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  • 1
    Electronic Resource
    Electronic Resource
    p53 gene mutations and expression of p53 and mdm2 proteins in invasive breast carcinoma (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 388-394 
    Details
    ISSN: 1432-1335
    Keywords: Key words p53 ; mdm2 ; p53 gene mutation ; Breast carcinoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the study was to analyze p53 gene mutations and the expression of p53 and mdm2 proteins in 31 randomly selected invasive breast carcinomas. The results were then correlated with tumor grade, stage, estrogen receptor status, nodal status, and DNA ploidy. The expression of the proteins p53 and mdm2 was determined immunohistochemically using formalin-fixed, paraffin-embedded material. Screening for p53 mutation involved analysis of the highly conserved regions of the p53 gene (exons 5–9) by the polymerase chain reaction/single-strand conformation polymorphism (PCR-SSCP) technique. PCR products with band shifts were directly sequenced. Immunohistochemical staining of p53 was positive in 9 cases (29.0 %), only 2 of which showed a p53 gene mutation. These were identified as a C→G transversion at the second position of codon 278 in exon 8 and an A→G transition at the second position of codon 205 in exon 6. A third case with a mutation was observed (C→T transition, position 1 of codon 250 in exon 7) that did not show p53 immunohistochemically. Of the 9 p53-positive tumors, 2 were moderately differentiated (grade II). The remaining tumors were poorly differentiated (7/9). By contrast, p53-negative carcinomas were well differentiated (grade I) in most cases (P = 0.02). DNA cytometry in 8 of the 9 p53-positive carcinomas revealed an aneuploid stem line. The majority of the p53-negative tumors were diploid (P = 0.01). Mdm2 oncoprotein was detected in 10 tumors (32.2 %), 4 of which were p53-positive, including the 3 with mutations. The grading of the mdm2-positive tumors was moderate or poor, G1 carcinomas were always noted to be mdm2-negative (P = 0.04). Overexpression of p53 protein is a complex mechanism and does not merely indicate the detection of mutations in the p53 gene. This study has shown that p53 expression correlates with tumor grade and DNA ploidy. Mdm2 expression was also associated with the tumor grade. Immunohistological demonstration of the p53 protein alone is insufficient as a basis for comment on the functional state of the p53 gene and gene product. The interrelation between recognition of the p53 protein and gene mutation needs more careful assessment to define their roles in the control of neoplasia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01240122
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  • 2
    Electronic Resource
    Electronic Resource
    Gastrointestinale Stromatumoren (GIST) – Probleme in Diagnostik und Therapie (1999)
    Springer
    Der Chirurg 70 (1999), S. 807-812 
    Details
    ISSN: 1433-0385
    Keywords: Key words: Stromal tumors ; GIST ; Surgical therapy ; Gastrointestinal tract. ; Schlüsselwörter: Stromatumoren ; GIST ; chirurgische Therapie ; Gastrointestinaltrakt.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Die gastrointestinalen Stromatumoren (GIST) sind eine seltene, auch heute noch nicht vollständig aufgeklärte Gruppe von Neoplasien des Magen-Darm-Trakts. Trotz vieler Fortschritte der diagnostischen Möglichkeiten ist eine Zuordnung der GIST hinsichtlich ihrer Histogenese und Dignität nicht eindeutig. Im Zeitraum von 1994 bis 1998 wurden in der Klinik für Chirurgie 18 Patienten mit einem GIST operiert. Dabei handelte es sich um 12 (67 %) gastrale und 6 (33 %) intestinale Stromatumoren. Der Primärtumor konnte bei allen Patienten durch eine R0-Resektion entfernt werden. Bei 6 Patienten kam es zu einer hämatogenen Lebermetastasierung, die Größe des Primärtumors betrug bei diesen Patienten mehr als 10 cm. Eine extrahepatische Fernmetastasierung ließ sich in allen untersuchten Fällen nicht nachweisen. Eine Lymphknotenmetastasierung konnte in den regionären Lymphknoten nicht festgestellt werden. Eine systematische Lymphadenektomie ist nicht indiziert. Die histologische Beurteilung der Dignität erfolgte auf der Grundlage der von Lewin, Weinstein und Riddell vorgeschlagenen Richtlinien. Das derzeit gesicherte therapeutische Vorgehen besteht in der kurativen Resektion des Primärtumors sowie der Metastasen mit histologisch tumorfreien Resektionsrändern. Das Tumorrezidiv ist ebenso zu behandeln. Adjuvante oder neoadjuvante chemotherapeutische Ansätze zeigen bisher keine Erfolge.
