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  • 1
    Electronic Resource
    Electronic Resource
    Human Histopathology of Electroanatomic Mapping After Cooled-Tip Radiofrequency Ablation to Treat Ventricular Tachycardia in Remote Myocardial Infarction (2005)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 16 (2005), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: Catheter ablation of ventricular tachycardia (VT) in remote myocardial infarction (MI) often requires excessive mapping procedures. Documentation of the electrical substrate via electrogram amplitude may help to identify regions of altered myocardium resembling exit areas of reentrant VTs. Methods and Results: A patient with multiple symptomatic monomorphic VTs (biventricular ICD, remote MI) underwent electroanatomic substrate mapping (CARTO™) for VT ablation. Regions of scar (bipolar electrogram amplitudes ≤0.5 mV), normal myocardium (≥1.5 mV), and “altered” myocardium (0.5–1.5 mV) were identified. Ablation was directed to regions with “altered” myocardium based on pace map correlation. After ablation the clinical VT did not reoccur. The patient died due to worsening of heart failure 7 days afterward. During postmortal evaluation specified sites of electroanatomic mapping were correlated to histopathological findings. Annotated scar areas were documented to consist of areas with massive fibrosis (≥80% of mural composition). Ablations were found to span through regions with intermediate fibrosis (21–79%) mapped as “altered” myocardium. Ablation produced transmural coagulation necrosis of mesh-like fibrotic tissue with interspersed remnants of myocardial cells up to a maximum depth of 7.0 mm. Subendocardial intramural bleedings were universal findings 7 days after ablation. Conclusions: Electroanatomic substrate mapping for VT ablation sufficiently identified regions of scar and normal myocardium. Regions with bipolar electrogram amplitudes between 0.5 and 1.5 mV were found to correlate to areas of “intermediate” fibrosis (21–79%) with only remnant strands of myocardial cells and were identified as target region for ablation. Cooled-tip endocardial radiofrequency ablation lead to transmural coagulation necrosis up to a depth of 7.0 mm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.2005.40826.x
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  • 2
    Electronic Resource
    Electronic Resource
    Total Pulmonary Vein Occlusion as a Consequence of Catheter Ablation for Atrial Fibrillation Mimicking Primary Lung Disease (2003)
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 14 (2003), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: Catheter ablation has recently been used for curative treatment of atrial fibrillation. Methods and Results: Three of 239 patients who underwent ablation close to the pulmonary vein (PV) ostia at our institute developed severe hemoptysis, dyspnea, and pneumonia as early as 1 week and as late as 6 months after the ablation. Because the patients were arrhythmia-free, the treating physician initially attributed the symptoms to new-onset pulmonary disease (e.g., bronchopulmonary neoplasm). After absent PV flow was confirmed by transesophageal echocardiography, transseptal contrast injection depicted a totally occluded PV in all three patients. Successful recanalization, even in chronically occluded Pvs, was performed in all patients. During follow-up, Doppler flow measurements by transesophageal echocardiography demonstrated restenosis in all primarily dilated PV, which led to stent implantation. Conclusion: PV stenosis/occlusion after catheter ablation of atrial fibrillation occurs in a subset of patients. However, because in-stent restenosis occurred in two patients after 6 to 10 weeks, final interventional strategy for PV stenosis or occlusion remains unclear. To prevent future PV stenosis or occlusion, a decrease in target temperature and energy of radiofrequency current or the use of new energy sources (ultrasound, cryothermia, microwave) seems necessary. (J Cardiovasc Electrophysiol, Vol. 14, pp. 366-370, April 2003)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2003.02334.x
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  • 3
    Electronic Resource
    Electronic Resource
    Patterns of chromosomal imbalances in benign solitary fibrous tumours of the pleura (2000)
    Springer
    Virchows Archiv 437 (2000), S. 248-255 
    Details
    ISSN: 1432-2307
    Keywords: Keywords Fibrous pleural tumour ; Solitary fibrous tumour ; Sarcomatoid mesothelioma ; Comparative genomic hybridisation ; Paraffin material
