Park Geun Soo, Joo Young Eun, Kim Hyun Soo, Choi Sung Kyu, Rew Jong Sun, Park Chang Soo, Kim Sei Jong
Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Korean J Gastroenterol. 2005 Sep;46(3):196-203.
BACKGROUND/AIMS: Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a recently clarified tumor suppressor gene located in 10q23.3. Alterations of this gene are associated with tumor progression and unfavorable outcome in various human cancers. Recently, PTEN has a possible role in angiogenesis by modulating angiogenic factor including vascular endothelial growth factor (VEGF). The aim of this study was to investigate the roles of PTEN and VEGF status for angiogenesis in human gastric cancer.
We conducted an immunohistochemical investigation of PTEN and VEGF expression in 90 cases of paraffin section obtained from gastric cancer patients undergone surgical treatment.
Negative expression of PTEN and positive expression of VEGF in gastric cancer tissues, were demonstrated in 40.0% and 77.8% of cases, respectively. However, no significant correlation was found between PTEN, VEGF expression and various clinicopathological parameters. PTEN expression did not correlate significantly with VEGF expression (p=0.301). High microvessel density (MVD) was significantly associated with lymph node metastasis and poor survival (p=0.014, 0.011, respectively). The mean MVD value of PTEN negative tumors was 90.4+/-43.0 and significantly higher than that of PTEN positive tumors (p=0.028). The mean MVD value of VEGF positive tumors was 86.4+/-6.7 and significantly higher than that of VEGF negative tumors (p=0.002). The mean MVD value of PTEN negative and VEGF positive tumors was 98.0+/-42.2, and significantly higher than those of the others.
These results suggest that loss of PTEN expression may play a critical role in tumor progression and metastasis by stimulating tumor angiogenesis in human gastric cancer.
背景/目的:第10号染色体缺失的磷酸酶及张力蛋白同源物(PTEN)是一种最近才明确的肿瘤抑制基因,位于10q23.3。该基因的改变与多种人类癌症的肿瘤进展及不良预后相关。最近,PTEN可能通过调节包括血管内皮生长因子(VEGF)在内的血管生成因子在血管生成中发挥作用。本研究的目的是探讨PTEN和VEGF状态在人类胃癌血管生成中的作用。
我们对90例接受手术治疗的胃癌患者的石蜡切片进行了PTEN和VEGF表达的免疫组织化学研究。
胃癌组织中PTEN阴性表达和VEGF阳性表达分别在40.0%和77.8%的病例中得到证实。然而,PTEN、VEGF表达与各种临床病理参数之间未发现显著相关性。PTEN表达与VEGF表达无显著相关性(p=0.301)。高微血管密度(MVD)与淋巴结转移及不良生存显著相关(分别为p=0.014、0.011)。PTEN阴性肿瘤的平均MVD值为90.4±43.0,显著高于PTEN阳性肿瘤(p=0.028)。VEGF阳性肿瘤的平均MVD值为86.4±6.7,显著高于VEGF阴性肿瘤(p=0.002)。PTEN阴性且VEGF阳性肿瘤的平均MVD值为98.0±42.2,显著高于其他肿瘤。
这些结果表明,PTEN表达缺失可能通过刺激人类胃癌的肿瘤血管生成在肿瘤进展和转移中起关键作用。