    Notes: Summary. Gastrointestinal stromal tumors (GIST), which form a rare group of neoplasias of the gastrointestinal tract, have not yet been fully investigated. Although good progress has been made in their diagnosis, classification of these lesions with regard to their histogenesis and biological behavior remains problematic. Between 1994 and 1998, 18 GIST patients underwere operation in the Department of Surgery. Twelve of these patients (67 %) had stromal tumors in the stomach, and six (33 %) had intestinal stromal tumors. The primary tumor could be removed in all patients with R0 resection. Six patients developed hematogenous liver metastasis, with the size of their primary tumor exceeding 10 cm. Extrahepatic distant metastases were not found in any case. Lymphadenectomy showed that lymph node metastases did not occur. Histological evaluation was made according to the guidelines of Lewin, Weinstein and Riddell. Currently established therapy is limited to complete surgical resection of the primary tumor and its metastases. Adjuvant or neoadjuvant chemotherapy approaches have failed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001040050728
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of MDR1/p-glycoprotein and multidrug resistance-associated protein in childhood solid tumours (1997)
    Springer
    Virchows Archiv 430 (1997), S. 99-105 
    Details
    ISSN: 1432-2307
    Keywords: Multidrug resistance ; P-glycoprotein Neuroblastoma ; Nephroblastoma ; Reverse transcriptase polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We evaluated the expression of MDR1/p-glycoprotein in paediatric tumours using reverse transcriptase polymerase chain reaction (RT-PCR), RNA dot blot analysis, and immunohistochemistry on formalin fixed paraffin-embedded material with JSB-1 and C-219 monoclonal antibodies, and compared these three techniques. The expression of multidrug resistance-associated protein (MRP) gene was examined by RT-PCR assay. We studied MDR1/p-glycoprotein and MRP expression in 13 samples from 10 neuroblastoma patients, 11 samples from 10 nephroblastoma patients, 2 rhabdomyosarcomas, 1 adrenocortical carcinoma and 10 benign tumours or tumour-like lesions. Eleven of 13 neuroblastomas, 7 of 11 nephroblastomas, 2 rhabdomyosarcomas, 1 adrenocortical carcinoma, and 7 of 10 benign tumours or tumour-like lesions showed MDR1 PCR products. By RNA dot blot analysis, MDR1 transcripts were detectable in 11 of 34 specimens. Immunohistochemically, we detected positive reaction products for JSB-1 in 26 of 36 samples. There was a significant correlation between the immunoreactivity for JSB-1 and the expression of MDR1 mRNA expression by RTPCR (P=0.0001). However, the presence of p-glycoprotein immunostaining does not correlate with the MDR1 expression shown by RT-PCR in every case. As for MRP mRNA expression, 9 of 13 neuroblastomas and 10 of 11 nephroblastomas revealed PCR products.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01008030
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  • 4
    Electronic Resource
    Electronic Resource
    No correlation of c-myc overexpression and p53 mutations in liposarcomas (1998)
    Springer
    Virchows Archiv 433 (1998), S. 315-321 
    Details
    ISSN: 1432-2307
    Keywords: Key words Liposarcoma ; c-myc gene expression ; p53 gene mutations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Although it is well known that oncogenesis is a multistep process involving the activation of normal cellular genes to become oncogenes and/or the inactivation of tumor suppressor genes, this process has seldom been investigated in soft tissue tumours. We screened a group of 36 liposarcomas for genetic abnormalitis in the p53 tumour suppressor gene and c-myc oncogene. Altered c-myc gene expression was examined by differential RT-PCR assay. p53 Gene mutations in exons 4–8 were analysed by using PCR-SSCP analysis and direct sequencing. Elevated c-myc expression was found in 6 of 31 liposarcomas (19.4%). p53 Gene mutations were observed in 5 of 36 liposarcomas (13.9%). Both genetic alterations were associated with the histological subtype of liposarcomas. Whereas c-myc gene expression was a characteristic of myxoid/round cell liposarcomas, p53 gene mutations were found more frequently in pleomorphic variants. Liposarcomas of the well-differentiated subtype showed neither p53 gene mutations nor altered c-myc gene expression. Our results indicate that the c-myc oncogene and the p53 tumor suppressor gene do not seem to cooperate in the oncogenesis of liposarcomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050255
