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  • 1
    Keywords: CELLS ; EXPRESSION ; CELL ; Germany ; human ; SYSTEM ; DISTINCT ; PROTEIN ; EPITHELIA ; MOLECULES ; TISSUE ; TISSUES ; SKIN ; GLYCOPROTEIN ; ELEMENTS ; SURFACE ; LOCALIZATION ; GLANDS ; SEGMENTS ; calnexin ; ESTABLISHMENT ; MUCINS ; salivary gland ; sebaceous gland ; SEBACEOUS GLANDS
    Abstract: Calnexin (Cnx) has been characterized as a membrane-bound protein that transiently interacts in a unique chaperone system with newly synthesized glycoproteins in order to allow the establishment of their proper tertiary and, in most cases, quarternary structures. The aim of the study was to identify and to locate the expression of Cnx in the three major salivary glands of humans by different methods. Strong expression of Cnx protein and mRNA were generally found in serous salivary secretory units. With regard to mucous secretory units, expression of Cnx was only detectable at a low level in mucous acinar cells of sublingual glands, but not of submandibular glands. Expression of Cnx was always preserved in the surface epithelium of intralobar and interlobular duct segments. In addition, expression of Cnx was detected in sebaceous glands of parotid tissues, with a distribution pattern resembling that seen in sebaceous glands of the normal skin. In conclusion, production of saliva is associated with the expression of Cnx. Synthesis of molecules in mucous secretory units is not necessarily associated with a strong Cnx expression, whereas synthesis in serous secretory units apparently is. The tissue- specific Cnx expression is also paralleled by the observation that the secretions produced by the major salivary glands differ in their composition and amount
    Type of Publication: Journal article published
    PubMed ID: 12507291
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  • 2
    Abstract: Various mesenchymal malignancies with a spindle cell morphology may mimic monophasic synovial sarcomas. We analysed, whether detection of SYT-SSX1/2 fusion transcripts, present as a consequence of a specific translocation [t(X;18)(p11.2;q11.2)] found in synovial sarcomas, are useful to confirm the diagnosis of synovial sarcoma. A nested RT-PCR protocol was established for the detection of SYT-SSX1/2 fusion transcripts. After RNA extraction of snap frozen tissue reverse transcription was carried out. In a nested PCR, the resulting cDNA samples were amplified and visualized on agarose gels. DNA sequencing of PCR products enabled the assignment of fusion transcripts to either the SYT-SSX1 or the SYT-SSX2 variant. We detected SYT-SSX1/2 fusion transcripts in seven monophasic and three biphasic synovial sarcomas. 20 out of 21 control tumour including leiomyosarcomas, malignant peripheral nerve sheath tumours, gastrointestinal stromal sarcomas and fibrosarcomas were negative in RT-PCR analysis. One case of recurrent spindle cell sarcoma originally classified as a fibrosarcoma revealed a SYT-SSX2 fusion transcript. These data provide further evidence that the RT-PCR amplification of SYT-SSX1/2 fusion transcripts permits the specific identification of synovial sarcomas. This diagnostic approach may be especially useful in cases with equivocal histomorphology.
    Type of Publication: Journal article published
    PubMed ID: 10095437
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  • 3
    Keywords: CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; CELL ; Germany ; human ; GENE-EXPRESSION ; PROTEIN ; transcription ; METABOLISM ; EPITHELIA ; MONOCLONAL-ANTIBODY ; TISSUE ; TUMORS ; TISSUES ; SEQUENCE ; ACID ; ACIDS ; antibodies ; antibody ; ADENOMAS ; SURFACE ; MONOCLONAL-ANTIBODIES ; EPITHELIAL-CELLS ; fatty acids ; FATTY-ACIDS ; adenocarcinoma ; ADENOCARCINOMAS ; carcinoma,epithelial tumors,fatty acid metabolism,small intestine ; CHAIN ACYL-COA ; DEPENDENT REGULATION ; fatty acid metabolism ; SMALL-INTESTINE
    Abstract: Fatty acids are implicated in tumorigenesis, but data are limited concerning endogenous fatty acid metabolism of tumor cells in adenomas and adenocarcinomas of the small intestine. The recently cloned human acyl-CoA-synthetase 5 (ACS5) is predominantly found in the small intestine and represents a key enzyme in providing cytosolic acyl-CoA thioesters. Protein synthesis and mRNA expression of ACS5 were studied in human intestinal tissues using different methods, including a newly established monoclonal antibody. In the healthy small intestine, expression of ACS5 was restricted to the villus surface epithelium but was not detectable in enterocytes lining crypts. ACS5 protein and mRNA were progressively diminished in epithelial cells of adenomas and adenocarcinomas of the small intestine. In conclusion, altered expression of ACS5 is probably related to the adenoma-carcinoma sequence of small intestinal epithelial tumors due to an impaired acyl-CoA thioester synthesis. (C) 2003 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 14608540
