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首页> 外文期刊>Modern Pathology >Loss of Stk11/Lkb1 Expression in Pancreatic and Biliary Neoplasms
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Loss of Stk11/Lkb1 Expression in Pancreatic and Biliary Neoplasms

机译：胰腺和胆道肿瘤Stk11 / Lkb1表达的损失。

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We have documented previously somatic mutations of STK11/LKB11, the gene responsible for Peutz-Jeghers syndrome (PJS), in a small proportion of sporadic pancreatic adenocarcinomas, intraductal papillary mucinous neoplasms (IPMNs), and biliary adenocarcinomas. In this report, we characterize the expression of Stk11, the protein product of the STK11 gene, in a larger series of pancreatic and biliary neoplasms. First, the specificity of the Stk11 antibody was established in 23 neoplasms (22 IPMNs and 1 biliary adenocarcinoma) with known STK11 gene status. Complete absence of labeling was seen in the neoplastic cells of 3 of the 3 (100%) cases with previously documented biallelic inactivation of the STK11 gene, whereas 16 of the 20 (80%) IPMNs, presumably with at least one wild-type STK11 gene, retained Stk11 expression in the neoplastic cells. The marked decrease or absence of Stk11 expression in four neoplasms with wild-type STK11 suggests that additional mechanisms may account for the lack of Stk11 expression. Subsequently, to further evaluate Stk11 expression in pancreatic and biliary neoplasms, tissue microarrays (TMAs) were constructed from a series of nearly 100 ductal adenocarcinomas and biliary neoplasms. Stk11 expression was lost in 4 of the 56 (7%) pancreatic adenocarcinomas and 1 of the 38 (2.6%) biliary cancers by immunohistochemistry; the absence of labeling was confirmed by repeated immunohistochemical labeling of complete tissue sections for the same cases. Thus, Stk11 expression is abrogated in a small proportion of pancreatic and biliary neoplasms. The inactivation of Stk11 in 27% (6/22) of IPMNs versus 7% (4/56) of pancreatic adenocarcinomas suggests genetic disparities in the pathogenesis of these closely related neoplasms. Immunohistochemical analysis for Stk11 expression may be a valid surrogate for genetic analysis of STK11 gene mutations in cancers.
机译：我们已经在少数散发性胰腺腺癌，导管内乳头状黏液性肿瘤（IPMNs）和胆道腺癌中记录了STK11 / LKB11（负责Peutz-Jeghers综合征（PJS）的基因）的体细胞突变。在本报告中，我们表征了STK11基因的蛋白质产物Stk11在更大范围的胰腺和胆道肿瘤中的表达。首先，在已知STK11基因状态的23例肿瘤（22个IPMN和1个胆道腺癌）中确定了Stk11抗体的特异性。在先前记录的STK11基因双等位基因失活的3例病例中，有3例（100％）的肿瘤细胞中完全没有标记，而20例（80％）IPMN中的16例，大概至少有一个野生的- STK11型基因，在肿瘤细胞中保留了Stk11表达。在野生型STK11的四个肿瘤中，Stk11表达的明显降低或不存在表明其他机制可能解释了Stk11表达的缺乏。随后，为了进一步评估Stk11在胰腺和胆道肿瘤中的表达，从一系列近100种导管腺癌和胆道肿瘤中构建了组织微阵列（TMA）。通过免疫组织化学，在56例（7％）的胰腺腺癌和38例（2.6％）的胆道癌中，Stk11表达缺失。通过对相同病例的完整组织切片进行重复免疫组织化学标记，可以确认没有标记。因此，Skt11表达被胰腺和胆道肿瘤中的一小部分所废除。在IPMN中，有27％（6/22）个IPMN中的Stk11失活，而胰腺腺癌中有7％（4/56）的Stk11失活表明这些密切相关的肿瘤在发病机理上存在遗传差异。 Stk11表达的免疫组织化学分析可能是癌症中STK11基因突变的遗传分析的有效替代方法。

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