIAP1 expression was rare in a cohort of cystic tumors. cIAP2 mRNA levels were significantly higher (2.4 fold) in PDAC than in the normal tissues. cIAP2 protein was overexpressed in PDAC and was detectable in low-grade and high-grade PanIN lesions. Moreover, cIAP2 was frequently expressed in pancreatic cystic tumors. cIAP1 and cIAP2 mRNA and protein were detected in all the examined cell lines. Survival analysis revealed a shorter survival in patients with cIAP1/cIAP2-positive tumors. CONCLUSIONS: cIAP1 might contribute to the regulation of the apoptotic process in the normal and in the neoplastic pancreas, depending on its subcellular localization. cIAP2 overexpression is a frequent and early event in pancreatic cancer progression and could therefore potentially influence important pathophysiological aspects of PDAC, such as anoikis or chemoresistance
    Type of Publication: Journal article published
    PubMed ID: 16775116
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  • 2
    Keywords: RECEPTOR ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; CELL ; Germany ; TISSUE ; LINES ; TIME ; FAMILY ; INDUCTION ; TISSUES ; CONTRAST ; CELL-LINES ; DOWN-REGULATION ; MEMBER ; MEMBERS ; PHOSPHORYLATION ; BREAST-CANCER ; antibodies ; antibody ; immunohistochemistry ; ASSAY ; CARCINOMA CELLS ; CELL-LINE ; LINE ; CANCER-CELLS ; BETA ; RT-PCR ; adenocarcinoma ; p21 ; CELL-SURFACE ; RECEPTORS ; DIFFERENTIAL EXPRESSION ; cell lines ; pancreatic cancer ; CELL-GROWTH ; signaling ; PANCREATIC-CANCER ; FAMILIES ; DUCTAL ADENOCARCINOMA ; independent growth ; ENHANCED EXPRESSION ; TGF-beta 1 ; HEPARAN-SULFATE PROTEOGLYCANS ; LEVEL ; pancreatic ; ASSAYS ; SULFATE ; downregulation ; lymph node ; LYMPH-NODE ; correlation ; VIEW ; DECREASED SURVIVAL ; activin ; bone morphogenic protein ; CONTROLS CELLULAR-RESPONSES ; glypican ; heparan sulfate proteoglycans ; SMAD PROTEINS
    Abstract: Glypican 1 (GPC1) is a cell surface heparan sulfate proteoglycan that acts as a co-receptor for heparin-binding growth factors as well as for members of the TGF-beta family. GPC1 plays a role in pancreatic cancer by regulating growth factor responsiveness. In view of the importance of members of the TGF-beta family in pancreatic cancer, in the present study, the role of GPC1 in TGF-beta, BMP and activin signaling was analyzed. Quantitative RT-PCR and immunohistochemistry were utilized to analyze GPC1 and TGF-beta, BMP and activin receptor expression levels. Panc-1 and T3M4 pancreatic cancer cells were transfected in a stable manner with a GPC1 antisense expression construct. Anchorage-dependent and -independent growth was determined by MTT and soft agar assays. TGF-beta 1, activin-A and BMP-2 responsiveness was determined by MTT assays and immunoblotting with p21, p-Smad1, and p-Smad2 antibodies. QRT-PCR demonstrated increased GPC1 mRNA levels in pancreatic ductal adenocarcinoma (PDAC) compared to normal pancreatic tissues (NPT), as described previously. There was a significant correlation between GPC1 mRNA levels and T beta RII, act-R1a, act-R1b, act-R2a, BMP-R1a, and BMP-R2 mRNA expression in NPT. In contrast, GPC1 mRNA expression correlated directly with act-R1a and BMP-R1a in NO PDAC cases and with act-R2a and BMP-R1a in lymph node positive cases. Down-regulation of GPC1 resulted in increased doubling time in Panc-1 but not in T3M4 cells, and decreased anchorage-independent growth in both cell lines. GPC1 down-regulation resulted in a slightly altered response towards TGF-beta 1, activin-A and BMP-2 in terms of growth, p21 induction and Smad2 phosphorylation. In conclusion, enhanced GPC1 expression correlates with BMP and activin receptors in pancreatic cancer. GPC1 down-regulation suppresses pancreatic cancer cell growth and slightly modifies signaling of members of the TGF-beta family of growth factors
    Type of Publication: Journal article published
    PubMed ID: 17016645
