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KMID : 0357920140480040276
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Korean Journal of Pathology
2014 Volume.48 No. 4 p.276 ~ p.282
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Differential Features of Microsatellite-Unstable Colorectal Carcinomas Depending on EPCAM Expression Status
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Kim Jung-Ho
Bae Jeong-Mo
Kim Kyung-Ju
Rhee Ye-Young
Kim Young-Hoon
Cho Nam-Yun
Lee Hye-Seung
Chang Mee-Soo
Kang Gyeong-Hoon
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Abstract
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Background: Recent studies have revealed that a small subset of Lynch syndrome-associated colorectal carcinomas (CRCs) is caused by a germline EPCAM deletion-induced MSH2 epimutation. Based on the finding of this genetic alteration, we investigated the implications of EPCAM expression changes in microsatellite instability-high (MSI-H) CRCs.
Methods: Expression of EPCAM and DNA mismatch repair proteins was assessed by immunohistochemistry in 168 MSI-H CRCs. Using DNA samples of these tumors, MLH1 promoter methylation status was also determined by methylation-specific real-time polymerase chain reaction method (MethyLight).
Results: Among 168 MSI-H CRCs, complete loss (CL) and focal loss (FL) of EPCAM expression was observed in two (1.2%) and 22 (13.1%) cases, respectively. Both of the EPCAM-CL cases were found in MSH2-negative tumors without MLH1 promoter methylation. However, only nine of the 22 EPCAM-FL tumors had MSH2 deficiency. Of the 22 EPCAM-FL tumors, 13 showed MLH1 loss, and among them, nine cases were determined to have MLH1 methylation. EPCAM-FL was significantly associated with advanced stage (p=.043), distant metastasis (p=.003), poor differentiation (p=.001), and signet ring cell component (p=.004).
Conclusions: Loss of EPCAM expression is differentially associated with clinicopathological and molecular features, depending on the completeness of the loss, in MSI-H CRCs.
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KEYWORD
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EPCAM, DNA mismatch repair, Microsatellite instability, Colorectal neoplasms
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