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Solitary fibrous tumours (SFTs) of the pleura, in contrast to malignant mesothelioma, occur independently of previous asbestos exposure. They are benign tumours, but may recur if the stalk to the adjacent pleural or lung tissue remains in situ during surgical removal. The molecular pathology of SFTs is largely unknown. We used comparative genomic hybridisation (CGH) to characterise 12 localised SFTs and 12 predominantly sarcomatoid mesotheliomas. Fifty-eight percent of the investigated SFTs did not show any chromosomal imbalances. The most frequent defects were losses on chromosome arms 13q (33%), 4q and 21q (17% each). Significant gains were seen at chromosome 8 and at 15q in two cases each. There was no correlation between tumour size and molecular pathology findings. In contrast, 75% of the mesotheliomas carried chromosomal defects. On average, the mesotheliomas showed over three times as many defects per tumour as the SFTs. Localisation of several frequent losses and gains were similar to those of the SFTs. Therefore, in individual cases, a clear distinction between SFTs and sarcomatoid mesotheliomas is not possible based on CGH analysis alone. Further molecular characterisation of this rare tumour entity will be necessary to elucidate possible genes involved in early tumorigenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280000235
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  • 4
    Electronic Resource
    Electronic Resource
    Intracellular distribution of β-catenin in colorectal adenomas, carcinomas and Peutz-Jeghers polyps (1999)
    Springer
    Journal of cancer research and clinical oncology 125 (1999), S. 297-304 
    Details
    ISSN: 1432-1335
    Keywords: Key words Adenoma ; APC ; β-Catenin ; Colorectal cancer ; Peutz-Jeghers polyps
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The interaction of the adenomatous polyposis coli (APC) tumor-suppressor protein and the intracellular cell-adhesion protein β-catenin is crucial for the development of colorectal tumors. Since functional nuclear complexes of β-catenin with transcription factors have been identified recently, the knowledge of level and distribution of β-catenin in sporadic colorectal tumors will give important insights into the intracellular mechanism of sporadic colorectal tumor initiation and progression. In contrast to the familiar adenomatous polyposis syndrome and to the majority of sporadic colorectal tumors, Peutz-Jeghers (PJ) syndrome is not caused by mutations in the APC gene. Since PJ syndrome is an inherited disease with an increased risk for gastrointestinal adenocarcinoma, whether β-catenin plays a similarly important role for the development of PJ polyps should be further investigated. For these reasons we analyzed the distribution of β-catenin in a total of 60 sporadic colorectal tumors at different stages of progression and in 6 PJ polyps. In addition to the localization at the cell-to-cell border membranes, fluorescence immunohistochemistry revealed a nuclear accumulation of β-catenin in single tumor cells of 10/14 small adenomas with mild dysplasia and in 14/16 adenomas with moderate dysplasia. Further tumor progression is accompanied by an expansion of cells with increased level of nuclear and cytoplasmic β-catenin. These cells were observed in 5/16 adenomas with moderate dysplasia and in 15/15 adenomas with severe dysplasia. In all adenocarcinomas investigated, as well as in the corresponding lymph node metastases, a subpopulation of tumor cells exhibited a remarkably increased level of β-catenin within the entire cytoplasm and the nucleus. In contrast to the situation in sporadic colorectal tumors, nuclear and cytoplasmic β-catenin was not increased in PJ polyps. These results point to an extensive redistribution of β-catenin, which starts early in colorectal tumorigenesis. The nuclear accumulation in single cells of small adenomas can be considered as the first visible sign of the loss of APC function. Thus the immunohistochemical detection of β-catenin distribution could serve as a criterion for estimating the malignant potential in the clinico-pathological evaluation of colon tumors during their early progression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050277
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  • 5
    Electronic Resource
    Electronic Resource
    Expression and localization of thrombomodulin in preneoplastic bronchial lesions and in lung cancer (1997)
    Springer
    Virchows Archiv 430 (1997), S. 209-212 
    Details
    ISSN: 1432-2307
    Keywords: Thrombomodulin ; Lung cancer ; Preneoplasia ; Squamous cell carcinoma ; Epithelial differentiation ; Keratinisation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Thrombomodulin (TM) is an endothelial surface glycoprotein that acts as a natural anticoagulant. It inhibits thrombin and accelerates the activation of the anticoagulant protein C. TM has been detected in dermal keratinocytes, where it is associated with terminal differentiation. It can also be detected in various types of squamous malignant neoplasms and in malignancies of endothelial and mesothelial origin, such as Kaposi's sarcoma or malignant mesothelioma, but is absent in pulmonary adenocarcinomas (AC). Seventy-two lung tumour specimens [33 squamous cell carcinomas (SQCC), 23 AC, 1 large cell carcinoma, 8 small cell lung cancers (SCLC) and 7 multidifferentiated tumours (MT)] were analysed immunohistochemically