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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: EXPRESSION ; tumor ; carcinoma ; Germany ; NEW-YORK ; GENE ; TISSUE ; TUMORS ; TISSUES ; DELETION ; LESIONS ; MICROARRAY DATA ; MUTATION ; METASTASIS ; inactivation ; MUTATIONS ; HEAD ; adenocarcinoma ; ADENOCARCINOMAS ; beta-catenin ; MICROARRAY ANALYSIS ; point mutation ; CLUSTER ; MASSES ; molecular ; FEATURES ; pancreas ; DUCTAL ADENOCARCINOMA ; ACINAR-CELL-CARCINOMA ; AUTOPSY ; CLUSTER-ANALYSIS ; DPC4/SMAD4 ; p16(INK4A)
    Abstract: An unusual pancreatic tumor with microcystic and tubulopapillary features was observed in a 53-year-old woman. The tumor presented as a large, focally cystic mass in the head of the pancreas, which compressed the surrounding structures. The histological and immunohistochemical analysis revealed a neoplasm that could not be assigned to any of the known pancreatic tumor types. At the molecular level, the tumor showed inactivation of the DPC4/SMAD4 gene, deletion of exon 1 of the p16(INK4A) gene and a point mutation at codon 34 (GGA〉AGA) of beta-catenin. Transcriptional profiling analyses and subsequent correspondence cluster analysis demonstrated that the transcriptional profile of the tumor differed distinctly from that of ductal adenocarcinomas, pancreatic cystic tumors and normal pancreatic tissues. These data suggest that the neoplasm most likely represents a new pancreatic tumor entity, which we would like to refer to as microcystic tubulopapillary tumor
    Type of Publication: Journal article published
    PubMed ID: 15014986
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  • 6
    Keywords: brain ; CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; human ; IN-VIVO ; LUNG ; VIVO ; COMMON ; lung cancer ; LUNG-CANCER ; NEW-YORK ; GENE ; GENOME ; EPITHELIA ; TISSUE ; TUMORS ; MICE ; INDUCTION ; TISSUES ; DOWN-REGULATION ; BREAST ; breast cancer ; BREAST-CANCER ; MOUSE ; IN-SITU ; UP-REGULATION ; MUTATION ; EXTRACELLULAR-MATRIX ; MUTATIONS ; SUPERFAMILY ; EPITHELIAL-CELLS ; GLANDS ; BEHAVIOR ; LUNG-CARCINOMA ; TERMINAL DIFFERENTIATION ; galectin-3 ; MALIGNANT BRAIN-TUMORS ; SCAVENGER RECEPTOR ; MATRIX ; AGGLUTININ
    Abstract: Deleted in malignant brain tumors 1 (DIMBT1) has been proposed as a candidate tumor suppressor for brain and epithelial cancer. Initial studies suggested loss of expression rather than mutation as the predominant mode of DMBT1 inactivation. However, in situ studies in lung cancer demonstrated highly sophisticated changes of DMBT1 expression and localization, pointing to a chronological order of events. Here we report on the investigation of DMBT1 in breast cancer in order to test whether these principles might also be attributable to other tumor types. Comprehensive mutational analyses did not uncover unambiguous inactivating DMBT1 mutations in breast cancer. Expression analyses in the human and mouse mammary glands pointed to the necessity of DMBT1 induction. While age-dependent and hormonal effects could be ruled out, 9 of 10 mice showed induction of Dmbt1 expression after administration of the carcinogen 7,12-dimethybenz(alpha)anthracene prior to the onset of tumorigenesis or other histopathological changes. DMBT1 displayed significant up-regulation in human tumor-flanking tissues compared to in normal breast tissues (P 〈 0.05). However, the breast tumor cells displayed a switch from lumenal secretion to secretion to the extracellular matrix and a significant down-regulation compared to that in matched normal flanking tissues (P 〈 0.01). We concluded that loss of expression also is the predominant mode of DMBT1 inactivation in breast cancer. The dynamic behavior of DMBT1 in lung carcinoma is fully reflected in breast cancer, which suggests that this behavior might be common to tumor types arising from monolayered epithelia. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14732920
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  • 7
    Keywords: RECEPTOR ; INHIBITOR ; tumor ; TUMORS ; PATIENT ; ACTIVATION ; PHOSPHORYLATION ; TYROSINE KINASE INHIBITOR ; PROGRESSION ; COMPARATIVE GENOMIC HYBRIDIZATION ; cytogenetics ; MUTATION ; TUMOR PROGRESSION ; MUTATIONS ; PROGNOSTIC-SIGNIFICANCE ; INTERSTITIAL-CELLS ; CHROMOSOMAL IMBALANCES ; COPY NUMBER CHANGES ; SMOOTH-MUSCLE TUMORS ; C-KIT ; CD117 (KIT) ; DIFFERENTIAL-DIAGNOSIS ; gastrointestinal stromal tumor ; imatinib (STI571/Glivec (R)) ; KIT mutation ; NERVE SHEATH TUMORS
