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  • 1
    Electronic Resource
    Electronic Resource
    Assessment of invasive growth pattern and lymphocytic infiltration in colorectal cancer (1996)
    Oxford UK : Blackwell Science Ltd
    Histopathology 28 (1996), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A total of 122 specimens of colorectal cancer were re-assessed in relation to the reporting of invasive growth pattern (expanding vs. infiltrating) and presence or absence of peritumoral lymphocytic infiltrate as used in the Jass prognostic classification. Jass agreed with 69% of cases reported as infiltrating and 90% of those reported as expanding. This parameter was distributed similarly amongst Dukes B and C cases in the original assessment (P = 0.27), whereas in the reviewed data infiltrating cases were more likely to be staged as Dukes C (P = 0.04). Jass agreed with 44% of lymphocyte present and 94% of lymphocyte absent assessments. The original lymphocyte assessments showed no significant differences in distribution between Dukes A and B cases (P = 0.12) or B and C cases (P = 0.75), whereas the reviewed data showed significant differences for A vs. B (P = 0.015) and B vs. C cases (P = 0.0025). Criteria for assessment were circulated to eight observers who revisited 20 of the cases in which there was disagreement. Consensus agreement with Jass was achieved in nine of 10 cases for invasive growth pattern and seven of 10 cases for lymphocyte infiltration (with two being evenly split). Most observers showed at least fair levels of agreement with Jass and some achieved excellent levels of agreement. This study indicates that assessment of criteria used in the Jass prognostic system for colorectal cancer is less than optimal in routine practice, but is improved through the provision of simple guidelines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.1996.d01-467.x
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  • 2
    Electronic Resource
    Electronic Resource
    When can complete regression of low-grade gastric lymphoma of mucosa-associated lymphoid tissue be predicted after Helicobacter pylori eradication? (2000)
    Oxford, UK : Blackwell Science Ltd
    Histopathology 37 (2000), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims: Recent studies suggest that primary low-grade gastric lymphomas of mucosa-associated lymphoid tissue (MALT) are cured in many cases between 1 and 18 months after H. pylori eradication. The aim of this study is to elucidate when complete regression (CR) of MALT lymphoma can be histologically predicted after H. pylori eradication.Methods and results: Twenty-one patients with low-grade gastric MALT lymphoma were treated with triple therapy (amoxicillin, clarythromycin and proton pump inhibitor) for 14 days. Subsequently, they were followed up by sequential endoscopy and biopsy (number of biopsy specimens for each endoscopy is 3–8, with an average of 4) from 91 to 657 days (average: 309 ± 165 days). Eradication of H. pylori infection was achieved in all patients. Nine patients were free of lymphoma at 1 to 2 months after eradication and remained in CR at 163–657 days. Twelve patients showed residual lymphoma at 1 to 2 months after eradication. Five out of 12 patients revealed only one or two small foci of lymphoma-cell aggregation and showed a high incidence (80%) of CR at the latest biopsy (135–434 days, average 276 ± 115 days after eradication), while seven patients showed diffuse remains of lymphoma cells and indicated CR in only one case (14%) at 362 days, partial regression in five cases at 130–431 days (average 227 ± 114 days), and no change in one case at 91 days after eradication.Conclusions: These results suggest that CR of low-grade MALT lymphoma can be predicted at 1 to 2 months after eradication therapy by checking histological changes of MALT lymphoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.2000.00927.x
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  • 3
    Electronic Resource
    Electronic Resource
    Sensitivity of biopsy site in evaluating regression of gastric atrophy after Helicobacter pylori eradication treatment (2002)
    Oxford UK : Blackwell Science Ltd.
