AMACR is associated with advanced pathologic risk factors in sporadic colorectal adenomas

Table 1 Incidence of various dysplasia histological phenotypes n (%)

Clinically oriented	Biologic potential	Total cases	Subgroups
Low grade dysplasia	Mild	16 (29.1)	6 (10.9)
	Moderate		10 (18.2)
High grade dysplasia	Severe	35 (63.6)	15 (27.3)
	In situ carcinoma		17 (30.9)
	Intramucosal carcinoma		3 (5.5)
Infiltrative carcinoma	Submucosal carcinoma	4 (7.3)

Table 2 AMACR expression in sporadic colorectal adenomas n (%)

Vienna classification of GI neoplasia	Biologic potential	Staining
		Negative	Weak	Strong	Subtotal positive	Total
Low grade (n = 16)	Mild	13 (81.3)	3 (18.8)	0 (0)	3 (18.8)	16
	moderate
High grade (n = 35)	Severe	9 (60)	6 (40)	0 (0)	6 (40)	15
	In situ carcinoma	2 (11.8)	3 (17.6)	12 (70.6)1	15 (88.2)	17
	Intramucosal carcinoma	1	0	2	2	3
Infiltrative carcinoma (n = 4)	Submucosal carcinoma	1	1	2	3	4
		26 (47.3)	13 (23.7)	16 (29)	29 (52.7)	55

¹In 3 cases (#48, 49, 52 in Figure 1A) higher grade focus and focus of most intense staining did not match, as described in Materials and Methods, Interpretation. AMACR: α-methylacyl CoA racemase; GI: Gastrointestinal.

Table 3 AMACR expression in relation to pathological features of adenomas n (%)

	n	Staining
		Negative	Weak	Strong	Total positivity
Configuration	55
Tubular	18	11 (61)	6 (33)	1 (6)	7 (39)
Villous	17	5 (29.4)	1 (5.9)	11 (64.7)	12 (76.5)
Tubulovillous	20	10 (50)	6 (30)	4 (20)	10 (50)
Size	55
< 1 cm	10	8 (80)	1 (10)	1 (10)	2 (20)
≥ 1 cm	45	18 (40)	12 (26.7)	15 (33.3)	27 (60)

Table 4 AMACR staining in areas with mild/moderate or severe dysplasia n (%)

Higher grade component	Staining
	Negative	Weak	Strong	Total positivity
Present (n = 33)	12 (36.4)	11 (33.3)	10 (30.3)	21 (63.6)
Absent (n = 40)	31 (77.5)	9 (22.5)	0 (0)	9 (22.5)