Differential Features of Microsatellite-Unstable Colorectal Carcinomas Depending on EPCAM Expression Status
´ëÇѺ´¸®ÇÐȸÁö 2014³â 48±Ç 4È£ p.276 ~ p.282
±èÁ¤È£(Kim Jung-Ho) - SMG-SNU Boramae Medical Center Department of Pathology
¹èÁ¤¸ð(Bae Jeong-Mo) - Seoul National University College of Medicine Department of Pathology
±è°æÁÖ(Kim Kyung-Ju) - Seoul National University College of Medicine Department of Pathology
(Rhee Ye-Young) - Seoul National University College of Medicine Department of Pathology
±è¿µÈÆ(Kim Young-Hoon) - Seoul National University College of Medicine Department of Pathology
Á¶³²À±(Cho Nam-Yun) - Seoul National University College of Medicine Cancer Research Institute
ÀÌÇý½Â(Lee Hye-Seung) - Seoul National University Bundang Hospital Department of Pathology
Àå¹Ì¼ö(Chang Mee-Soo) - SMG-SNU Boramae Medical Center Department of Pathology
°°æÈÆ(Kang Gyeong-Hoon) - Seoul National University College of Medicine Department of Pathology
Abstract
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.
Å°¿öµå
EPCAM, DNA mismatch repair, Microsatellite instability, Colorectal neoplasms
KMID :
0357920140480040276
¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸
µîÀçÀú³Î Á¤º¸
À¯È¿¼º°á°ú(Recomendation)