Gene expression profiling: Canonical molecular changes and clinicopathological features in sporadic colorectal cancers

Table 2 Number of differentially expressed genes in terms of molecular changes and clinicopathological features

Parameters	No. of patients (missing)	No. of differentiallyexpressed genes (P < 0.01), total (up/down)
Molecular changes1, -/+
APC mutations	55/27 (2)	83 (41/42)
Wnt-activated	45/38 (1)	82 (37/45)
MMR defects	70/14	238 (122/116)
RAF-mediated	58/26	108 (59/49)
Altered p53 expression	24/59 (1)	125 (57/68)
Crossover	64/19 (1)	92 (44/48)
Clinicopathologic features
Tumor location2, R/L + P	27/57	1628 (936/692)
R/L/P	27/29/28	1263
AJCC stage3, I + II/III + IV	50/34	195 (103/92)
Tumor differentiation, WD + MD/PD + muc	75/9	151 (69/82)
Synchronous adenoma, -/+	55/29	152 (92/60)
LVN invasion, -/+	57/27	279 (147/132)

¹Wnt-activated: explored by β-catenin assay, AXIN2 measurement, and GSK-3β immune staining; MMR defect: analyzed by MSI assay, MLH1 5'-promoter measurement or 3'-methylation, and MLH1 or MSH2 immune staining; RAF-mediated alterations: assayed by detection of mutations in BRAF V600E and KRAS exons 12 and 13, and MEK immune staining; Crossover: When a tumor carried both APC/Wnt-mediated alterations and MMR defects or RAF-mediated alterations.

²R: Caecum-splenic flexure of transverse colon; L: Splenic flexure of transverse colon-sigmoid colon; P: Rectum.

³According to the American Joint Committee on Cancer (6th ed., 2001). WD, MD, PD, and muc, well-, moderately-, poorly-differentiated, and mucinous; MMR: Mismatch repair.