Differential Features of Microsatellite-Unstable Colorectal Carcinomas Depending on EPCAM Expression Status
Korean Journal of Pathology
;
: 276-282, 2014.
Article
in English
| WPRIM
| ID: wpr-70531
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
DNA
/
Immunohistochemistry
/
Colorectal Neoplasms
/
Microsatellite Repeats
/
Cellular Structures
/
Microsatellite Instability
/
DNA Mismatch Repair
/
Real-Time Polymerase Chain Reaction
/
Methylation
/
Neoplasm Metastasis
Language:
English
Journal:
Korean Journal of Pathology
Year:
2014
Type:
Article
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