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  • 1
    Keywords: CELL ; neoplasms ; GENE ; GENES ; HYBRIDIZATION ; DIFFERENTIATION ; TUMORS ; tumour ; BIOLOGY ; chromosome ; COMPARATIVE GENOMIC HYBRIDIZATION ; MUTATION ; PCR ; MUTATIONS ; MUSCLE ; INVOLVEMENT ; POLYMERASE-CHAIN-REACTION ; SERIES ; CHAIN-REACTION ; pathology ; CHILDREN ; IMBALANCES ; AUSTRALIA ; LOCATION ; CHROMOSOMAL IMBALANCES ; CGH ; tumour suppressor gene ; molecular ; CHAIN ; FEATURES ; SUPPRESSOR GENE ; polymerase chain reaction ; SPINE ; MUTATIONAL ANALYSIS ; LEVEL ; analysis ; methods ; SUPPRESSOR ; tumour suppressor ; LOSSES ; genomic ; ENGLAND ; EXONS ; histopathology ; COMPARATIVE-GENOMIC-HYBRIDIZATION ; INTRACRANIAL NEUROTHEKEOMA ; nerve sheath myxoma ; neurothekeoma ; NF-2 ; S-100 PROTEIN
    Abstract: Aims: To report the demographic, clinical and molecular profile of a series of intraspinal nerve sheath myxomas. Nerve sheath myxomas are diagnostically challenging, mainly cutaneous spindle cell neoplasms exhibiting Schwann cell differentiation. They are frequently mistaken for neurothekeomas and their genetic features are essentially unknown. Methods and results: Ten spinal nerve sheath myxomas with a preferential location in the lumbar spine (70%) were investigated. Presenting symptoms consisted of sciatic pain (100%), muscle weakness and paraesthesia (60% each). Intraoperatively, all tumours were attached to a spinal nerve. Chromosomal imbalances by comparative genomic hybridization were found in 8/10 cases, consisting of -22q (80%) and -19 (30%). Polymerase chain reaction analysis of the NF2 gene (exons 1-16) revealed two tumours with mutations in exon 8 and 14, respectively. Conclusions: Although these 10 nerve sheath myxomas exhibited Schwann cell differentiation and frequently showed loss of chromosome 22q typically encountered in peripheral nerve tumours, only two cases demonstrated mutations of the NF2 gene. This may indicate involvement of other tumour suppressor genes on 22q in nerve sheath myxomas and shows that they are more closely related at the molecular level to sporadic schwannomas, underscoring the presumption that they are true nerve sheath tumours
    Type of Publication: Journal article published
    PubMed ID: 17222254
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  • 2
    Keywords: SURVIVAL ; carcinoma ; Germany ; antibody ; leukemia ; COLORECTAL CANCERS ; SARCOMA ; GLIOMAS ; HUMAN BREAST ; BRAIN-TUMORS ; IDH1 ; GLIOBLASTOMAS ; L-2-HYDROXYGLUTARIC ACIDURIA ; ISOCITRATE-DEHYDROGENASE 1 ; haematopoietic tumors ; IDH1 CODON 132
    Abstract: Aims: Mutations in the isocitrate dehydrogenase 1 gene have been identified recently to play a key role in diffuse astrocytoma and oligodendroglioma as well as in acute myeloid leukaemia. In glioma, IDH1R132H is the most common mutation type, which is associated with younger patient age and longer patient survival compared to wild-type status. Sequencing analyses of carcinomas and lymphomas have detected IDH1 mutations in only a small fraction of cases. In those studies, IDH1R132H was also the most frequent mutation. The aim of the present study was to analyse a comprehensive series of human tumours for IDH1R132H mutation. Methods and results: A total of 1844 formalin-fixed paraffin-embedded tumours, including carcinomas, sarcomas and haematopoietic tumours were investigated immunohistochemically using a mutationspecific antibody for IDH1 R132H. Our positive control series consisted of a collection of diffuse astrocytomas and oligodendrogliomas. No IDH1R132H mutation was found in this series. Conclusions: IDH1R132H mutations occur almost exclusively in glioma and acute myeloid leukaemia
    Type of Publication: Journal article published
    PubMed ID: 21707716
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  • 3
    Keywords: EXPRESSION ; SURVIVAL ; THERAPY ; RISK ; prognosis ; BREAST-CANCER ; PROGRESSION ; METASTASIS ; metastases ; MELANOMA ; ADHESION ; MIGRATION ; INVOLVEMENT ; L1 ; CELL-ADHESION MOLECULE ; ADENOID CYSTIC CARCINOMA ; OVARIAN CARCINOMAS ; CEACAM1
