Ahn Ji Yong, Son Da Hye, Choi Kee Don, Roh Jin, Lim Hyun, Choi Kwi-Sook, Lee Jeong Hoon, Kim Do Hoon, Song Ho June, Lee Gin Hyug, Jung Hwoon-Yong, Kim Jin-Ho, Han Seungbong, Park Young Soo
Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, Asan Digestive Disease Research Institute, Seoul, Korea.
Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Asan Digestive Disease Research Institute, Seoul, Korea.
Gastrointest Endosc. 2014 Dec;80(6):1005-13.e2. doi: 10.1016/j.gie.2014.04.020. Epub 2014 Jun 11.
Little is known about gastric neoplasms arising from hyperplastic polyps (HPs).
To investigate the risk factors associated with neoplasms within HPs and to evaluate the role of alterations of the p16-cyclin D1-pRb pathway in the malignant transformation of HPs.
Retrospective, case-control study.
Tertiary-care center.
Between May 1995 and January 2011, a total of 809 HPs >1 cm were investigated. Associated neoplasms were present in 30 HPs (case group); 30 HPs without neoplasms were selected as a control group.
Gastric polypectomy.
The risk factors associated with neoplasms within HPs and immunohistochemical expression of p16, cyclin D1, p53, and Ki-67 between case and control groups.
Of the 809 HPs, 15 had associated dysplasia, and 15 had carcinoma. Multivariate analysis showed that neoplasm was associated with patient age (odds ratio [OR] 1.159; 95% confidence interval [CI], 1.243-2.044; P < .001), polyp size (OR 1.103; 95% CI, 1.055-1.152; P < .001), and polyp lobulation (OR 4.549; 95% CI, 1.759-11.0766; P < .001) but not with location, multiplicity, intestinal metaplasia, growth pattern, or Helicobacter pylori infection. Loss of p16 expression and high Ki-67 expression were observed in dysplastic areas of HPs compared with the control group (p16 = 14.3% vs 60%; P = .001, Ki-67 = 60.7% vs 36.7%; P < .001). However, no significant differences were found in nondysplastic areas in both groups.
Single-center, retrospective study.
HPs >1 cm may indicate the presence of neoplasms. Loss of p16 and high Ki-67 expression may be markers of HP-associated dysplasia.
关于增生性息肉（HP）引发的胃肿瘤，人们了解甚少。
研究与HP内肿瘤相关的危险因素，并评估p16 - 细胞周期蛋白D1 - pRb通路改变在HP恶变中的作用。
回顾性病例对照研究。
三级医疗中心。
1995年5月至2011年1月期间，共对809个直径大于1厘米的HP进行了研究。30个HP存在相关肿瘤（病例组）；选取30个无肿瘤的HP作为对照组。
胃息肉切除术。
与HP内肿瘤相关的危险因素以及病例组和对照组之间p16、细胞周期蛋白D1、p53和Ki - 67的免疫组化表达。
809个HP中，15个伴有发育异常，15个伴有癌。多因素分析显示，肿瘤与患者年龄（比值比[OR]1.159；95%置信区间[CI]，1.243 - 2.044；P <.001）、息肉大小（OR 1.103；95% CI，1.055 - 1.152；P <.001）和息肉分叶（OR 4.549；95% CI，1.759 - 11.0766；P <.001）相关，但与位置、多发性、肠化生、生长模式或幽门螺杆菌感染无关。与对照组相比，在HP发育异常区域观察到p16表达缺失和Ki - 67高表达（p16 = 14.3%对60%；P =.001，Ki - 67 = 60.7%对36.7%；P <.001）。然而，两组非发育异常区域未发现显著差异。
单中心回顾性研究。
直径大于1厘米的HP可能提示存在肿瘤。p16缺失和Ki - 67高表达可能是HP相关发育异常的标志物。
