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Table 1 Core Gene Pathway Alterations and Association with Tumor Differentiation in KRASmut PDAC

From: TP53 missense mutation reveals gain-of-function properties in small-sized KRAS transformed pancreatic ductal adenocarcinoma

Mutated pathway in KRASmut PDAC

Moderate and well differentiated n=260

P

Poor differentiated n=284

P

TP53

 Missense

94 (36.1%)

1

144 (50.7%)

0.001†

 Truncating

53 (20.4%)

1

53 (18.7%)

0.612†

 Others*

2 (0.8%)

1

11 (3.9%)

0.018†

 Overall mutated

149 (57.3%)

1

208 (73.3%)

<0.001†

Cell cycle

 CDKN2A

37 (14.2%)

1

52 (18.3%)

0.199†

 Overall mutated

42 (16.2%)

1

58 (20.4%)

0.199†

 TGFb

62 (23.8%)

1

60 (21.1%)

0.447†

2-3 mutated pathways**

63 (24.2%)

1

91 (32.0%)

0.043†

Trithorax

52 (20.0%)

1

70 (24.6%)

0.194†

HRD

39 (15.0%)

1

46 (16.2%)

0.701†

MMRD

6 (2.3%)

1

6 (2.1%)

0.877†

RNA processing

11 (4.2%)

1

8 (2.8%)

0.370†

PI3K-Akt

3 (1.2%)

1

3 (1.1%)

1.000‡

WNT

26 (10.0%)

1

22 (7.7%)

0.355†

NOTCH

10 (3.8%)

1

10 (3.5%)

0.841†

Hedgehog

7 (2.7%)

1

7 (2.5%)

0.867†

DNA modification

6 (2.3%)

1

11 (3.9%)

0.295†

  1. *Other mutation subtypes included mixed cases, in-frame insertion or deletion and silent mutation
  2. **Alterations of 2-3 pathways among TP53, cell cycle pathway and TGFb pathway; †Chi-squared test; ‡Fisher exact test