Deletion analysis of the p16 tumor suppressor gene in gastrointestinal mucosa-associated lymphoid tissue lymphomas.
Deletion analysis of the p16 tumor suppressor gene in gastrointestinal mucosa-associated lymphoid tissue lymphomas.
复制标题
胃肠粘膜相关淋巴组织淋巴瘤中p16抑癌基因的缺失分析。
作者：
Peter Neumeister;Gerald Hoefler;Christine Beham;Helmut H. Schmidt;U. Apfelbeck;Helmut Schaider;Werner Linkesch;Heinz Sill
背景与目标
胃肠道粘膜相关淋巴组织（MALT）淋巴瘤发生和发展的分子机制尚不清楚。本研究的目的是分析p16抑癌基因在胃和结肠MALT淋巴瘤。
方法
从28例低级别（n = 12）和高级别（n = 14）胃MALT淋巴瘤患者和2例结肠MALT淋巴瘤患者中获得肿瘤样本。从具有至少80%肿瘤细胞的显微切割区域提取DNA。为了检测纯合性p16缺失，使用半定量聚合酶链反应测定，其中p16外显子1或外显子2与作为内部对照的不相关序列共扩增。
结果
在14例高级别胃MALT淋巴瘤中有2例（14%）发现纯合子p16缺失。这两名患者都有幽门螺杆菌相关性胃炎;然而，从胃炎区域提取的DNA显示正常的p16补体。在任何低度胃或结肠MALT淋巴瘤标本中均未发现缺失。
结论
在胃MALT淋巴瘤的一个子集中，获得了纯合p16缺失，并可能导致从低度恶性转化为高度恶性。
BACKGROUND & AIMS
The molecular mechanisms responsible for initiation and progression of gastrointestinal mucosa-associated lymphoid tissue (MALT) lymphomas are largely unknown. The aim of this study was to analyze the p16 tumor suppressor gene in MALT lymphomas of the stomach and colon.
METHODS
Tumor samples were obtained from 28 patients with low-grade (n = 12) and high-grade (n = 14) gastric MALT lymphomas and from 2 patients with colonic MALT lymphomas. DNA was extracted from microdissected areas with at least 80% tumor cells. To detect homozygous p16 deletions, a semiquantitative polymerase chain reaction assay was used, whereby either p16 exon 1 or exon 2 was coamplified with an unrelated sequence as internal control.
RESULTS
Homozygous p16 deletions were found in 2 of 14 (14%) cases with high-grade gastric MALT lymphomas. Both patients had Helicobacter pylori-associated gastritis; however, DNA extracted from areas of gastritis showed a normal p16 complement. No deletion was found in any of the low-grade gastric or the colonic MALT lymphoma specimens.
CONCLUSIONS
In a subset of gastric MALT lymphomas, homozygous p16 deletions are acquired and may contribute to the transformation from a low-grade to a high-grade malignancy.
影响因子：
20.3
作者：
T. Hirama;H. Koeffler
通讯作者：
T. Hirama;H. Koeffler