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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 119 (1993), S. 155-159 
    ISSN: 1432-1335
    Keywords: MNNG ; Carcinogenesis ; Gastric mucosa ; Rats ; Lectins ; Glycoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect ofN-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on the mucin phenotype of non-metaplastic gastric mucosa in the rat was studied histochemically. Animals were exposed to MNNG in drinking water (83 mg/l) for 12 weeks. Carcinogen treatment was then discontinued and the animals (27 in the treatment group and 25 in the control group) were examined after another 44 weeks. Glycosylation was analysed with histochemical stains for sialomucins and sulphomucins and with peroxidase-conjugated lectins (GS-II, SBA, DBA, UEA-I, and WGA). Sialo-and sulphomucins remained quantitatively unchanged, only a slight increase of acid mucins in the antral glands was observed. The analysis of the lectin binding patterns, however, revealed a significant increase for WGA-binding glycoproteins in the surface mucous cells and gastric pits, while DBA binding was significantly decreased (P〈0.05). GS-II lectin bound specifically to the proliferative compartment in the gastric fundus, consisting of mucous neck cells, and was significantly increased after MNNG treatment. No specific alterations were detected in lectin binding to parietal or chief cells. It is concluded, therefore, that treatment of gastric mucosa with MNNG alters the glycoprotein metabolism before intestinal metaplasia can be observed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Breast cancer research and treatment 59 (2000), S. 185-192 
    ISSN: 1573-7217
    Keywords: BRCA1 mutation ; breast cancer ; disease-free survival ; overall survival ; pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Reports from different countries have been inconclusive in attempting to relate the BRCA1 mutation status to the survival of breast cancer patients. The purpose of this study was to investigate overall and disease-free survival for German hereditary breast cancer patients. Data on clinical outcome and data on age at diagnosis of breast cancer, histology, tumor size, lymph node status, histological grade, and laterality of 36 breast cancer patients from 12 families with a BRCA1 mutation and from one family with strong evidence for linkage to BRCA1 were compared with those of 49 hereditary breast cancer patients from 23 families that did not harbor a BRCA1 mutation. Overall and disease-free survival was estimated for both groups. BRCA1 mutation carriers had a significantly earlier age of diagnosis than non-carriers (p = 0.0001) and more frequently developed contralateral breast cancer (p = 0.04). Also, BRCA1-associated tumors more frequently were of larger size (p = 0.041) and higher grade of malignancy (p = 0.005) than non-BRCA1-associated tumors. Whereas no difference in overall survival was seen, disease-free survival at 10 years differed significantly with 53.3% for BRCA1 mutation carriers and 76% for non- carriers (p = 0.02). However, after stratification for age and in multivariate analysis for mutation status, age, and bilaterality, it was shown that the worse prognosis for BRCA1 mutation carriers disappeared. Our results suggest that the worse prognosis of BRCA1 mutation carriers in terms of disease-free survival may in large part be due to the age of onset of breast cancer in this population. Thus, BRCA1 mutation status does not appear to be an independent prognostic factor.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7217
    Keywords: breast cancer ; CD44 variants ; metastasis ; tumor progression marker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Splice variants of CD44 expressed in a metastasizing cell line derived from a rat pancreatic adenocarcinoma have been shown recently to confer metastatic potential onto non-metastasizing rat pancreatic carcinoma and sarcoma cell lines. Homologues of these variants have also been detected in a variety of human malignancies. Using antibodies raised against a bacterially expressed fusion protein containing variant CD44 sequences, we have explored the expression of variant CD44 glycoproteins on tumors of the female breast. The material examined included normal tissue, hyperplastic lesions, 103 primary invasive mammary carcinomas, 10in situ carcinomas, 12 local recurrences and 18 lymph node metastases. Using a polyclonal serum directed against several variant CD44 epitopes, normal mammary epithelia as well as ductal hyperplasias were negative for these splice variants, while the variant CD44 epitopes were detectable in all but six of the primary invasive carcinomas. From the reaction with various monoclonal antibodies and polyclonal sera specific for individual epitopes it is obvious that the tumors predominantly express CD44 variants encoded by exons v5 to v7. Interestingly, all investigated lymph node metastases reacted positively with the variant-specific antibodies, in contrast to primary tumors which reacted in 54% to 86% of the cases, depending on the antibody used. Statistical analysis revealed a significant correlation between expression of variant exons v3/v4 and v6 and increased tumor grade (p = 0.001 and p 〈 0.05, respectively; Fisher's exact test). Exon v6 is carried by the variants which confer metastatic capability in the rat. These results indicate that the expression of the CD44 variants is upregulated in mammary carcinomas and is closely linked to tumor anaplasia.
    Type of Medium: Electronic Resource
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