by staining with an anti-TM antibody in order to assess TM expression. All of the SQCC stained positively for TM. In contrast, only 9 AC and 4 MT and none of the SCLC showed positive anti-TM staining. Seven hyperplastic bronchial epithelial specimens and eight preneoplastic bronchial lesions (five cases of moderate dysplasia, two cases of severe dysplasia and one case of carcinoma in situ) were used as controls. Normal or hyperplastic areas of bronchial epithelium revealed no positive reaction. However, a distinct positive anti-TM staining pattern related to the degree of keratiniziation of dysplastic lesions was seen. The present results suggest that anti-TM immunostaining is a useful marker for squamous cell carcinoma in the differential diagnosis of pulmonary carcinoma, also indicating keratinocyte differentiation in dysplastic bronchial epithelium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01324803
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  • 6
    Electronic Resource
    Electronic Resource
    Expression of c-Met receptor and hepatocyte growth factor/scatter factor in synovial sarcoma and epithelioid sarcoma (1998)
    Springer
    Virchows Archiv 432 (1998), S. 337-342 
    Details
    ISSN: 1432-2307
    Keywords: Key words c-Met receptor ; Hepatocyte growth factor/scatter factor ; Synovial sarcoma ; Epithelioid sarcoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Overexpression of c-Met receptor/hepatocyte growth factor (scatter factor) system (c-Met/HGF/SF) as a physiologically paracrine cellular signaling system is thought to be involved in the progression of malignant tumours. In 26 synovial sarcomas and epithelioid sarcomas, c-Met and HGF/SF expression was analysed immunohistochemically. There were 10 biphasic synovial sarcomas, 7 of which showed moderate to strong c-Met expression in epithelial areas compared with the fibrous component, with corresponding expression of HGF/SF. Six of 9 monophasic fibrous synovial sarcomas showed only very faint c-Met and corresponding HGF/SF expression. In 7 epithelioid sarcomas strong expression of c-Met and HGF/SF was observed within epithelioid tumour cells. Non-radioactive in situ hybridization demonstrated the synthesis of c-Met receptor in tumor cells by detecting c-met-mRNA. This analysis shows that in synovial sarcomas and epithelioid sarcomas, tumour entities with epithelial and mesenchymal structures, c-Met and HGF/SF overexpression can be detected, indicating a role of this signaling system in these subtypes of sarcoma, and especially in the more epithelioid tumour phenotype. An autocrine interaction between overexpressed c-Met receptor and HGF/SF may be hypothesized.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050175
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  • 7
    Electronic Resource
    Electronic Resource
    Patterns of expression and secretion of vascular endothelial growth factor in malignant soft-tissue tumours (2000)
    Springer
    Journal of cancer research and clinical oncology 126 (2000), S. 219-225 
    Details
    ISSN: 1432-1335
    Keywords: Key words VEGF ; Sarcoma ; Expression ; Secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vascular endothelial growth factor (VEGF) is an important cytokine especially in the process of tumour angiogenesis. A total of 46 soft-tissue sarcomas were analysed for the expression and possible secretion of VEGF by immunohistochemistry, in-situ hybridisation, and enzyme-linked immunosorbent assays (ELISA). VEGF was demonstrated immunohistochemically in tumour tissue in 45 of 46 cases. The detection of mRNA transcripts yielded evidence of synthesis of VEGF in these sarcomas. ELISA could be performed in 21 cases. Higher concentrations of VEGF were found in tumour-related intraoperatively sampled venous blood in 16 out of 21 patients (76%) than in systemic concentrations taken preoperatively. The results indicated the secretion of VEGF by tumour cells although these raised concentrations were not statistically significant. In 12 out of these 16 patients (75%) a concurrent moderate to strong immunoexpression of VEGF was detected. The relevance of VEGF blood concentrations as a potential “progress parameter” for the course of disease remains questionable. This is mainly due to the lack of statistical significance in the difference between systemic VEGF concentrations in patients and those of a control group. Further long-term follow-up studies are needed, which should include patients with tumour recurrences.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050036
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  • 8
    Electronic Resource
    Electronic Resource
    Hepatocyte growth factor/scatter factor and its receptor c-Met are overexpressed and associated with an increased microvessel density in malignant pleural mesothelioma (1998)
    Springer
    Journal of cancer research and clinical oncology 124 (1998), S. 291-296 
    Details
    ISSN: 1432-1335