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  • 5
    Electronic Resource
    Electronic Resource
    The urokinase plasminogen activator (u-PA) and its inhibitor (PAI-1) in embryo-fetal bone formation in the human: an immunohistochemical study (1995)
    Springer
    Anatomy and embryology 192 (1995), S. 363-368 
    Details
    ISSN: 1432-0568
    Keywords: Plasminogen activator ; Plasminogen activator inhibitor ; Bone formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of urokinase plasminogen activator and plasminogen activator inhibitor-1 in human embryofetal bone formation between the 9th and the 20th week of gestation has been studied immunohistochemically. While mature osteocytes of the secondary spongiosa and resting chondrocytes of the bone epiphyses were negative for both antigens in each developmental stage, metabolically active parts of the osseocartilaginous system showed a strong immunoreactivity. Until the end of the 10th week of gestation urokinase plasminogen activator and plasminogen activator inhibitor-1 could not be demonstrated in the shaft of the preexisting cartilaginous models of bones, which correlates with the morphological developmental stage of the embryos. Later, osteoblasts and chondrocytes in the areas of enchondral ossification, and the perivascular chondrocytes of the epiphyseal secondary ossification centres, showed similarly high concentrations of urokinase plasminogen activator and plasminogen activator inhibitor-1. Moreover, the individual ossification stages of the different bones in embryo-fetal development could be demonstrated immunohistochemically. While humeri and femora showed diaphyseal immunoreactivities at an early stage, positive reactions in the phalanges were found only much later. Thus, the enzymes of the fibrinolytic system studied are clearly involved in the desmal and enchondral ossification process in the osseocartilaginous compartment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00710105
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  • 6
    Electronic Resource
    Electronic Resource
    Pathologie des Ewing-Sarkoms (1996)
    Springer
    Der Pathologe 17 (1996), S. 6-17 
    Details
    ISSN: 1432-1963
    Keywords: Schlüsselwörter Ewing-Sarkom ; Key words Ewing's sarcoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Ewing's sarcoma is a very rare tumor which has, however, attracted much oncological interest since the dramatic improvement of its prognosis under chemotherapy. Its histogenesis has been discussed controversially for a long time, including a possible origin in immature reticulum, myogenous, endothelial and undifferentiated mesenchymal cells. Repeated reports have also suggested a possible neuroectodermal genesis. Convincing arguments, however, have only been brought forward during recent years, since it was found that Ewing's sarcoma and malignant peripheral neuroectodermal tumor share a common chromosome translocation 11;22. In the meantime this hypothesis has been strengthened by numerous cell biological analyses. There seems to be no clear border between Ewing's sarcoma and malignant peripheral neuroectodermal tumors with definite neural differentiation. Histological differential diagnosis of Ewing's sarcoma has been improved by immunohistological methods. In most cases, they can be distinguished from lymphoma (leucocyte common antigen, B and T markers) and embryonal rhabdomyosarcoma (muscle specific actin, desmin) without problems. Apart from that, it is possible nowadays to obtain antibodies against the MIC 2-protein, which is preferably expressed in Ewing sarcoma. The diagnostics of Ewing's sarcoma and the malignant peripheral neuroectodermal tumor have considerably been enriched by the fact that the specific chromosome translocation t(11;22) can be proved molecular biologically. In contrast to the cytogenetic evidence, it is not necessary to establish cell cultures.
