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유방암에서 -Synuclein 과발현의 예후인자로서 유용성 및 HER-2/neu 유전자 증폭과 연관성
박찬흔 한국유방암학회 2007 Journal of breast cancer Vol.10 No.2
Purpose: Synuclein has been identified as an important neuroprotein for developing pathologic deposits in Alzheimer’s and Parkinson’s disease patients. -synuclein is also known as a breast cancer-specific gene 1 thats’s not found in normal breast tissues but it has been reported to be overexpressed in breast cancer, ovarian cancer and other tumors. To evaluate the availability of -synuclein expression as a prognostic factor for infiltrative breast cancer, we analyzed its correlation with the clinical parameters and the HER-2/neu gene expression. Methods: Two hundred fiffty samples of breast cancer tissues embedded in paraffin and that were obtained from the infiltrative breast cancer patients who were operated in our institution from January 1995 to December 2000 were analyzed with employing the tissue microarray technique. The expression of -synuclein was studied with immunohistochemistry and with using -synulcein antibodies. One hundred thirty one cases that showed favorable staining were selected and studied retrospectively. Results: Fiffty five% (71/131) of the patients showed -synuclein overexpression. The histopathological findings that significantly correlated with -synuclein overexpression were the number of metastatic lymph nodes (p<0.01) and the cancer stage (p<0.01). Using the same tissue mircoarray, the HER-2/neu gene expression and -synuclein expression also showed statistically significant correlation (p=0.04). Conclusion: -synuclein overexpression showed significant correaltion with lymph node metastasis and cancer stage. It also showed significant relevance with the HER-2/neu gene expression, and that is already known to be a prognostic factor for breast cancer. Therefore -synuclein may be a useful prognostic factor for infiltrative breast cancer and further studies on the its correlation with survival, local recurrence, and distant metastasis should be conducted.
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유방의 침윤성 관암에서 주요 종양 억제유전자의 이형접합 소실
박찬흔 한국유방암학회 2007 Journal of breast cancer Vol.10 No.1
Purpose: Breast cancer is one of the most frequent malignant tumors in Korea. The major tumor suppressor genes (TSGs) such as p16, Rb, E-cadherin and p53 may play important roles in cell cycle regulation, apoptosis and the regulation of the expression of other genes as well as tumor suppression. Microsatellite alteration such as loss of heterozygosity (LOH) have been reported to be a novel mechanism of carcinogenesis and a useful prognostic factor for many malignant tumors. Also, LOH is also known to be related with allelic loss of various TSGs. This study evaluated LOH of 4 TSGs in invasive ductal carcinomas (IDCs) and we correlated these results with the clinicopathological factors. Methods: LOH analysis was carried out using a polymerase chain reaction with 12 polymorphic microsatellite markers of 4 TSGs in 50 surgically resected tumors and their non-tumorous counterparts. Results: There was no detectable LOH in the normal tissue. LOH was detected in 86% of the 50 cases of IDCs. LOH was detected on al chromosomes and this showed a statistical difference between benign tumor and malignant tumor. LOH of p16, Rb, E-cadherin and p53 TSGs was detected in 36%, 26%, 54% and 60% of the tumors, respectively. LOH of the p16 and Rb genes was inversely correlated with tumor grade 1. The low rate of detecting LOH on the E-cadherin gene was noted in T1 tumor and stage I disease. LOH of the p53 gene correlated well with the tumor size and stage. The LOH-High results correlate well with the tumor size and stage and the LOH-High results are similar to those of the p53 gene LOH. Conclusion: These results suggest that LOH of the 4 major TSGs may contribute to the development and invasion of IDCs. Also, the combined use of various LOH markers may help in deciding the prognosis of IDCs.
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박찬흔 한국유방암학회 2007 Journal of breast cancer Vol.10 No.1
Purpose: Breast cancer shows various molecular and genetic alterations in its development and progression. Microsatellite alterations, and especially microsatellite instability (MSI) and loss of heterozygosity (LOH), have recently been postulated as a novel mechanism of carcinogenesis and as a useful prognostic factor for several gastrointestinal malignancies. LOH is related to the allelic loss of various tumor suppressor genes; however, MSI has been found to be the result of an erroneous DNA mismatch repair system and this has been known to be involved in the carcinogenesis of the hereditary non-polyposis colon cancers and some portion of the sporadic colorectal or gastric cancers. Yet MSI has rarely been studied in invasive ductal carcinoma. Our objectives were to evaluate the MSI and p53 protein expression in invasive ductal carcinomas and to correlate this with various clinicopathological factors. Methods: The MSI analysis was performed by using polymerase chain reaction with five polymorphic microsatellite markers (the BAT25, BAT26, D2S123, D5S346 and D17S250 loci as recommended by the 1998 NCI International Workshop on Microsatellite Instabilitis and RER phenotypes) in 50 surgically resected tumors and each of their non-tumorous counterpart. The p53 protein expression was studied using unohistochemistry. Results: MSI and a p53 protein expression were detected in 22% and 54% of the tumors and non-tumorous tissues, respectively. MSI was more frequently detected in tumor grade I, T-stage I, non-metastatic tumor and tumor stage I. Also there were rare cases showing a high grade and stage with metastasis in the MSI-high group, in which more than 3 microsatellite loci had MSI. The p53 expression results correlated well with a higher tumor grade. Correlation between MSI and the p53 expression was not found. Conclusion: These results may suggest that MSI may be involved in some portions in mammary carcinogenesis and tumor invasion. Also the clinical use of the MSI status may help to determine a better prognosis among invasive ductal cancer patients.
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유방의 침윤성 관암종에서 염색체 17p13의 이형접합 소실과 p53 단백 발현
박찬흔 한국유방암학회 2006 Journal of breast cancer Vol.9 No.4
Purpose: The p53 gene is located on chromosome 17p13 and may play important roles in cell cycle regulation, apoptosis and the regulation of the expression of other genes as well as tumor suppression. In addition, the p53 gene is believed to play an important role in the progression of various human malignant tumors through mutation and overexpression. There have been few studies on loss of heterozygosity (LOH) study on 17p13 in invasive ductal carcinoma. This study evaluated a 17p13 LOH and protein expression in invasive ductal carcinomas and correlated these results with the clinicopathological factors. Methods: LOH analysis was carried out using a polymerase chain reaction with four polymorphic microsatellite markers (D17S796, TP53, D17S5, D17S513) in 50 surgically resected tumors and their non-tumorous counterparts. The p53 protein expression level was examined using immunohistochemistry. Results: A LOH and protein expression was detected in 66% and 54% of the tumors, respectively. The LOH rates ranged from 26.3% (D17S513) to 33.3% (TP53). There was no detected LOH or protein expression in the non-tumor parts. The LOH results correlate well with the tumor size and stage. The protein expression results correlate well with the tumor histological grade. There was no correlation between the LOH and protein loss. Conclusion: 17p13 LOH and p53 gene abnormalities may be associated with tumorigenesis and tumor invasion. In addition, the combined use of both methods may help in early detection as well as for determining the prognosis of an invasive ductal carcinoma. 17p13 LOH and p53 protein expression may contribute to tumor progression through reciprocal complementation in some portions of the invasive ductal carcinoma.
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