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Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma

BACKGROUND: Microsatellite instability (MSI) at tri- or tetranucleotide repeat markers (elevated microsatellite alterations at selected tetranucleotide repeat, EMAST) has been recently described. But, the underlying genetic mechanism of EMAST is unclear. This study was to investigate the prevalence...

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Autores principales: Choi, Yoo Duk, Choi, Jin, Kim, Jo Heon, Lee, Ji Shin, Lee, Jae Hyuk, Choi, Chan, Choi, Ho Sun, Lee, Min Cheol, Park, Chang Soo, Juhng, Sang Woo, Nam, Jong Hee
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637840/
https://www.ncbi.nlm.nih.gov/pubmed/19116039
http://dx.doi.org/10.1186/1756-9966-27-88
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author Choi, Yoo Duk
Choi, Jin
Kim, Jo Heon
Lee, Ji Shin
Lee, Jae Hyuk
Choi, Chan
Choi, Ho Sun
Lee, Min Cheol
Park, Chang Soo
Juhng, Sang Woo
Nam, Jong Hee
author_facet Choi, Yoo Duk
Choi, Jin
Kim, Jo Heon
Lee, Ji Shin
Lee, Jae Hyuk
Choi, Chan
Choi, Ho Sun
Lee, Min Cheol
Park, Chang Soo
Juhng, Sang Woo
Nam, Jong Hee
author_sort Choi, Yoo Duk
collection PubMed
description BACKGROUND: Microsatellite instability (MSI) at tri- or tetranucleotide repeat markers (elevated microsatellite alterations at selected tetranucleotide repeat, EMAST) has been recently described. But, the underlying genetic mechanism of EMAST is unclear. This study was to investigate the prevalence of EMAST, in type I endometrial carcinoma, and to determine the correlation between the MSI status and mismatch repair genes (MMR) or p53. METHODS: We examined the 3 mono-, 3 di-, and 6 tetranucleotide repeat markers by PCR in 39 cases of type I endometrial carcinoma and performed the immunohistochemistry of hMSH2, hMLH1, and p53 protein. RESULTS: More than two MSI at mono- and dinucleotide repeat markers was noted in 8 cases (MSI-H, 20.5%). MSI, at a tetranucleotide repeat, was detected in 15 cases (EMAST, 38.5%). In remaining 16 cases, any MSI was not observed. (MSS, 42.1%), MSI status was not associated with FIGO stage, grade or depth of invasion. The absence of expression of either one of both hMSH2 or hMLH1 was noted in seven (87.5%) of eight MSI-H tumors, one (6.3%) of 16 MSS tumors, and five (33.3%) of 15 EMAST tumors. (p = 0.010) The expression of p53 protein was found in one (12.5%) of eight MSI-H tumors, five (31.3%) of 16 MSS tumors, and seven of 15 EMAST tumors. (p = 0.247) CONCLUSION: Our results showed that about 38.5% of type I endometrial carcinomas exhibited EMAST, and that EMAST was rarely associated with alteration of hMSH2 or hMLH1.
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spelling pubmed-26378402009-02-10 Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma Choi, Yoo Duk Choi, Jin Kim, Jo Heon Lee, Ji Shin Lee, Jae Hyuk Choi, Chan Choi, Ho Sun Lee, Min Cheol Park, Chang Soo Juhng, Sang Woo Nam, Jong Hee J Exp Clin Cancer Res Research BACKGROUND: Microsatellite instability (MSI) at tri- or tetranucleotide repeat markers (elevated microsatellite alterations at selected tetranucleotide repeat, EMAST) has been recently described. But, the underlying genetic mechanism of EMAST is unclear. This study was to investigate the prevalence of EMAST, in type I endometrial carcinoma, and to determine the correlation between the MSI status and mismatch repair genes (MMR) or p53. METHODS: We examined the 3 mono-, 3 di-, and 6 tetranucleotide repeat markers by PCR in 39 cases of type I endometrial carcinoma and performed the immunohistochemistry of hMSH2, hMLH1, and p53 protein. RESULTS: More than two MSI at mono- and dinucleotide repeat markers was noted in 8 cases (MSI-H, 20.5%). MSI, at a tetranucleotide repeat, was detected in 15 cases (EMAST, 38.5%). In remaining 16 cases, any MSI was not observed. (MSS, 42.1%), MSI status was not associated with FIGO stage, grade or depth of invasion. The absence of expression of either one of both hMSH2 or hMLH1 was noted in seven (87.5%) of eight MSI-H tumors, one (6.3%) of 16 MSS tumors, and five (33.3%) of 15 EMAST tumors. (p = 0.010) The expression of p53 protein was found in one (12.5%) of eight MSI-H tumors, five (31.3%) of 16 MSS tumors, and seven of 15 EMAST tumors. (p = 0.247) CONCLUSION: Our results showed that about 38.5% of type I endometrial carcinomas exhibited EMAST, and that EMAST was rarely associated with alteration of hMSH2 or hMLH1. BioMed Central 2008-12-31 /pmc/articles/PMC2637840/ /pubmed/19116039 http://dx.doi.org/10.1186/1756-9966-27-88 Text en Copyright © 2008 Choi et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Choi, Yoo Duk
Choi, Jin
Kim, Jo Heon
Lee, Ji Shin
Lee, Jae Hyuk
Choi, Chan
Choi, Ho Sun
Lee, Min Cheol
Park, Chang Soo
Juhng, Sang Woo
Nam, Jong Hee
Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma
title Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma
title_full Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma
title_fullStr Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma
title_full_unstemmed Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma
title_short Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma
title_sort microsatellite instability at a tetranucleotide repeat in type i endometrial carcinoma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637840/
https://www.ncbi.nlm.nih.gov/pubmed/19116039
http://dx.doi.org/10.1186/1756-9966-27-88
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