    Keywords: Key words HGF/SF ; c-Met receptor ; Malignant mesothelioma ; autocrine loop ; angiogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hepatocyte growth factor/scatter factor (HGF/SF) stimulates cell proliferation, motility and invasiveness via its receptor c-Met during embryogenesis and repair processes. It induces angiogenesis, promoting endothelial cell migration and capillary-tube formation in vivo. Co-expression of HGF/SF and c-Met receptor results in enhanced tumour growth, invasiveness and a mesenchymal-epithelial transition in some experimental tumours. Since mesothelioma cells have been reported to express c-Met receptor and to migrate in response to HGF/SF, we investigated human malignant pleural mesotheliomas for the demonstration of possible co-expression of the growth factor and its receptor. The microvessel density of the tumours was also analysed in order to assess the influence of HGF/SF expression on tumour angiogenesis. Thirty-nine paraffin-embedded specimens of malignant pleural mesotheliomas were immunostained by anti-HGF/SF and anti-c-Met antibodies and semiquantitatively evaluated. c-Met mRNA expression was visualised in ten tumour samples by a fluorescent in situ hybridisation method. Microvessel density was calculated by counting microvessels with a high-power field (200×) on von-Willebrand-factor-stained slides. We found an increased production of HGF/SF in 33/39 tumours and a corresponding overexpression of c-Met receptor in 29/39 specimens. The FISH method detected increased transcription of c-Met mRNA in malignant cells and in neighbouring vascular endothelial cells. HGF/SF-positive mesotheliomas had significantly higher microvessel densities compared to their HGF/SF-negative counterparts. The observed co-expression of HGF/SF and c-Met in malignant pleural mesotheliomas suggests a possible self-stimulation (autocrine loop) of tumour cells. On the basis of the significantly higher microvessel density values of malignant mesotheliomas overexpressing HGF/SF, we postulate, that HGF/SF may be an additional relevant factor in tumour angiogenesis in malignant pleural mesotheliomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050171
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  • 9
    Electronic Resource
    Electronic Resource
    Expression of type IV collagenase correlates with the expression of vascular endothelial growth factor in primary non-small cell lung cancer (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 652-658 
    Details
    ISSN: 1432-1335
    Keywords: Key words Type IV collagenase ; Vascular endothelial growth factor ; Angiogenesis ; non-small cell lung cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tumor growth and metastasis are angiogenesis-dependent processes initiated and regulated by a number of cytokines. Vascular endothelial growth factor (VEGF) is a potent angiogenic protein with a selective mitogenic effect on vascular endothelial cells, known to be involved in physiological (embryogenesis) and pathophysiological (rheumatoid arthritis, tumor) angiogenesis. An increased expression of matrix metalloproteinase type IV collagenase has been reported in invading endothelial cells in vitro and in malignant cells, degrading structures of the basement membranes in various human malignancies. In the present study we investigated the expression of the genes for type IV collagenase and vascular endothelial growth factor (VEGF) in 40 cases of primary non-small-cell lung cancer (NSCLC). Specimens were immunostained by an antibody directed against VEGF and mRNA transcripts of VEGF and type IV collagenase were localized by non-radioactive in situ hybridization. VEGF mRNA was detected in 33 neoplasms, while in 23 cases transcripts of the type IV collagenase gene were visualized by digoxigenin-labeled cDNA probes. Transcripts of both mRNAs were detected in malignant cells. Furthermore, anti-VEGF immunostaining was present in newly formed microvessels close to the atypical cells, and mRNA of type IV collagenase was present in stromal cells adjacent to the tumor. A statistically significant correlation was found between the expression of type IV collagenase and VEGF (P=0.0061). These data suggest a double role for type IV collagenase in the metastatic process of NSCLC: (1) facilitating the invasion of tumor cells by the proteolytic cleavage of the basement membrane and (2) similarly supporting the endothelial cell invasion essential for tumor angiogenesis. Furthermore, our findings sustain the hypothesis that metastatic spread and angiogenesis are associated with a clonal expansion of highly angiogenic and invasive tumor cell clones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050120
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  • 10
    Electronic Resource
    Electronic Resource
    Neoplastic cells in the cerebrospinal fluid in intravascular lymphomatosis (2000)
    Springer
    Journal of neurology 247 (2000), S. 656-658 
    Details
    ISSN: 1432-1459
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00007809
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