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Original Articles
- The p53 Mutation and DNA Ploidy in Human Metastatic Breast Cancer.
- Seong Jin Cho, Ae Ree Kim, Nam Hee Won
- Korean J Pathol. 1997;31(2):135-144.
- 1,549 View
- 11 Download
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Abstract
PDF - The p53 gene, one of the tumor suppressor genes, is believed to play an important role through mutation and overexpression in the progression of various human malignant tumors. To compare the p53 mutation status between the primary and metastatic lesions of breast cancers and to investigate the mutational pattern of p53, immunohistochemistry (IHC) and polymerase chain reaction and single strand conformational polymorphism (PCR-SSCP) were performed in 25 cases of breast cancers with paraffin embedded tissue. Mutant protein products or point mutation were detected through IHC or PCR-SSCP method. And flow cytometrical (FCM) analysis were performed in the same paraffin blocks to correlate the DNA ploidy and p53 mutation. The following results are summarized. 1. The detection of the p53 gene mutation and overexpression of the p53 protein were measured in 40% and 48%, respectively, in 25 primary tumors, either or both methods was detected in 64%. 2. A concordance rate of the p53 protein expression between the primary and metastatic lesions of 25 breast cancers was 100%, but the concordance rate of the p53 gene mutation was 72%. 3. The correlation between the p53 mutation and the DNA aneuploidy was not statistically significant (p=0.38) 4. A p53 mutation by IHC or PCR-SSCP was more frequently detected in grade III breast cancers than in grade I or II. 5. Among 5 to 9 exons of the p53 gene, exon 7 was the most frequent mutation spot in this study. 6. Additional mutation of the p53 gene was developed in the three metastatic lesions. With the above results it is suggested that the p53 protein overexpression by immunohistochemistry is not correlated with the p53 mutation by PCR-SSCP. The p53 mutation pattern between the primary and metastatic lesions are not idenitical and an additional point mutation can occur in the metastatic lesion. The DNA aneuploidy is more frequently detected in the cases with the p53 protein overexpression than in the p53 protein negative, but it is not statistically significant.
- Alteration of p53 Tumor Suppressor Gene in Hyperplastic Lesions and Adenocarcinomas of Uterine Endometrium - Immunohistochemistry and PCR-SSCP.
- Eun Kyung Kim, Chan Kum Park, Gu Kong, Moon Hyang Park, Jung Dal Lee
- Korean J Pathol. 1997;31(7):662-671.
- 1,568 View
- 12 Download
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Abstract
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- To investigate the role of the p53 gene in the development of endometrial adenocarcinoma and to study the relation between alteration of the p53 gene and histologic grade, the author studied the alteration of thep53 gene in hyperplastic lesions and adenocarcinomas of the uterine endometrium. The study was carried out with immunohistochemical stain and PCR-SSCP. The materials included ten cases of endometrial hyperplasia (five simple and five atypical complex) and 18 cases of endometrial adenocarcinoma. Overexpression of the p53 protein were found in one of five atypical complex hyperplasias (20%) and 11 of 18 adenocarcinomas (61.1%). The intensity of p53 overexpression appeared to have increasing tendency with higher histologic grade of adenocarcinomas. Among the II cases of adenocarcinoma that overexpressed p53 protien, five cases (45.5%) were found to have mutations by PCR-SSCP. One was grade 1 (20%), two were grade 11 (25%), and two were grade III (40%). The sites of mutation were three exon 8, one exon 5, and one exon 6. In conclusion, alteration of the p53 gene may paly a role in the development of endometrial adenocarcinoma and appears to occur as a late event in carcinogenesis.HHowever, inactivation of the p53 gene in early stage of tumor development cannot be excluded.
- A Comparative Study of Immunohistochemistry and PCR-SSCP for Detection of p53 Mutation In Gastric Carcinoma.
- Jong Soon Kim, Jae Hyuk Lee, Min Cheol Lee, Chang Soo Park, Sang Woo Juhung
- Korean J Pathol. 1998;32(1):21-28.
- 1,626 View
- 23 Download
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Abstract
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- Mutation of the p53 tumor-suppressor gene in exons 4 through 9 was examined in 34 cases of primary advanced gastric cancer using PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) and the results were compared with p53 protein expression as determined by immunohistochemistry (IHC) using a monoclonal antibody(DO-1). p53 protein detected by IHC was observed in 14 cases (41.2%) and genotypic mutation detected by PCR-SSCP in exons 4-9 was observed in 13 cases (38.2%) One case showed an aberrant band on PCR-SSCP both in Exon 7 and Exon 8/9. p53 alteration detected by either IHC or PCR-SSCP was observed in 19 cases (55.9%), but only 8 cases (23.5%) showed both p53 mutation and protein expression. We also tried to obtain the correlation between relative intensity of the shifted bands on PCR-SSCP and percentage of positive cells by IHC, but a significant correlation was not seen between relative intensity of shifted bands on PCR-SSCP and positve cell ratio. A discrepancy between p53 protein expression and p53 mutation is observed in primary gastric carcinomas. The reason for this discrepancy are not apparent. However, examination of gastric carcinomas for mutations in other exons may identify a better correlation with protein overexpression. The results obtained in this study suggest that the negative reaction for p53 immunohistochemistry may not necessarily mean no genetic alteration of the p53 locus.
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