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  • 3
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; carcinoma ; CELL ; Germany ; INHIBITION ; THERAPY ; HEPATOCELLULAR-CARCINOMA ; PROTEIN ; TISSUE ; LINES ; MICE ; PATIENT ; IMPACT ; INDUCTION ; CELL-LINES ; treatment ; hepatocellular carcinoma ; resistance ; AGE ; metastases ; NUDE-MICE ; CELL-LINE ; chemotherapy ; leukemia ; LINE ; MODULATION ; p53 ; CANCER-PATIENTS ; CARCINOMAS ; CISPLATIN ; CANCER PATIENTS ; cell lines ; CANCER-THERAPY ; protein expression ; P53 STATUS ; GEMCITABINE ; RE ; cancer therapy ; GENDER ; dexamethasone ; GLUCOCORTICOID-INDUCED APOPTOSIS ; NAUSEA ; HISTOLOGY ; corticosteroids ; GLUCOCORTICOIDS ; correlation ; GAMMA-IRRADIATION ; viability ; 5-FU ; xenograft
    Abstract: The glucocorticoid dexamethasone is frequently used as co-treatment in cytotoxic cancer therapy, e.g. to prevent nausea, to protect normal tissue or for other reasons. While the potent pro-apoptotic properties and the supportive effects of glucocorticoids to tumour therapy in lymphoid cells are well studied, the impact to cytotoxic treatment of colorectal and hepatocellular carcinoma is unknown. We tested apoptosis-induction, viability, tumour growth and protein expression using 8 established cell lines, 18 surgical specimen and a xenograft on nude mice. In the presence of dexamethasone we found strong inhibition of apoptosis in response to 5-FU, cisplatin, gemcitabine or gamma-irradiation, enhanced viability and tumour growth of colorectal and hepatocellular carcinomas. No correlation with age, gender, histology, TNM, the p53 status and induction of therapy resistance by dexamethasone cotreatment could be detected. These data show that glucocorticoid-induced resistance occurs not occasionally but is common in colorectal and hepatocellular carcinomas implicating that the use of glucocorticoids may be harmful for cancer patients. (c) 2005 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16338063
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  • 4
    Keywords: APOPTOSIS ; CELLS ; SURVIVAL ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; MODEL ; PATHWAY ; TISSUE ; TUMORS ; NF-KAPPA-B ; TUMOR-NECROSIS-FACTOR ; INDUCTION ; TISSUES ; treatment ; resistance ; chemotherapy ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; EXTRACELLULAR-MATRIX ; EPITHELIAL-CELLS ; MAMMARY EPITHELIAL-CELLS ; RADIATION-INDUCED APOPTOSIS ; GLYCOGEN-SYNTHASE KINASE-3 ; corticosteroids ; GLUCOCORTICOIDS ; DEXAMETHASONE-INDUCED APOPTOSIS ; OVARIAN FOLLICULAR CELLS ; PACLITAXEL-INDUCED APOPTOSIS ; PHOSPHATIDYLINOSITOL 3-KINASE/AKT PATHWAY
    Abstract: More than a quarter of a century ago, the phenomenon of glucocorticoid-induced apoptosis in the majority of hematological cells was first recognized. More recently, glucocorticoid-induced antiapoptotic signaling associated with apoptosis resistance has been identified in cells of epithelial origin, most of malignant solid tumors and some other tissues. Despite these huge amount of data demonstrating differential pro- and anti-apoptotic effects of glucocortioids, the underlying mechanisms of cell type specific glucocorticoid signaling are just beginning to be described. This review summarizes our present understanding of cell type-specific pro- and anti-apoptotic signaling induced by glucocorticoids. In the first section we give a summary and update of known glucocorticoid-induced pathways mediating apoptosis in hematological cells. We shortly introduce mechanisms of glucocorticoid resistance of hematological cells. We highlight and discuss the emerging molecular evidence of a general induction of survival signaling in epithelial cells and carcinoma cells by glucocorticoids. We provide a model for glucocorticoid-induced resistance in cells growing in a tissue formation. Thus, attachment to the extracellular matrix and cell-cell contacts typical for e.g. epithelial and tumor cells may be crucially involved in switching the balance of several interacting pathways to survival upon treatment with glucocorticoids
