Liang J-T, Huang K-C, Jeng Y-M, Lee P-H, Lai H-S, Hsu H-C
Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, Republic of China.
Br J Surg. 2004 Mar;91(3):355-61. doi: 10.1002/bjs.4447.
Tumour angiogenesis, cyclo-oxygenase (COX) 2 expression, K-ras mutation and p53 overexpression are commonly involved in colorectal tumorigenesis, but their interrelationship and clinicopathological effects remain inconclusive.
Clinicopathological data from 114 consecutive patients with primary stage III colorectal cancer were evaluated prospectively. Microvessel density (MVD) of the tumour was defined by counting the number of microvessels in hotspots, visualized by immunocytochemical staining of endothelial CD34. K-ras mutation was analysed by the restriction enzyme cleavage method. COX-2 expression and p53 overexpression were determined by immunocytochemistry.
Increased MVD in hotspots was significantly associated with COX-2 expression (P < 0.001), K-ras mutation (P = 0.007) and p53 overexpression (P = 0.006). COX-2 expression was not associated with either K-ras mutation or p53 overexpression. Clinicopathologically, greater MVD and COX-2 expression were significantly associated with vascular invasion of cancer cells (MVD, P = 0.027 and COX-2 expression, P = 0.006), but p53 overexpression and K-ras mutation were not. Multivariate analysis indicated that greater MVD (P = 0.002) and p53 overexpression (P = 0.016) were significant independent predictors of tumour recurrence, whereas COX-2 expression (P = 0.634) and K-ras mutation (P = 0.356) were not.
Tumour angiogenesis may be associated with tumour metastasis and is significantly influenced by K-ras mutation, p53 overexpression and COX-2 expression in patients with colonic cancer.
肿瘤血管生成、环氧化酶（COX）-2表达、K-ras突变和p53过表达通常参与结直肠癌的发生，但它们之间的相互关系及临床病理影响仍不明确。
对114例连续的原发性III期结直肠癌患者的临床病理资料进行前瞻性评估。通过对内皮细胞CD34进行免疫细胞化学染色，计数热点区域微血管数量来确定肿瘤的微血管密度（MVD）。采用限制性内切酶切割法分析K-ras突变。通过免疫细胞化学检测COX-2表达和p53过表达。
热点区域MVD增加与COX-2表达（P<0.001）、K-ras突变（P=0.007）和p53过表达（P=0.006）显著相关。COX-2表达与K-ras突变或p53过表达均无关联。在临床病理方面，较高的MVD和COX-2表达与癌细胞血管侵犯显著相关（MVD，P=0.027；COX-2表达，P=0.006），但p53过表达和K-ras突变则不然。多因素分析表明，较高的MVD（P=0.002）和p53过表达（P=0.016）是肿瘤复发的显著独立预测因素，而COX-2表达（P=0.634）和K-ras突变（P=0.356）则不是。
肿瘤血管生成可能与肿瘤转移有关，并且在结肠癌患者中受K-ras突变、p53过表达和COX-2表达的显著影响。
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