    Notes: Zusammenfassung Das Ewing-Sarkom ist ein sehr seltener Tumor, der jedoch in den Blickpunkt des onkologischen Interesses gelangt ist, seit seine Prognose unter Chemotherapie sich dramatisch verbessert hat. Die Ansichten zu seiner Histogenese waren lange Zeit strittig. Es wurde eine Herkunft von unreifen Retikulumzellen, myogenen Zellen, Endothelzellen und undifferenzierten Mesenchymzellen diskutiert. Auch auf eine mögliche neuroektodermale Genese ist immer wieder hingewiesen worden. Überzeugende Argumente hierfür wurden jedoch erst in den letzten Jahren vorgelegt, nachdem sich herausgestellt hat, daß das Ewing-Sarkom und der maligne periphere neuroektodermale Tumor eine gemeinsame Chromosomentranslokation aufweisen t(11;22). Mittlerweile wurde diese Hypothese durch zahlreiche zellbiologische Untersuchungen erhärtet. Offensichtlich gibt es fließende Übergänge von den Ewing-Sarkomen zu malignen peripheren neuroektodermalen Tumoren mit eindeutiger neuraler Differenzierung. Die histologische Differentialdiagnostik des Ewing-Sarkoms wurde durch immunhistologische Methoden verbessert. Eine Abgrenzung gegen Lymphome (Leucocyte common antigen, B- und T-Marker) und embryonale Rhabdomyosarkome (Muskelspezifisches Aktin, Desmin) ist so meist problemlos möglich. Darüber hinaus stehen jetzt Antikörper gegen das MIC 2-Protein zur Verfügung, das vorzugsweise im Ewing-Sarkom exprimiert wird. Eine wesentliche Bereicherung hat die Diagnostik des Ewing-Sarkoms und des malignen peripheren neuroektodermalen Tumors dadurch erfahren, daß die spezifische Chromosomentranslokation t(11;22) auch molekularbiologisch nachweisbar ist. Im Gegensatz zum zytogenetischen Nachweis ist es hierfür nicht erforderlich, Zellkulturen anzulegen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002920050129
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  • 7
    Electronic Resource
    Electronic Resource
    MDM2 amplification and loss of heterozygosity at Rb and p53 genes: no simultaneous alterations in the oncogenesis of liposarcomas (1998)
    Springer
    Journal of cancer research and clinical oncology 124 (1998), S. 532-540 
    Details
    ISSN: 1432-1335
    Keywords: Key wordsMDM2 amplification ; Rb LOH ; p53 LOH ; p53 mutation ; Liposarcoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: The present study aimed to investigate the status of alterations of the MDM2, Rb and p53 genes in a series of 45 liposarcomas. Furthermore, the possible correlation with histological and clinical parameters was studied. Methods: MDM2 amplification was examined by non-radioactive Southern blot hybridization with a human MDM2 cDNA probe. Mutations in the p53 gene were screened by polymerase chain reaction/single-strand conformation polymorphism analysis and direct sequencing. To study loss of heterozygosity (LOH) at the tumor-suppressor genes Rb and p53, we used four polymorphic intragenic Rb markers (introns 1, 17, 20, and 25) and two p53 markers (intron 1 and exon 4). Results: MDM2 amplification was found in 19 of 45 liposarcomas (42.2%). The frequency of LOH in Rb and p53 was nearly identical (22%). In 4 of 9 tumors (44.4%) with LOH, allelic loss was a concurrent event in both genes. Of 45 liposarcomas, 6 (13.3%) showed p53 mutations. Overall, alterations of the p53/MDM2/Rb pathway occurred in 30 of 45 liposarcomas (66.6%). In contrast to myxoid and pleomorphic variants, well-differentiated liposarcomas were characterized by a high frequency of MDM2 amplification, a lack of LOH of Rb and p53, and p53 mutations. Conclusions: Obviously MDM2 amplification and LOH at the Rb and p53 genes do not occur simultaneously in the oncogenesis of liposarcomas, as is the case for MDM2 amplification and p53 gene mutations (with one exception). We suggest that well-differentiated, myxoid and pleomorphic liposarcomas are characterized by a different pattern of molecular alterations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050211
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  • 8
    Electronic Resource
    Electronic Resource
    p53 gene mutations in soft-tissue sarcomas – correlations with p53 immunohistochemistry and DNA ploidy (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 211-218 
    Details
    ISSN: 1432-1335
