Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231-2410, USA.
Am J Surg Pathol. 2012 Feb;36(2):235-41. doi: 10.1097/PAS.0b013e3182376e36.
Although vascular invasion is a well-established indicator of poor prognosis for patients with infiltrating ductal adenocarcinoma of the pancreas (PDAC), the histopathologic characteristics of vascular invasion are not well described. Hematoxylin and eosin-stained slides from 209 surgically resected infiltrating PDACs were systematically evaluated for the presence or absence of microscopic vascular invasion. For the cases with vascular invasion, we further categorized the histologic pattern of invasion into conventional and pancreatic intraepithelial neoplasia-like (PanIN-like). In addition, several histopathologic factors in the surrounding blood vessels, including lymphocytic infiltration and luminal fibrosis, were carefully assessed. Data were compared with clinicopathologic variables, including patient survival. Microscopic vascular invasion was observed in 136 of the 209 PDACs (65.1%). Vascular invasion mimicking pancreatic intraepithelial neoplasia (PanIN-like invasion) was observed in 94 of the 136 cases (69.1%) with vascular invasion. Microscopic vascular invasion was associated with increased tumor size (P=0.04), higher pT classification (P=0.003), lymph node metastasis (P<0.0001), and perineural invasion (P=0.005). Vascular invasion was inversely correlated with neo-adjuvant therapy (P<0.0001). Examination of adjacent blood vessels revealed that peritumoral blood vessels with intimal lymphocytes (P=0.002), intimal (P=0.007) and medial (P=0.001) fibrosis, and cancer cells in vascular wall (P<0.0001) were all highly associated with the intraluminal vascular invasion. In univariate analysis, patients whose cancers had microscopic vascular invasion (median survival, 15.3 mo) had a significantly worse survival than did patients with carcinomas without vascular invasion (25.1 mo; P=0.01, log-rank test). Microscopic vascular invasion is a poor prognostic indicator and can histologically mimic PanIN.
虽然血管侵犯是浸润性胰腺导管腺癌（PDAC）患者预后不良的一个公认指标，但血管侵犯的组织病理学特征描述得并不清楚。对 209 例手术切除的浸润性 PDAC 的苏木精和伊红染色切片进行了系统性评估，以确定是否存在微血管侵犯。对于有血管侵犯的病例，我们进一步将侵犯的组织学模式分为常规型和胰腺上皮内肿瘤样（PanIN 样）。此外，还仔细评估了周围血管中的几个组织病理学因素，包括淋巴细胞浸润和管腔纤维化。将数据与包括患者生存在内的临床病理变量进行了比较。在 209 例 PDAC 中有 136 例（65.1%）观察到微血管侵犯。在有血管侵犯的 136 例中，有 94 例（69.1%）表现为类似于胰腺上皮内肿瘤（PanIN 样侵犯）。微血管侵犯与肿瘤体积增大（P=0.04）、更高的 pT 分级（P=0.003）、淋巴结转移（P<0.0001）和神经周围侵犯（P=0.005）有关。血管侵犯与新辅助治疗呈负相关（P<0.0001）。对相邻血管的检查显示，肿瘤周围血管内膜有淋巴细胞（P=0.002）、内膜（P=0.007）和中膜（P=0.001）纤维化以及血管壁内的癌细胞，均与管腔内血管侵犯高度相关。在单因素分析中，有微血管侵犯的患者（中位生存时间 15.3 个月）的生存情况明显比没有血管侵犯的患者（25.1 个月；P=0.01，对数秩检验）差。微血管侵犯是一个预后不良的指标，在组织学上可以模拟 PanIN。
