Laboratory of Pathology, Georgios Gennimatas General Hospital, Thessaloniki 54635, Greece.
World J Gastroenterol. 2010 May 28;16(20):2476-83. doi: 10.3748/wjg.v16.i20.2476.
To analyze alpha-methylacyl CoA racemase (AMACR) expression in relation to various dysplasia phenotypes and clinicopathological parameters of sporadic colorectal adenomas.
Fifty-five cases of sporadic colorectal adenomas were categorized according to the Vienna classification for Gastrointestinal Neoplasia. These corresponded to a total of 98 different intra-lesion microscopic fields that were further independently assigned a histological grade based on the old nomenclature (mild, moderate, severe dyplasia and carcinoma in situ). AMACR expression was evaluated by immunohistochemistry and statistical analysis was performed to investigate possible associations with various clinicopathologic parameters of adenomas i.e. gender, age, localization, grade of dysplasia, size and configuration.
Patient age ranged from 41 to 84 years (mean 65 +/- 13.2 years); 37 patients were males and 18 were females. Adenomas ranged in size between 0.5 and 30 cm (mean 2 +/- 1.3 cm), including 18 tubular, 16 villous, 20 mixed or tubulovillous, and 1 giant sessile villous adenoma. AMACR expression was observed in 3 out of 16 (18.8%) of low-grade vs 23 out of 35 (62.8%) of high-grade lesions (P = 0.002). Most adenomas exhibiting high grade dysplasia with in situ carcinoma-like areas stained positive for AMACR (15/17 or 88.2%) as compared to adenomas with high grade dysplasia which contained severe dysplasia-like foci (6/15 or 40%), (P = 0.005). In AMACR positive adenomas featuring severe dysplasia-like or in situ carcinoma-like areas, AMACR staining was not necessarily observed in the in situ component. Positivity in intra-lesion of mild, moderate or severe dysplasia-like foci was more often encountered in adenomas harboring in situ, intramucosal or infiltrative carcinoma [21/33 (63.6%) vs 9/40 (22.5%), P < 0.001]. Strong AMACR expression was found in 11 out of 17 villous adenomas, but in only 1 out of 18 tubular lesions (P = 0.005). Larger lesions, i.e. > 1 cm stained more frequently for AMACR than smaller ones [27/45 (60%) vs 2/10 (20%), P = 0.02]. Overall, AMACR expression was associated with the grade of dysplasia, as well as with the size and configuration of adenomas, i.e. the consensus risk factors applied to colorectal adenoma patient surveillance.
It may be worthy to further evaluate the possible use of AMACR as an additional risk factor for the assessment of colorectal adenoma patients.
分析α-甲基酰基辅酶 A 消旋酶（AMACR）在散发性结直肠腺瘤不同异型增生表型和临床病理参数中的表达。
根据胃肠道肿瘤维也纳分类，对 55 例散发性结直肠腺瘤进行分类。这些病例共对应 98 个不同的病变内微观区域，根据旧命名法（轻度、中度、重度异型增生和原位癌）进一步独立分配组织学分级。通过免疫组织化学评估 AMACR 表达，并进行统计学分析以研究与腺瘤的各种临床病理参数（即性别、年龄、定位、异型增生程度、大小和形态）之间可能的关联。
患者年龄为 41 至 84 岁（平均 65±13.2 岁）；男性 37 例，女性 18 例。腺瘤大小为 0.5 至 30cm（平均 2±1.3cm），包括 18 个管状、16 个绒毛状、20 个混合或管状绒毛状和 1 个巨大无蒂绒毛状腺瘤。低级别病变中 AMACR 表达为 3 例（18.8%），高级别病变中为 23 例（62.8%）（P=0.002）。与包含重度异型增生样灶的腺瘤（6/15 或 40%）相比，表现为高级别异型增生伴原位癌样区域的大多数腺瘤（15/17 或 88.2%）呈 AMACR 阳性（P=0.005）。在 AMACR 阳性的高级别异型增生或原位癌样区域的腺瘤中，原位成分中不一定观察到 AMACR 染色。在伴有原位、黏膜内或浸润性癌的腺瘤中，更常观察到病变内的轻度、中度或重度异型增生样灶的阳性[21/33（63.6%）比 9/40（22.5%），P<0.001]。17 个绒毛状腺瘤中有 11 个表达强烈的 AMACR，但 18 个管状病变中只有 1 个（P=0.005）。大于 1cm 的病变比小于 1cm 的病变更常染色 AMACR[27/45（60%）比 2/10（20%），P=0.02]。总的来说，AMACR 表达与异型增生程度以及腺瘤的大小和形态有关，即共识风险因素适用于结直肠腺瘤患者的监测。
进一步评估 AMACR 作为结直肠腺瘤患者评估的附加危险因素可能是值得的。
