The Role of Chromosomal Instability and Epigenetics in Colorectal Cancers Lacking β-Catenin/TCF Regulated Transcription
Table 2
Immunohistochemical evaluation of protein expression of the selected target genes in various tumor categories.
Gene
Chr
Status in RKO
Pilot study,
% loss in MSS sporadic cancers, ( value)
% loss in MSI sporadic cancers, ( value)
% loss in sporadic adenoma, ( value)
% loss in Lynch-colon cancers, ( value)
% loss in FCCX, ( value)
1
IFI16
1q22
Upregulated
Loss 43% not correlated with β-catenin localization
ND
ND
ND
ND
ND
2
RGS4
1q23.3
Upregulated
RGS4 nuclear localization in 56% of tumors correlated with nuclear β-catenin
58% cytoplasmic (NS)
50% cytoplasmic (NS)
ND
ND
ND
3
MCTP1
5q15
Upregulated
50% membranous, 50% cytoplasmic, not correlated with β-catenin localization
ND
ND
ND
ND
ND
4
DGKI
7q32.3–q33
Upregulated
Loss correlated with localization
55% (0.0001)
69% (0.0001)
30% (NS)
63% (0.0001)
50% (0.002)
5
OBCAM/OPCML
11q25
Upregulated
Loss in 55% but not correlated with β-catenin localization
60% (NS)
50% (NS)
70% (NS)
68% (NS)
15% (NS)
6
GLIPR1
12q21.2
Upregulated
Loss correlated with localization
33% (0.005)
27% (0.005)
27% (0.001)
44% (0.001)
40% (0.035)
value is for loss of the expression versus β-catenin subcellular localization. Highlighted in bold are GLIPR1 and DGKI findings which correlated with β-catenin status in a pattern similar to that observed in the microarray. ND, not done; NS, not significant.