    Abstract: Recent morphological and molecular genetic findings have greatly expanded our understanding of gastrointestinal stromal tumors (GISTs). GISTs are now defined by their overexpression of CD117 (KIT), the receptor for the stem cell factor, and can thus be discriminated from smooth muscle tumors. Cytogenetically, GISTs are characterized even in early lesions by frequent entire or partial loss of the chromosomes 14 and 22 and terminal deletions of the chromosomal arm 1p. During tumor progression further chromosomal imbalances accumulate. Following the first report on activating KIT mutations in GISTs, several studies have addressed the role of wild-type and mutant KIT in GISTs and demonstrated activating KIT mutations in the majority of cases. Moreover, KIT tyrosine phosphorylation is even present in KIT mutation-negative GISTs, implicating KIT activation as a central event in the pathogenesis of GISTs. Imatinib (ST1571/Glivec((R))) is a selective inhibitor of BCR/ABL, PDGFR and KIT receptor-tyrosine kinases. First therapeutic applications of imatinib in patients with progressive GISTs have yielded promising results. This review focusses on the morphological and molecular findings in GISTs which have opened up a new therapeutic perspective
    Type of Publication: Journal article published
    PubMed ID: 12739051
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  • 8
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; tumor ; SUPPORT ; SYSTEM ; GENE ; PROTEIN ; PROTEINS ; DIFFERENTIATION ; TUMORS ; LINES ; COMPLEX ; COMPLEXES ; DOMAIN ; INDUCTION ; mechanisms ; SKIN ; MUTATION ; HETEROZYGOSITY ; MELANOMA ; CARCINOMA-CELLS ; EXCHANGE ; EPITHELIAL-CELLS ; squamous cell carcinoma ; epidermis ; TERMINAL DIFFERENTIATION ; DMBT1 ; SALIVARY AGGLUTININ ; basal cell carcinoma ; galectin-3 ; MALIGNANT BRAIN-TUMORS
    Abstract: DMBT1 and galectin-3 are potential interacting proteins with presumably complex roles in tumorigenesis. While at present a variety of mechanisms are discussed for DMBT1 and its participation in cancer, galectin-3 is commonly known to exert tumor-promoting effects. However, in vitro studies in a rodent system have suggested that DMBT1/galectin-3 interaction in the ECM triggers epithelial differentiation, which would point to tumor-suppressive properties. To improve the understanding of DMBT1/galectin-3 action in cancer, we carried out studies in skin cancer of different origins. Mutational analyses of DMBT1 identified a missense mutation in 1 of 13 melanoma cell lines. It led to an exchange of an evolutionary conserved proline residue for serine and located within the second CUB domain of DMBT1. Immunohistochemical analyses demonstrated absence of DMBT1/galectin-3 expression from melanocytes but induction of DMBT1 expression in 1 of 8 nevi and 1 of 11 melanomas and of galectin-3 expression in 3 of 8 nevi and 4 of 8 melanomas. These data suggest that DMBT1 and galectin-3 are unlikely to act as classical tumor suppressors in melanomas. DMBT1 and galectin-3 appear to be secreted to the ECM by epithelial cells within the epidermis and the hair follicle. Compared to the flanking normal epidermis, skin tumors of epithelial origin frequently displayed downregulation of DMBT1 (18 of 19 cases) and galectin-3 (12 of 12 cases). Thus, loss of DMBT1/ galectin- 3 expression may play a role in the genesis of epithelial skin cancer. This would support the view that galectin-3 can exert tumor-suppressive effects in certain scenarios, and DMBT1/galectin-3-mediated differentiation represents a candidate mechanism for this effect. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12673672
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  • 9
    Keywords: CANCER ; tumor ; carcinoma ; Germany ; KINASE ; PATHWAY ; GENE ; DNA ; BASE ; FREQUENCY ; FREQUENCIES ; MUTATION ; COMPONENT ; MELANOMA ; PCR ; MUTATIONS ; EXCHANGE ; CONSTITUTIVE ACTIVATION ; CUTANEOUS MELANOMA ; BRAF ; ABSENCE ; FEATURES ; HIGH PREVALENCE ; KRAS MUTATIONS ; uveal melanoma
    Abstract: Background & Aims: Anorectal melanoma (AM) is a rare but highly malignant tumor, displaying histologic and immunohistochemical features very similar to cutaneous melanoma (CM). Because BRAF mutations were recently identified in the majority of CM and nevi, we investigated AM for BRAF mutations and mutations of NRAS, an additional component of the MAPK-signalling pathway. Methods: DNA from formalin-fixed and paraffin-embedded AM was PCR amplified and sequenced. Results: We detected BRAF mutations in 2 of 19 cases and NRAS mutations in none of the cases. Mutations in exon 15 of BRAF were present in only I tumor (I of 19 cases). The A1800T base exchange represented a novel mutation and resulted in a K600N transition in an AM from a 96-year-old white man who presented with rectal bleeding and painful sitting of a few weeks' duration. The second positive AM case, a 69-year-old white man who presented with painless rectal bleeding and clinical symptoms of an intestinal constipation showed a novel missense mutation (C1327T leading to R443W conversion) in BRAF exon 11. None of the AM cases displayed the oncogenic V599E mutation preponderating in CM. Conclusions: With regard to the frequency of V599E BRAFmutations, AM significantly differs from CM (P less than or equal to .0001), which suggests that BRAF mutations distinguish anorectal from cutaneous melanoma at the molecular level
    Type of Publication: Journal article published
    PubMed ID: 15578519
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  • 10
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