    Abstract: Aims: The up-regulation of the cell adhesion molecule L1 has been associated with impaired prognosis in several cancers. This study aimed to identify potential prognostic markers, including L1, in adenoid cystic carcinoma of the salivary glands (ACCs), which might give additional insight into the molecular mechanisms underlying malignant progression. Methods and results: The expression of L1 was analysed in 34 primary ACCs (nine tubular, 15 cribriform, nine solid, one mixed) and correlated with recurrence, metastasis, overall survival and clinicopathological parameters. Independent of the histological subtype, intense L1 expression in the primary tumours was associated significantly with metastasis (P = 0.02) and death (P = 0.044). In the subgroup of cribriform ACCs, 10 of 15 tumours contained pseudocysts, which were associated with significantly lower recurrence rates (P = 0.003), lower metastasis rates (P = 0.009) and a prolonged overall survival (P = 0.004). Conclusions: Determination of L1 expression in primary ACCs improves risk estimations. As up-regulation of L1 expression predicts fatal prognosis, L1 might be involved functionally in growth and spread of ACC and might thus present a molecular target for future therapeutic strategies
    Type of Publication: Journal article published
    PubMed ID: 21884209
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  • 4
    Keywords: EXPRESSION ; ACCUMULATION ; MICE ; SKELETAL-MUSCLE ; INSULIN-RESISTANCE ; adipophilin ; DIFFERENTIATION-RELATED PROTEIN ; FATTY LIVER ; PERILIPIN ; PAT-FAMILY
    Abstract: AIMS: Lipid droplets (LDs) are dynamic storage compartments for energy-rich fats that are nearly ubiquitously present in eukaryotic cells, exerting tissue-specific functions in metabolically active cell types, and are increased in conditions following cellular damage or lipid overload. The LD-cytoplasm interface is stabilized by amphiphilic proteins of the PAT/perilipin family (perilipin/perilipin-1, adipophilin/perilipin-2, and TIP47/perilipin-3). We evaluated the value of adipophilin immunohistochemistry for the diagnosis of diseases associated with LD accumulation. METHODS AND RESULTS: In human tissues, adipophilin-positive LDs were especially prominent in steroidogenic cells of the adrenal gland, testis, and ovary, in hepatocytes and hepatic stellate cells, in cardiac, striated and smooth myocytes, in lactating mammary gland epithelial cells, and in plurivacuolar adipocytes. Variable amounts of adipophilin-positive LDs were also detected almost ubiquitously in epithelial cells of the gastrointestinal tract and skin. In diseases associated with lipid storage, adipophilin was strongly expressed in lipid-laden macrophages in atherosclerosis, in cardiomyopathies, kidney diseases, hepatocyte steatosis, colon ischaemia, and at the border of organ infarcts. CONCLUSIONS: Adipophilin immunohistochemistry visualizes small LDs in tissues under physiological and disease conditions that are not visible by conventional light microscopy. Immunohistology for adipophilin may facilitate histomorphological diagnosis of diseases and definition of the extent of metabolic dysregulation, such as in organ infarcts, cardiomyopathies, kidney diseases, and microvesicular steatosis.
    Type of Publication: Journal article published
    PubMed ID: 23347084
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  • 5
    Keywords: EXPRESSION ; GENE ; COPY-NUMBER ; SARCOMA ; CHROMOSOMAL IMBALANCES ; SPECTRUM ; LIPOMATOUS HEMANGIOPERICYTOMA ; NODULAR FASCIITIS ; LIPOSARCOMAS ; DEFINE
    Abstract: AIMS: Nuclear relocation of STAT6 has been shown in tumours with NAB2-STAT6 fusion, and has been proposed as an ancillary marker for the diagnosis of solitary fibrous tumours (SFTs). The aim of this study was to verify the utility of STAT6 immunohistology in diagnosing SFT. METHODS AND RESULTS: A total of 689 formalin-fixed paraffin-embedded tumours comprising 35 pleural SFTs and 654 other mesenchymal tumours were investigated for STAT6 expression using immunohistochemistry. Nine dedifferentiated liposarcomas (DDLSs) and five SFTs were also examined for the presence of NAB2-STAT6 fusion at the protein level using the proximity ligation assay (PLA), and for copy number variants (CNVs) with the Illumina Infinium Human Methylation450 array. Thirty-four of 35 SFTs showed strong nuclear STAT6 expression. Furthermore, five of 68 DDLSs, two of 130 undifferentiated pleomorphic sarcomas and one of 63 cases of nodular fasciitis showed moderate to strong nuclear STAT6 expression. The PLA indicated the presence of NAB2-STAT6 fusion protein in SFTs, but signal was also detected in some DDLSs. Copy number analysis showed an overall low frequency of chromosomal imbalances in SFTs, but complex karyotypes in DDLSs, including amplification of STAT6 and MDM2 loci. CONCLUSIONS: The detection of nuclear relocation of STAT6 with immunohistochemistry is a characteristic of SFTs, and may serve as a diagnostic marker that indicates NAB2-STAT6 fusion and helps to discriminate SFTs from histological mimics.