    Alimentary pharmacology & therapeutics 16 (2002), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Helicobacter pylori infection is a major cause of the progress of gastric glandular atrophy, a high-risk background factor in the development of gastric cancer. Regression of gastric atrophy is critical to prevention of cancer by H. pylori eradication treatment. However, it is controversial whether gastric atrophy regresses after H. pylori eradication.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To determine the most sensitive and appropriate biopsy site for evaluation of regression of atrophy after treatment.〈section xml:id="abs1-3"〉〈title type="main"〉Subjects and methods:Thirty-eight patients who showed regression of gastric atrophy in histology after treatment were investigated. Four biopsy specimens from the lesser and greater curvatures in the antrum and corpus were evaluated before and after treatment according to the Updated Sydney System.〈section xml:id="abs1-4"〉〈title type="main"〉Results:Regression of atrophy after treatment was seen in 30 of 38 biopsy specimens from the lesser curvature of the corpus (79%), and this site was most sensitive. Odds ratio of this site to the others was 8.28. Regression of atrophy in this site was observed at 12.2 months in the younger patients and 15.9 months in the elder patients.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:Biopsy sampling from the lesser curvature of the corpus is the most sensitive and appropriate for evaluation of regression of gastric atrophy after H. pylori eradication treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.16.s2.17.x
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  • 4
    Electronic Resource
    Electronic Resource
    Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non-polyposis colorectal cancer (1997)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Histopathology 30 (1997), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non-polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non-polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra- and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki-67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.1997.d01-589.x
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  • 5
    Electronic Resource
    Electronic Resource
    Correlation of p53 protein expression with apoptotic incidence in colorectal neoplasia (1995)
    Springer
    Virchows Archiv 427 (1995), S. 27-32 
    Details
    ISSN: 1432-2307
    Keywords: Apoptosis ; p53 Expression ; Colorectal cancer ; Ki-67
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The wild-type p53 gene suppresses cell proliferation and induces apoptosis when it is transfected into human colon cancer cell lines. Therefore, mutation of the p53 gene, which correlates closely with p53 protein overexpression, would be predicted to activate cell proliferation and limit apoptosis. We tested this hypothesis by correlating p53 protein expression with cell proliferation and apoptosis in 70 neoplasms (29 adenomas and 41 carcinomas) using p53 and Ki-67 immunohistochemical staining and DNA nick end labelling. The p53 immunoreactivity was independent of the Ki-67 positivity. The apoptotic incidence was less frequent (P〈0.005) in tumours with diffuse p53 protein overexpression than in those with the sporadic overexpression, defined as p53 staining of isolated or scattered expression. In addition, apoptotic incidence only correlated directly (P〈0.05) with Ki-67 positivity in tumours with sporadic p53-protein expression. These results indicate that p53 protein that is expressed sporadically in colorectal neoplasms is probably wild-type protein and induces apoptosis in response to active cell proliferation. In contrast, diffusely overexpressed p53 protein in colorectal neoplasms is probably mutant and correlates with a reduction in apoptotic cell death independently of cell proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00203734
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  • 6
    Electronic Resource
    Electronic Resource
    Histological and Genetic Changes in Malignant Transformation of Gallbladder Adenoma (1999)
    Springer
    Annals of oncology 10 (1999), S. 136-139 
    Details
    ISSN: 1569-8041
    Keywords: carcinoma-in-adenoma ; carcinoma ; gallbladder adenoma ; genetic pathways of carcinoma ; K-ras ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Design: Elucidate the histological and genetic changes in malignant transformation of adenoma of the gallbladder. Materials and methods: Forty-three adenomas and 20 intramucosal tumors of carcinoma-in-adenomas were studied for histological and genetic changes (particularly K-ras mutation and p53 protein overexpression by immunohistochemistry) in malignant transformation. The genetic changes were compared with those of 164 carcinomas without anomalous union and 17 carcinomas with anomalous union of pancreatico-biliary duct. Results: Atypical cell foci, i.e. spindle cell foci, were observed only in the adenoma area, with a frequency of 23% in 39 adenomas, and of 45% in 20 tumors of carcinoma-in-adenoma. 129 of 130 spindle cell foci examined were negative for Ki-67 staining and all the spindle cell foci were negative for p53 stain. K-ras mutation and p53 overexpression were not found in all adenomas, pure and with carcinoma i.s., and only one carcinoma (1/16, 6%) with adenoma showed p53 overexpression. K-ras mutation was low (10%, 4/40) in carcinomas without adenoma, but high in carcinomas with anomalous union of pancreatico-biliary duct. While, p53 overexpression was high and similar in carcinomas with and without anomalous union. Conclusions: These results suggest that there are three distinct pathways in gallbladder carcinogenesis; that is, de novo carcinoma develops from a predominant p53 alteration with low K-ras mutation, de novo carcinoma with anomalous union from K-ras mutation and p53 mutation, and carcinoma-in-adenoma from K-ras-, p53-, and probably APC-gene-related, as yet unknown, alteration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008330012536
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