    Type of Publication: Journal article published
    PubMed ID: 17191112
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  • 5
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; neoplasms ; DIAGNOSIS ; NEW-YORK ; microarray ; transcription ; TISSUE ; DNA ; MICROARRAY DATA ; MUTATIONS ; Jun ; PHENOTYPE ; vimentin ; HEAD ; adenocarcinoma ; pathology ; BEHAVIOR ; MICROARRAY ANALYSIS ; expression profiling ; TUMOR CELLS ; DIFFERENTIAL-DIAGNOSIS ; CELL CARCINOMA ; OF-THE-LITERATURE ; pancreas ; review ; DUCTAL ADENOCARCINOMA ; AUTOPSY ; analysis ; pancreatic ; TUMOR-CELL ; GENOTYPE ; DNA-MICROARRAY ; USA ; pancreatic ductal adenocarcinoma ; MYOEPITHELIAL CARCINOMA ; pancreatic neoplasm ; PSEUDOPAPILLARY TUMORS
    Abstract: Pancreatic neoplasms have been reliably classified on the basis of their histopathology and immunophenotype. In this study, we report on a pancreatic tumor whose phenotype and genotype could not be assigned to any known tumor entity. The tumor was observed in the pancreatic head of a 54-year-old woman. It was found to be a solid infiltrating carcinoma with abundant clear cells. Apart from cytokeratin, the tumor cells expressed vimentin, S100, and MUC-1. DNA microarray analysis revealed a transcription profile clearly differing from that of normal pancreatic tissue and pancreatic ductal adenocarcinoma. Despite metastatic behavior, the tumor displayed a more favorable course than conventional pancreatic ductal adenocarcinoma. We suggest that this tumor be called solid type clear cell carcinoma of the pancreas
    Type of Publication: Journal article published
    PubMed ID: 17453235
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  • 6
    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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  • 7
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; tumor ; CELL ; Germany ; human ; DISTINCT ; GENES ; HYBRIDIZATION ; PROTEIN ; SAMPLE ; SAMPLES ; transcription ; TISSUE ; TUMORS ; COMPLEX ; COMPLEXES ; primary ; renal ; colon ; RATS ; TISSUES ; CONTRAST ; DOWN-REGULATION ; BREAST ; BREAST-CANCER ; IDENTIFICATION ; IN-SITU ; immunohistochemistry ; MALIGNANCIES ; UP-REGULATION ; BRCA1 ; metastases ; CANCER-CELLS ; COLON-CANCER ; LOCALIZATION ; RT-PCR ; TRACT ; RECEPTORS ; pancreatic cancer ; chronic pancreatitis ; protein expression ; HUMAN TISSUES ; F ; in situ hybridization ; colon cancer ; TGF-BETA ; gastric cancer ; MAC30 ; PRIMARY TUMORS
    Abstract: Meningioma-associated protein, MAC30, is a protein with unknown function and cellular localization that is differentially expressed in certain malignancies. In the present study, the expression of MAC30 in a variety of normal and cancerous human gastrointestinal tissues, with special emphasis on pancreatic tissues was analyzed. Quantitative RT-PCR was utilized to compare MAC30 expression levels. In situ hybridization and immunohistochemistry were carried out to localize MAC30 mRNA and protein expression in normal and cancerous tissue samples of the esophagus, stomach, colon and pancreas. Furthermore, the effects of TGF-beta on the transcription of MAC30 mRNA were examined in pancreatic cancer cells. MAC30 mRNA was expressed in a wide variety of normal human tissues, being most abundant in testicular and gastric tissue samples. MAC30 mRNA levels were significantly increased in breast and colon cancer, but significantly decreased in pancreatic and renal cancer. TGF-beta down-regulated MAC30 mRNA levels in certain pancreatic cancer cells. MAC30 protein was localized in normal pancreatic tissues, mainly in acinar and islet cells, and in normal colon, gastric and esophageal tissues especially in the mucosal cells. MAC30 was strongly present in tubular complexes in pancreatic cancer tissues but weak to absent in pancreatic cancer cells of primary tumors and metastases. In contrast, esophageal, gastric and colon tumors displayed strong MAC30 immunoreactivity in the cancer cells. In conclusion, MAC30 is expressed in various normal and diseased human tissues. MAC30 up-regulation in certain tumors and down-regulation in others suggests that this protein plays a distinct role in human malignancies