    Type of Publication: Journal article published
    PubMed ID: 24702701
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  • 6
    Keywords: SURVIVAL ; carcinoma ; ACTIVATION ; protein expression ; EGFR ; C-MET ; GENE COPY NUMBER ; ALK ; TUMOR REGISTRY
    Abstract: BACKGROUND: CMET represents an emerging therapy target for monoclonal antibodies and tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC). METHODS: We investigated CMET gene amplification status by fluorescence in-situ hybridization (FISH) and CMET protein expression by immunohistochemistry in a large series of 209 NSCLC brain metastases (BM; 165 adenocarcinoma, 20 squamous cell carcinoma, 11 adenosquamous carcinomas, 11 large cell carcinomas and two large cell neuroendocrine carcinomas) and correlated our results to clinic-pathological parameters and molecular data from previous studies. RESULTS: We found CMET gene amplification in 36/167 (21.6%) and CMET protein expression in 87/196 (44.4%) of evaluable BM. There was a strong correlation between the presence of CMET gene amplification and CMET protein expression (P 〈 0.001, chi-square test). Furthermore, presence of CMET amplification correlated positively with presence of ALK amplifications (P = 0.039, chi-square test) and high HIF1 alpha index (P = 0.013, Mann-Whitney U-test). Neither CMET expression nor CMET gene amplification status correlated with patient outcome parameters or known prognostic factors. CONCLUSIONS: CMET overexpression and CMET amplification are commonly found in NSCLC BM and may represent a promising therapeutic target.
    Type of Publication: Journal article published
    PubMed ID: 25039982
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  • 7
    Abstract: AIM: Nuclear alpha-thalassemia/mental retardation X-linked (ATRX) loss and alternative lengthening of telomeres (ALT) are linked in distinct malignancies. We therefore aimed to determine the nuclear ATRX expression correlated with ALT in a comprehensive series of sarcomas. METHODS: 573 formalin-fixed paraffin-embedded sarcomas comprising 28 entities were investigated for nuclear ATRX expression by immunohistochemistry. Telomere-specific FISH was used to determine the ALT phenotype in 50 sarcomas with complete or heterogeneous ATRX loss. RESULTS: Complete nuclear ATRX loss was detected in 58 of 573 sarcomas, all high-grade, with the highest prevalence in undifferentiated pleomorphic sarcomas (38%) and pleomorphic liposarcomas (38%), followed by dedifferentiated liposarcomas (24%), osteosarcomas (21%), leiomyosarcomas (17%), myxofibrosarcomas (11%) and malignant peripheral nerve sheath tumours (4%). Interestingly, further 20 sarcomas, all belonging to the aforementioned entities with complete ATRX loss, presented with a heterogeneous ATRX expression pattern. ALT was observed in 41/42 sarcomas with complete ATRX loss, but only in 2/8 sarcomas with heterogeneous expression. CONCLUSION: Nuclear ATRX loss, either complete or heterogeneous, is encountered in a considerable number of high-grade sarcomas with non-specific genetic alterations. A causal relationship with ALT might be indicated at least in cases with a complete nuclear ATRX loss. This article is protected by copyright. All rights reserved.
