Dorer Russell, Odze Robert D
Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA.
Am J Surg Pathol. 2006 Jul;30(7):871-7. doi: 10.1097/01.pas.0000213268.30468.b4.
Alpha-methylacyl-CoA racemase (AMACR) catalyzes the racemization of alpha-methyl, branched carboxylic coenzyme A thioesters, and is overexpressed in a variety of neoplasms, such as prostate and colon cancer. The aim of this study was to evaluate AMACR expression in the metaplasia-dysplasia-carcinoma sequence in Barrett's esophagus (BE), ulcerative colitis (UC), and Crohn's disease (CD) and to determine whether its expression can be used to detect dysplastic epithelium in these conditions. One hundred thirty-four routinely processed biopsy and/or resection specimens from 134 patients with BE [M/F ratio: 5.7, mean age: 67 y (36 negative (intestinal metaplasia only), 14 indefinite for dysplasia (IND), 16 low-grade dysplasia (LGD), 32 high-grade dysplasia (HGD), and 36 invasive adenocarcinoma (ACA)] and 74 specimens from 74 patients with inflammatory bowel disease (IBD) [56 with ulcerative colitis, 18 with Crohn's disease, M/F ratio: 1.8, mean age: 55 y (17 negative, 7 IND, 26 LGD, 10 HGD, and 14 ACA)] were immunostained with a monoclonal AMACR antibody (p504S). The degree of cytoplasmic staining in all cases was evaluated in a blinded fashion according to the following grading system: 0, negative (0% cells positive); 1+, 1% to 10% cells positive; 2+, 10% to 50% cells positive; or 3+, >50% cells positive. In patients with BE, AMACR was not expressed in any negative foci (0%) but was significantly increased (P<0.0001) in foci of LGD (38%), HGD (81%), and ACA (72%). Three of 14 (21%) IND foci from 3 BE patients were only focally positive (grade 1: 7%, 2: 14%). However, 1 of these 3 patients had follow-up information available and had developed ACA subsequently. Similarly, in patients with IBD, AMACR was not expressed in any foci considered negative for dysplasia, but was significantly increased (P<0.0001) in foci of LGD (96%), HGD (80%), and ACA (71%). Only 1/7 (14%) IND focus from 1 patient was focally positive (grade 1). The sensitivity for the detection of LGD and HGD in BE and IBD was 38% and 81%, and 96% and 80%, respectively, for the 2 types of disorders. The specificity was 100% for both BE and IBD. AMACR is involved in the neoplastic progression in BE and IBD. The high degree of specificity of AMACR for dysplasia/carcinoma in BE and IBD suggests that it may be useful to detect neoplastic epithelium in these conditions.
α-甲基酰基辅酶A消旋酶(AMACR)催化α-甲基、支链羧酸辅酶A硫酯的消旋化反应,在多种肿瘤中过表达,如前列腺癌和结肠癌。本研究旨在评估AMACR在巴雷特食管(BE)、溃疡性结肠炎(UC)和克罗恩病(CD)的化生-发育异常-癌序列中的表达情况,并确定其表达是否可用于检测这些疾病中的发育异常上皮。对134例BE患者的134份常规处理的活检和/或切除标本[男/女比例:5.7,平均年龄:67岁(36例阴性(仅肠化生),14例发育异常不确定(IND),16例低级别发育异常(LGD),32例高级别发育异常(HGD),36例浸润性腺癌(ACA)]以及74例炎症性肠病(IBD)患者的74份标本[56例溃疡性结肠炎,18例克罗恩病,男/女比例:1.8,平均年龄:55岁(17例阴性,7例IND,26例LGD,10例HGD,14例ACA)]用单克隆AMACR抗体(p504S)进行免疫染色。根据以下分级系统以盲法评估所有病例的细胞质染色程度:0级,阴性(0%细胞阳性);1+级,1%至10%细胞阳性;2+级,10%至50%细胞阳性;或3+级,>50%细胞阳性。在BE患者中,AMACR在任何阴性病灶中均无表达(0%),但在LGD(38%)、HGD(81%)和ACA(72%)病灶中显著增加(P<0.0001)。3例BE患者的14个(21%)IND病灶中有3个仅局灶阳性(1级:7%,2级:14%)。然而,这3例患者中有1例有随访信息,随后发生了ACA。同样,在IBD患者中,AMACR在任何被认为发育异常阴性的病灶中均无表达,但在LGD(96%)、HGD(80%)和ACA(71%)病灶中显著增加(P<0.0001)。1例患者的7个(14%)IND病灶中只有1个局灶阳性(1级)。BE和IBD中检测LGD和HGD的敏感性分别为38%和81%,以及96%和80%。BE和IBD的特异性均为100%。AMACR参与BE和IBD的肿瘤进展。AMACR对BE和IBD中发育异常/癌的高度特异性表明,它可能有助于检测这些疾病中的肿瘤上皮。