Table 2 Molecular characteristics of colorectal carcinomas according to acetyl-CoA synthetase-2 expression status

From: Downregulation of acetyl-CoA synthetase 2 is a metabolic hallmark of tumor progression and aggressiveness in colorectal carcinoma

 

Acetyl-CoA synthetase-2-low (n=771)

Acetyl-CoA synthetase-2-high (n=335)

P-value

CpG island methylator phenotype

  

0.008

 CpG island methylator phenotype-negative

368 (48%)

133 (40%)

 

 CpG island methylator phenotype-low

356 (46%)

188 (56%)

 

 CpG island methylator phenotype-high

47 (6%)

14 (4%)

 

Microsatellite instability

  

0.305

 Microsatellite stable

664 (86%)

286 (85%)

 

 Microsatellite instability-low

53 (7%)

18 (6%)

 

 Microsatellite instability-high

54 (7%)

31 (9%)

 

KRAS mutation (n=1044)

  

0.975

 Wild-type

531 (73%)

235 (73%)

 

 Mutant-type

193 (27%)

85 (27%)

 

BRAF mutation (n=979)

  

0.279

 Wild-type

660 (96%)

276 (94%)

 

 Mutant-type

27 (4%)

16 (6%)

 

KRT7 (CK7) expression (n=1100)

  

0.008

 Negative

690 (90%)

317 (95%)

 

 Positive

76 (10%)

17 (5%)

 

KRT20 (CK20) expression (n=1094)

  

0.031

 Intact

620 (81%)

289 (87%)

 

 Decreased

141 (19%)

44 (13%)

 

CDX2 expression (n=1084)

  

0.019

 Intact

718 (93%)

324 (97%)

 

 Decreased

53 (7%)

11 (3%)

 

MKI67 (Ki-67) labelling index, median (min–max)

10.4 (0.10–71.0)

18.8 (0.1–81.6)

< 0.001a

  1. aWilcoxon’s rank-sum test.