    Type of Publication: Journal article published
    PubMed ID: 15375745
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  • 8
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; tumor ; carcinoma ; FACTOR RECEPTOR ; Germany ; GENES ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; MICE ; TIME ; PATIENT ; COMPLEX ; COMPLEXES ; DONOR ; DOMAIN ; TISSUES ; 5-FLUOROURACIL ; TRANSPORT ; IN-SITU ; LESIONS ; immunohistochemistry ; MALIGNANCIES ; ASSAY ; UP-REGULATION ; PROSTATE-CANCER ; NUDE-MICE ; chemotherapy ; CANCER-CELLS ; LOCALIZATION ; adenocarcinoma ; sensitivity ; CISPLATIN ; MICROARRAY ANALYSIS ; OVEREXPRESSION ; expression profiling ; microdissection ; pancreatic cancer ; REGULATOR ; chronic pancreatitis ; CELL-GROWTH ; in situ hybridization ; MALIGNANCY ; GEMCITABINE ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; INCREASE ; independent growth ; TRANSFECTION ; ENHANCED EXPRESSION ; LEVEL ; ASSAYS ; downregulation ; PROLIFERATIVE ACTIVITY ; CHLORIDE ; chloride channel ; COLO-357 CELLS ; DECREASED SURVIVAL ; NA+/K+-ATPASE ; TGF-BETA RESPONSIVENESS ; TGFP
    Abstract: The expression and localization of FXYD domain containing ion transport regulator 3 (FXYD3), a transmembrane protein that acts as a chloride channel or chloride channel regulator, was analyzed in pancreatic tissues derived from donors and patients suffering from chronic pancreatitis (CP) or pancreatic ductal adenocarcinoma (PDAC) as well as in pancreatic cancer cells using QRT-PCR, laser-capture microdissection and microarray analysis, in situ hybridization and immunohistochemistry. FXYD3 antisense expressing T3M4 pancreatic cancer cells were generated and compared to control cells using anchorage-dependent and independent growth assays, and xenotransplantation into nude mice. FXYD3 mRNA levels were 3.4-fold increased in PDAC tissues compared to donor specimens (p = 0.006), and 3.9-fold increased in microdissected cancer cells compared to normal pancreatic ductal cells (p = 0.02). FXYD3 was localized in the tubular complexes and PanIN lesions of both CP and PDAC, as well as in pancreatic cancer cells. Downregulation of FXYD3 by stable antisense transfection increased significantly the doubling time of T3M4 pancreatic cancer cells from 44 +/- 2 hr to 55 +/- 12 hr (p = 0.02). Nude mice transplanted with antisense transfected cells displayed a significant increase in tumor doubling time from 3.3 days +/- 1.0 to 4.3 days +/- 0.43 (p = 0.058). Anchorage-independent growth and sensitivity to 5-fluorouracil, gemcitabine and cisplatin as well as to MgCl2 were not dependent on the level of FXYD3 expression. In conclusion, overexpression of FXYD3 in pancreatic cancer may contribute to the proliferative activity of this malignancy. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16003754
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  • 9
    Keywords: CELLS ; tumor ; CELL ; Germany ; neoplasms ; imaging ; TOOL ; DISEASE ; DISEASES ; RESOLUTION ; SURGERY ; MECHANISM ; MARKER ; prognosis ; AUTOIMMUNE-DISEASE ; mechanisms ; T cell ; T cells ; T-CELL ; T-CELLS ; treatment ; MARKERS ; RESECTION ; LOCALIZATION ; HEAD ; ATROPHY ; FUTURE ; DIABETES-MELLITUS ; AUTOANTIBODIES ; autoimmune pancreatitis ; PRIMARY SCLEROSING CHOLANGITIS ; SJOGRENS-SYNDROME ; INFLAMMATORY-BOWEL-DISEASE ; FEATURES ; fibrosis ; INFILTRATION ; inflammatory bowel disease ; AUTOIMMUNE-DISEASES ; STENOSIS ; LEVEL ; pancreatic ; MASS ; autoimmune disease ; TOOLS ; DUCT ; serological ; Diabetes Mellitus ; surgical resection ; BOWEL ; EFFECTIVE STEROID-THERAPY ; ENTITY ; IgG4 ; pancreatic neoplasms ; pancreatic tumor ; PSEUDOTUMOROUS PANCREATITIS ; SERUM IGG4 ; steroids ; URSODEOXYCHOLIC ACID
