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. 2007 Feb 28;13(8):1187–1194. doi: 10.3748/wjg.v13.i8.1187

Table 1.

Association between p16 and MGMT methylation, K-ras mutations and clinicopathological features of colorectal cancer

Methylation (%) Mutations (%)
Variable p16 (n = 46) MGMT (n = 46) K-ras (n = 84)
Gender
Female 9/15 (60.0) 7/15 (46.7) 15/23 (65.2)a
Male 15/31 (48.4) 13/31 (41.9) 22/61 (36.1)
Dukes’ stage
A 5/9 (55.5) 5/9 (55.5) 8/21 (38.1)
B 7/10 (70.0) 4/10 (40.0) 12/24 (50.0)
C 8/15 (53.3) 8/15 (53.3) 17/39 (43.6)4
D 4/12 (33.3) 3/12 (25.0)
Differentiation
Poor 15/25 (60.0) 10/25 (40.0) 18/44 (40.9)
Moderate 8/18 (44.4) 10/18 (55.5) 16/26 (61.5)
Well 1/3 (33.3) 0/3 (0) 3/14 (21.4)
Macrosopic type2
Polypoid 11/23 (47.8) 14/23 (60.7)a 25/48 (52.1)
Flat 13/23 (56.5) 6/23 (26.1) 12/35 (34.3)
Histological type2
Mucinous 8/19 (42.1) 6/19 (31.6) 16/34 (47.1)
Tubular 16/27 (59.3) 14/27 (51.8) 21/49 (42.8)
Location2
Proximal 3/3 (100) 1/3 (33.3) 5/9 (55.5)
Distal 21/43 (48.8) 19/43 (44.2) 32/74 (43.2)
Progression (2 yr)1,3
Metastasis or/and death 11/25 (44.0) 9/25 (36.0) 29/44 (65.9)b
Without progression 12/19 (63.1) 11/19 (57.9) 7/37 (18.9)

Complete clinicopathological data were missing on one sample of colorectal cancer, and it was only included in analysis of genetic alterations;

a

P < 0.05;

b

P < 0.001 (all P values were revealed by χ2-test ); Data are missing on two1 subjects for p16 and MGMT methylation status analysis, and on one2 and three3 subjects for K-ras mutation analysis, respectively.

4

Data for C and D Dukes’ stages are considered together for K-ras mutation analysis.