    Type of Publication: Journal article published
    PubMed ID: 26291601
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  • 8
    Keywords: ACID, ASSOCIATION, BIOLOGY, BREAST-CANCER, CARCINOGENESIS, carcinoma, CELL, CELL CARCINOMA, CELLS, c
    Abstract: Aims: To investigate the modulation of cellular retinol-binding protein (CRBP)-1 and the desmosomal plaque proteins plakophilin (PKP)-1 and desmoplakin (DP) in correlation with the Ki67+ proliferation index (PI) during the progression of cervical squamous intraepithelial lesions (SIL) to squamous cell carcinoma (SCC). Methods: Using in situ imaging by brightfield and confocal laser scanning microscopy, the expression of CRBP-1 protein and transcripts, PKP-1, DP and the Ki67 PI were analysed in 38 low-grade (L) SIL, 56 high-grade (H) SIL, 49 SCC, 30 control cervices and 10 human papillomavirus-positive condylomatous lesions. Results: CRBP-1+ cells increased from 11.4% in the normal cervix to 80.3% in LSILs, 92.3% in HSILs and slightly decreased to 78.3% in invasive SCCs (P 〈 0.0001) in close association with the Ki67 PI (r = 0.41; P 〈 0.0001). PKP-1+ and DP+ cells were correlated (0.32; P 〈 0.0001) and decreased from normal (81% versus 92.3%) to LSIL (53.1% versus 85.3%), to HSIL (46.4% versus 67.5%) and SCC (35.1% versus 35.9%). The Ki67+ PI was inversely correlated with DP (-0.20, P = 0.0014) and PKP-1 (-0.19, P = 0.015). Condylomata retained low CRBP-1 and high expression of PKP-1 and DP. Conclusions: The gain of CRBP-1 and the loss of desmosomal proteins occur early in cervical carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 17593084
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  • 9
    Keywords: CELLS ; CELL ; MODEL ; DNA ; kidney ; MACROPHAGES ; RAT ; BIOLOGY ; ACID ; LESIONS ; PROGRESSION ; immunohistochemistry ; LYMPHOCYTES ; IMMUNITY ; pathology ; inflammation ; INJURY ; aristolochic acid ; CHINESE HERBS NEPHROPATHY ; DNA-ADDUCTS ; UROTHELIAL CARCINOMA ; FEATURES ; TGF-BETA ; DNA ADDUCT ; PHASE ; CELL BIOLOGY ; interstitial inflammation ; RENAL FIBROSIS ; CASE SERIES ; cytotoxic T cells ; FANCONIS-SYNDROME ; INTERSTITIAL RENAL FIBROSIS ; MURINE ADRIAMYCIN NEPHROPATHY
    Abstract: Aristolochic acid nephropathy revisited: a place for innate and adaptive immunity? Aims: The histological features of aristolochic acid nephropathy (AAN) consist of paucicellular interstitial fibrosis, severe tubular atrophy, and almost intact glomeruli with media lesions of interlobular arteries. As an early phase of interstitial inflammation preceded peritubular fibrosis in the rat model of AAN, the aim was to investigate the presence of inflammatory cells in human AAN. Methods and results: Reports of confirmed cases and case series of AAN were reviewed in terms of interstitial inflammation and found to have very conflicting results. This prompted us to search for and characterize inflammatory cells within the native kidneys provided from four end-stage AAN patients. Prior aristolochic acid exposure was attested by the intrarenal presence of the typical aristolactam I-derived DNA adduct. Besides the tubulointerstitial lesions usually seen in the cortex, a massive infiltration of macrophages, T and B lymphocytes was detected by immunohistochemistry in the medullary rays and in the outer medullae with some extension to the upper cortical labyrinth. Conclusions: In parallel with histological findings reported in the rat model, inflammatory cells are present preferentially in the interstitium of the medullary rays and of the outer medulllae in renal interstitium from human AAN cases, even in the terminal stages. Further studies must be undertaken to determine the respective roles of innate and adaptive immunity in the progression of AAN
    Type of Publication: Journal article published
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  • 10
    Keywords: CANCER ; EXPRESSION ; proliferation ; SURVIVAL ; GENE-EXPRESSION ; TUMOR PROGRESSION ; EXTRACELLULAR-MATRIX ; PATIENT SURVIVAL ; pancreatic adenocarcinoma ; MAMMALIAN HEPARANASE ; head and neck squamous cell carcinoma ; ENZYMATIC-ACTIVITY ; GASTRIC-CARCINOMA ; CANCER METASTASIS ; heparanase ; MOLECULAR-PROPERTIES
    Abstract: Aims: Cellular expression of heparanase, a degrading enzyme of the extracellular matrix, is associated with poorer prognosis in several cancers. The present analysis, has studied the role of heparanase in tumour growth and clinical outcome in patients with head and neck squamous cell carcinoma (HNSCC). Methods and Results: We analysed the cellular expression of the active form of heparanase in 71 human HNSCCs, using immunohistochemistry. The results were compared with clinicopathological data and, in 65 cases with immunoreactivity for the proliferation marker, MIB1. Cellular heparanase expression was detected in 41 of 71 (57.74%) cases; in particular, UICC IV-stage tumours showed high heparanase levels. Heparanase was localized mainly in the cytoplasm and, to a lesser extent, at the cell membrane. High levels of heparanase were significantly correlated with an almost four-fold decrease in MIB1 labelling (P = 0.006). Comparison with clinical outcome by multivariate analysis revealed that patients with high-level heparanase expression had prolonged overall survival (P = 0.029). Conclusions: Although heparanase was mainly found in late-stage HNSCCs, cellular heparanase expression in HNSCCs was associated with prolonged overall survival. We propose that the proliferation-reducing effect of high heparanase levels might outweigh the tumour-promoting effects of heparanase, especially in advanced tumours
    Type of Publication: Journal article published
    PubMed ID: 21585429
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