Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Language
Year range
1.
Chinese Journal of Pathology ; (12): 517-522, 2008.
Article in Chinese | WPRIM | ID: wpr-315136

ABSTRACT

<p><b>OBJECTIVE</b>To study the clonality of gastric carcinoma and precancerous lesions and its relationship with Ki-67 protein expression.</p><p><b>METHODS</b>Formalin-fixed paraffin embedded tissues were collected from 174 cases of gastric endoscopic biopsies and surgical removed specimens. The lesional tissues were isolated by Laser Capture Microdissection. Methylation sensitive restriction enzyme (HpaII) digestion and polymerase chain reaction (PCR) were used to detect the clonality at the polymorphic human androgen receptor gene locus on the X chromosome. PCR products were analyzed by capillary electrophoresis using applied Biosystems 3730 DNA Analyzer. In addition, a two-step immunohistochemical staining EnVision method was used to detect the expression of Ki-67 protein.</p><p><b>RESULTS</b>The frequency of detection of monoclonality and expression rate of Ki-67 were found increased in a stepwise fashion from gastrointestinal metaplasia, low grade intraepithelial neoplasia, high grade intraepithelial neoplasia to intestinal carcinoma (15.63%, 5/32; 22.22%, 10/45; 69.44%, 25/36 and 100.0%, 20/20; respectively). The presence of clonal proliferation was correlated with Ki-67 expression in low grade intraepithelial neoplasia (P < 0.01).</p><p><b>CONCLUSIONS</b>The presence of clonal proliferation and increased Ki-67 are increasingly detected in the lesions along the multi-step gastric carcinogenesis model. Clonal status is associated with the expression rate of Ki-67 to a certain extent, suggesting a combined application of both markers may be useful in assessing early stages of gastric carcinoma.</p>


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Middle Aged , Young Adult , Cell Line, Tumor , Ki-67 Antigen , Genetics , Metabolism , Neoplasm Staging , Precancerous Conditions , Genetics , Metabolism , Pathology , Stomach Neoplasms , Metabolism , Pathology
2.
Chinese Journal of Oncology ; (12): 192-195, 2006.
Article in Chinese | WPRIM | ID: wpr-308385

ABSTRACT

<p><b>OBJECTIVE</b>This study was designed to investigate the significance of hTERT mRNA in breast carcinogenesis and to explore the diagnostic efficacy, and to study the effect of tumor suppressor gene p53 on the expression of hTERT mRNA.</p><p><b>METHODS</b>The expression of hTERT mRNA was examined by in situ hybridization in 12 cases of normal breast tissue nearby cancer, 7 of simple ductal hyperplasia, 20 of atypical hyperplasia, 18 of ductal carcinoma in situ and 25 with invasive ductal carcinoma. The expression of p53 protein were examined by immunohistochemistry in 43 carcinomas.</p><p><b>RESULTS</b>hTERT was not detected in normal breast tissue nearby cancer and simple ductal hyperplasia. The positive rate of hTERT mRNA in atypical hyperplasia, ductal carcinoma in situ and invasive ductal carcinoma were 25.0%, 83.3% and 88.0%, respectively. The prevalence and intensity of hTERT mRNA expression were much greater in carcinoma than those in simple or atypical hyperplasia and normal breast tissue nearby cancer (P < 0.05). The expression of hTERT was not correlated with tumor size and lymph node metastasis (P > 0.05). The positive correlation between hTERT mRNA and p53 was found in breast carcinoma (r = 0.5540, P < 0.01).</p><p><b>CONCLUSION</b>hTERT mRNA expression is closely related to the malignant transformation of breast tissue. Semi-quantitative detection of hTERT mRNA expression in situ is helpful in differentiated diagnosis of carcinoma in situ and atypical hyperplasia. Inactivation of p53 may play a role in the transcriptive activation of hTERT gene in breast carcinoma.</p>


Subject(s)
Adult , Humans , Middle Aged , Breast , Metabolism , Pathology , Breast Neoplasms , Genetics , Metabolism , Pathology , Carcinoma, Ductal, Breast , Metabolism , Pathology , Carcinoma, Intraductal, Noninfiltrating , Metabolism , Pathology , Diagnosis, Differential , Disease Progression , Hyperplasia , Lymphatic Metastasis , RNA, Messenger , Genetics , Telomerase , Genetics , Tumor Suppressor Protein p53
SELECTION OF CITATIONS
SEARCH DETAIL