Table 4 Genetic alterations in interval and non-interval tumors involving the five major pathogenetic pathway in colorectal cancer (CRC)

From: Clinicopathologic and genetic characteristics of interval colorectal carcinomas favor origin from missed or incompletely excised precursors

Signaling pathway (genesa)

Interval colon cancer N = 20 n (%)

Matched non-interval colon cancerb N = 40 n (%)

P (matched comparison)

Wnt (APC, CTNNB1, TCF7L2, TCF7L1, FBXW7, ARID1A, SOX9)

18 (90)

37 (93)

0.73

P53 (ATM, TP53, CDKN1A, CDKN2A)

16 (80)

38 (95)

0.81

RTK/RAS (EGFR, ERBB2, NRAS, KRAS, BRAF)

14 (70)

35 (88)

0.13

PI3K (IGF1R, PIK3CA, PIK3C2B, PTEN, PIK3R1, AKT1, PRKDC, MET)

17 (85)

30 (75)

0.38

TGF beta (SMAD2, SMAD4, MYC, MECOM)

13 (65)

20 (50)

0.26

  1. aGenetic alterations include all single nucleotide variants or indels (truncation, missense, and homozygous deletion) and all copy number variations
  2. bMatched on 10-year age groups, tumor location, and gender
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