    Abstract: The term autoimmune pancreatitis (AIP) describes a nonalcoholic, chronic lymphoplasmocytic pancreatitis. The lymphoplasmocytic infiltration is characterized by periductal localization of predominantly CD4-positive T cells, fibrosis, and acinar atrophy, frequently resulting in stenosis of the main pancreatic and distal common bile ducts. Imaging studies often reveal a diffuse narrowing of the pancreatic main duct and swelling of the pancreatic head wrongly suggesting the presence of a malignant tumor. Clinical signs include mild abdominal pain,jaundice, recurrent episodes of acute pancreatitis, and even new-onset diabetes mellitus. Additionally, AIP can be associated with other autoimmune diseases such as Sjogren's syndrome, primary sclerosing cholangitis, chronic inflammatory bowel diseases, and retroperitoneal fibrosis. Serological markers include autoantibodies and increased levels of gamma globulin and especially IgG4. Steroids seem to be effective in improving clinical symptoms as well as in the resolution of pancreatic and bile duct narrowing. This distinguishes AIP from other forms of pancreatitis and from pancreatic neoplasms. Further studies of the underlying pathophysiologic mechanisms, prognosis, and new diagnostic tools are needed to provide adequate and effective treatment in the future. In this article, we summarize the current knowledge about AIP and present 17 cases that underwent surgical resection at our institution from 2003 to 2004
    Type of Publication: Journal article published
    PubMed ID: 17007063
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  • 10
    Keywords: brain ; APOPTOSIS ; CANCER ; CELLS ; GROWTH ; carcinoma ; CELL ; Germany ; THERAPY ; screening ; TISSUE ; LINES ; PATIENT ; MECHANISM ; CONTRAST ; CELL-LINES ; treatment ; BREAST ; breast cancer ; BREAST-CANCER ; resistance ; INDUCED APOPTOSIS ; CERVIX ; metastases ; CELL-LINE ; chemotherapy ; LINE ; MELANOMA ; RESECTION ; CISPLATIN ; cell lines ; CANCER-THERAPY ; LUNG-CARCINOMA ; neuroblastoma ; signaling ; MALIGNANT-CELLS ; RE ; cancer therapy ; SOLID TUMORS ; dexamethasone ; NAUSEA ; corticosteroids ; GLUCOCORTICOIDS ; prospective ; BONE ; EXTENT ; clinical studies ; surgical resection ; steroids
    Abstract: Glucocorticoids (GCs) such as dexamethasone (DEX) have been widely used as co-medication in cancer therapy because they have potent proapoptotic properties in lymphoid cells, can reduce nausea, and alleviate acute toxic effects in healthy tissue. However, GCs are used in a supportive-care role, even though no prospective clinical studies have assessed the effect of these steroids on the growth of solid tumours. Data from preclinical and, to some extent, clinical studies, suggest that GCs induce treatment resistance in some solid tumours. Since it is unknown whether GC-induced resistance occurs only occasionally or is a more common phenomenon, we performed a screening study using several established cell lines from bone, brain, breast and cervix carcinoma as well as melanoma and neuroblastoma together with fresh surgical resections from patients with breast cancer. We found that DEX inhibits cisplatin and 5-fluorouracil- induced apoptosis and promotes the growth of the majority of examined malignant cells. In contrast, and as expected, DEX acted pro-apoptotically and promoted the cytotoxic effect of chemotherapy in established and primary lymphoid cells. Thus, these data demonstrate the need for detailed molecular studies to clarify the mechanism of differential glucocorticoid signaling as well as controlled, prospective clinical studies
    Type of Publication: Journal article published
    PubMed ID: 17016664
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