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. 2008 Dec 31;27(1):88.
doi: 10.1186/1756-9966-27-88.

Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma

Yoo Duk Choi  1 , Jin Choi, Jo Heon Kim, Ji Shin Lee, Jae Hyuk Lee, Chan Choi, Ho Sun Choi, Min Cheol Lee, Chang Soo Park, Sang Woo Juhng, Jong Hee Nam
Affiliations

Microsatellite instability at a tetranucleotide repeat in type I endometrial carcinoma

Yoo Duk Choi et al. J Exp Clin Cancer Res. .

Abstract

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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Figures

Figure 1
Figure 1
MSI at mono- and dinucleotide repeat markers in type I endometrial carcinioma. Alterations in the electrophoretic mobility of PCR products from tumor compared with normal tissue DNA are seen (arrowheads). (N: normal, T: tumor).
Figure 2
Figure 2
MSI at tetranucleotide repeat markers (EMAST) in type I endometrial carcinioma. Alterations in the electrophoretic mobility of PCR products from tumor compared with normal tissue DNA are seen (arrowheads). (N: normal, T: tumor).
Figure 3
Figure 3
Examples of type I endometrial carcinoma with (A) loss of hMSH2 protein expression, (B) preservation of hMSH2 protein expression, (C) loss of hMLH1 protein expression, and (D) preservation of hMLH1 protein expression. Positive expression for hMSH2 or hMSH1 is noted in non-tumor cells. (A-D, X200).
See this image and copyright information in PMC

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