Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Hum Pathol. 2010 Jun;41(6):838-47. doi: 10.1016/j.humpath.2009.11.011. Epub 2010 Feb 25.
Hepatocellular carcinoma develops in a multistep process. Previous studies have revealed changes in blood supply in hepatocellular carcinoma during its carcinogenesis. However, little is known about the relationship between tumor vasculature and the biological behavior of moderately differentiated hepatocellular carcinoma which demonstrates varied degrees of biological behavior. We immunohistochemically assessed intratumoral arterial vessel density (by high-molecular-weight caldesmon and calponin) and microvessel density (by CD34) in 123 cases of moderately differentiated hepatocellular carcinomas, and compared these densities with clinicopathological findings. Arterial vessel density and microvessel density of 19 well-differentiated and 37 poorly differentiated hepatocellular carcinomas were also evaluated. The arterial vessel density of moderately differentiated hepatocellular carcinomas with capsule formation, infiltration to the capsule, portal venous invasion, and high Ki-67 labeling index was lower than that of moderately differentiated hepatocellular carcinomas without these pathological findings (high-molecular-weight caldesmon: P < .0001, P = .0074, P = .0009, P = .0244, calponin: P < .0001, P = .0695, P = .0033, and P = .0155, respectively). The low arterial vessel density group (<10) of moderately differentiated hepatocellular carcinomas tended to show poorer overall survival than the high arterial vessel density group (>or=10) (high-molecular-weight caldesmon: P = .0347, calponin: P = .0404). The arterial vessel density and microvessel density of moderately differentiated hepatocellular carcinomas were significantly higher than those of well-differentiated hepatocellular carcinomas (high-molecular-weight caldesmon: P = .022, calponin: P = .027, CD34: P = .036) and poorly differentiated hepatocellular carcinomas (high-molecular-weight caldesmon, calponin and CD34: P < .0001). The moderately differentiated hepatocellular carcinomas with lower arterial vessel density had more malignant potential than those with higher arterial vessel density. The changes of arterial vessel density in moderately differentiated hepatocellular carcinomas were suggested.
肝细胞癌的发生是一个多步骤的过程。先前的研究已经揭示了在肝癌发生过程中肝癌血供的变化。然而，对于中等分化的肝癌，其肿瘤血管与不同程度生物学行为之间的关系知之甚少。我们采用免疫组织化学方法检测了 123 例中等分化肝癌的肿瘤内动脉血管密度（用高分子量钙调蛋白和钙调蛋白）和微血管密度（用 CD34），并将这些密度与临床病理发现进行了比较。还评估了 19 例分化良好和 37 例分化不良的肝癌的动脉血管密度。有包膜形成、包膜浸润、门静脉侵犯和 Ki-67 标记指数高的中等分化肝癌的动脉血管密度低于无这些病理发现的中等分化肝癌（高分子量钙调蛋白：P<0.0001，P=0.0074，P=0.0009，P=0.0244，钙调蛋白：P<0.0001，P=0.0695，P=0.0033，P=0.0155）。中等分化肝癌的低动脉血管密度组（<10）的总生存时间倾向于低于高动脉血管密度组（≥10）（高分子量钙调蛋白：P=0.0347，钙调蛋白：P=0.0404）。中等分化肝癌的动脉血管密度和微血管密度明显高于高分化肝癌（高分子量钙调蛋白：P=0.022，钙调蛋白：P=0.027，CD34：P=0.036）和低分化肝癌（高分子量钙调蛋白、钙调蛋白和 CD34：P<0.0001）。动脉血管密度较低的中等分化肝癌比动脉血管密度较高的中等分化肝癌具有更大的恶性潜能。提示中等分化肝癌的动脉血管密度发生变化。
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