    Keywords: Key words Soft-tissue tumors ; p53 gene mutation ; p53 immunohistochemistry ; PCR SSCP analysis ; DNA ploidy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The significance of p53 mutations in a group of 67 soft-tissue tumors was examined using single-strand conformation polymorphism and direct sequencing analysis. Molecular findings were correlated with immunohistochemical detection of the p53 protein and DNA ploidy status. Mutations of the p53 gene were detected in 13 (19.5%) out of 67 cases of soft-tissue tumors. Only three were localized outside the conservative regions of the p53 gene. Six mutations were described for the first time in these tumors. Most of the mutations were point mutations in exons 5 – 8 and, in one case, a deletion at the 3′-splice site of exon 5 could be demonstrated. There was no significant correlation between the occurrence of p53 mutations and the histological grade, although a high number of mutations were defined in poorly differentiated tumors (grade 3). Molecular finding of a p53 gene mutation and immunohistochemical detection of p53 expression did not correlate, which may be due to the high percentage of nonsense mutations in our study (50%). We confirm that only DNA sequencing allows a unique identification and differentiation of mutations in the p53 gene. Other factors may be responsible for the detection of p53 protein in many cases. Histological grade correlated with aneuploidy. The frequency of mutations observed was in accordance with values quoted in the literature. Generally, p53 mutations and p53 overexpression are more likely to represent a late event in the oncogenesis of soft-tissue tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01240317
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  • 9
    Electronic Resource
    Electronic Resource
    Expression of multidrug resistance-associated protein gene in Ewing’s sarcoma and malignant peripheral neuroectodermal tumor of bone (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 237-239 
    Details
    ISSN: 1432-1335
    Keywords: Key words Ewing’s sarcoma ; Multidrug resistance gene ; Anti-cancer-drug resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The expression of multidrug resistance-associated protein (MRP) mRNA was examined in ten samples of Ewing’s sarcoma of bone (ES) and in one nude mice transplantable ES and two malignant peripheral neuroectodermal tumor (MPNT) cell lines using an RT-PCR assay. MRP mRNA expression was recognized in eight of the ten clinical specimen and in all three cell lines. On the other hand, the expression of multidrug resistance gene (MDR1) was demonstrated in three of the ten clinical samples and all three cell lines. Our results may contribute to elucidation of the mechanism of anti-cancer-drug resistance in this tumor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01240323
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  • 10
    Electronic Resource
    Electronic Resource
    p53 gene mutations and expression of p53 and mdm2 proteins in invasive breast carcinoma (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 388-394 
    Details
    ISSN: 1432-1335
    Keywords: p53 ; mdm2 ; p53 gene mutation ; Breast carcinoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the study was to analyzep53 gene mutations and the expression of p53 and mdm2 proteins in 31 randomly selected invasive breast carcinomas. The results were then correlated with tumor grade, stage, estrogen receptor status, nodal status, and DNA ploidy. The expression of the proteins p53 and mdm2 was determined immunohistochemically using formalin-fixed, paraffin-embedded material. Screening for p53 mutation involved analysis of the highly conserved regions of thep53 gene (exons 5–9) by the polymerase chain reaction/single-strand conformation polymorphism (PCR-SSCP) technique. PCR products with band shifts were directly sequenced. Immunohistochemical staining of p53 was positive in 9 cases (29.0%), only 2 of which showed ap53 gene mutation. These were identified as a C→G transversion at the second position of codon 278 in exon 8 and an A→G transition at the second position of codon 205 in exon 6. A third case with a mutation was observed (C→T transition, position 1 of codon 250 in exon 7) that did not show p53 immunohistochemically. Of the 9 p53-positive tumors, 2 were moderately differentiated (grade II). The remaining tumors were poorly differentiated (7/9). By contrast, p53-negative carcinomas were well differentiated (grade I) in most cases (P=0.02). DNA cytometry in 8 of the 9 p53-positive carcinomas revealed an aneuploid stem line. The majority of the p53-negative tumors were diploid (P=0.01). Mdm2 oncoprotein was detected in 10 tumors (32.2%), 4 of which were p53-positive, including the 3 with mutations. The grading of the mdm2-positive tumors was moderate or poor, G1 carcinomas were always noted to be mdm2-negative (P=0.04). Overexpression of p53 protein is a complex mechanism and does not merely indicate the detection of mutations in thep53 gene. This study has shown that p53 expression correlates with tumor grade and DNA ploidy. Mdm2 expression was also associated with the tumor grade. Immunohistological demonstration of the p53 protein alone is insufficient as a basis for comment on the functional state of thep53 gene and gene product. The interrelation between recognition of the p53 protein and gene mutation needs more careful assessment to define their roles in the control of neoplasia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01240122
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