Comethylation of p16 and MGMT genes in colorectal carcinoma: Correlation with clinicopathological features and prognostic value

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;

^aP < 0.05;

^bP < 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.

⁴Data for C and D Dukes’ stages are considered together for K-ras mutation analysis.

Table 2 Association between p16 and MGMT methylation, K-ras mutations and immunohistochemical features of colorectal cancer

	Methylation (%)		Mutations (%)
Variable	p16 (n = 46)	MGMT (n = 46)	K-ras (n = 84)
E-cadherin1,3
Absent	13/19 (68.4)	9/19 (47.4)	28/37 (75.7)b
Heterogeneous	4/14 (28.6)	7/14 (50.0)	4/23 (17.4)
Present	6/11 (54.5)	4/11 (36.4)	4/21 (19.0)
CD44 expression1,3
Absent	7/11 (63.6)	6/11 (54.5)	4/22 (18.2)
Low	6/9 (66.7)	4/9 (44.4)	5/17 (29.4)
Moderate	2/7 (28.6)	4/7 (57.1)	4/10 (40.0)
Extensive	8/17 (47.0)	6/17 (35.3)	23/32 (71.9)b
CD44 type2,4
Membranous	9/17 (52.9)	7/17 (41.2)	9/36 (25.0)
Cytoplasmic	13/26 (50.0)	12/26 (46.1)	27/44 (71.9)b
Laminin1,3
0-25%	5/8 (62.5)	5/8 (62.5)	2/15 (13.3)
25%-75%	5/12 (41.7)	5/12 (41.7)	5/22 (22.7)
> 75%	13/24 (54.2)	10/24 (41.7)	29/44 (65.9)b
PCNAi1,3
0	1/2 (50.0)	2/2 (100)	0/2 (0)
0-10%	5/9 (55.5)	4/9 (44.4)	3/17 (17.6)
10%-50%	6/9 (66.7)	5/9 (55.5)	3/20 (15.0)
> 50%	11/24 (45.8)	9/24 (37.5)	30/42 (71.4)b

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

^bP < 0.001 (all P values were revealed by χ²-test ); Data are missing on two¹ and three² subjects for p16 and MGMT methylation status analysis, respectively, and on three³ and four⁴ subjects for K-ras mutation analysis, respectively.