Wu T T, Watanabe T, Heitmiller R, Zahurak M, Forastiere A A, Hamilton S R
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2196, USA.
Am J Pathol. 1998 Jul;153(1):287-94. doi: 10.1016/S0002-9440(10)65570-8.
The incidence of esophageal adenocarcinoma has increased markedly in the past two decades, but the genetic alterations in this cancer and its precursor, Barrett mucosa, have not been characterized extensively. DNA replication errors and allelic losses of chromosomes 17p, 18q, and 5q were studied in 36 resected adenocarcinomas arising in the esophagus and esophagogastric junction, 56 Barrett adenocarcinomas, and 11 dysplasias in Barrett esophagus. The results were compared with clinical and pathological characteristics, including patient survival. Replication error positive cancer was rare (5.4%) in esophageal adenocarcinomas and was not found in Barrett mucosa. There was an increase in the prevalence of chromosomal losses in the Barrett mucosa-columnar dysplasia-adenocarcinoma sequence: 17p loss occurred in 14% of Barrett mucosae, 42% of low-grade dysplasias, 79% of high-grade dysplasias, and 75% of adenocarcinomas, respectively; loss of 18q in 32%, 42%, 73%, and 69%; and loss of 5q in 10%, 21%, 27%, and 46%. Clinical stage was a very strong prognostic factor for survival, and adenocarcinomas with allelic loss of both 17p and 18q had worse survival than cancers with no or one allelic loss (P = 0.002). Our results indicate that accumulation of genetic alterations follows the dysplasia-adenocarcinoma sequence in the esophagus and that losses of 18q and 17p occur earlier than 5q loss. Allelic loss of both 17p and 18q in esophageal adenocarcinoma identifies patients with poor prognosis.
在过去二十年中,食管腺癌的发病率显著上升,但这种癌症及其癌前病变巴雷特黏膜的基因改变尚未得到广泛研究。我们对36例食管及食管胃交界部切除的腺癌、56例巴雷特腺癌和11例巴雷特食管发育异常进行了DNA复制错误及17号染色体短臂(17p)、18号染色体长臂(18q)和5号染色体长臂(5q)的等位基因缺失研究。并将结果与包括患者生存情况在内的临床和病理特征进行了比较。食管腺癌中复制错误阳性的癌症很少见(5.4%),在巴雷特黏膜中未发现。在巴雷特黏膜-柱状上皮发育异常-腺癌序列中,染色体缺失的发生率增加:17p缺失分别发生在14%的巴雷特黏膜、42%的低级别发育异常、79%的高级别发育异常和75%的腺癌中;18q缺失分别为32%、42%、73%和69%;5q缺失分别为10%、21%、27%和46%。临床分期是生存的一个非常重要的预后因素,17p和18q等位基因均缺失的腺癌患者的生存率低于无或仅有一个等位基因缺失的癌症患者(P = 0.002)。我们的结果表明,食管中基因改变的积累遵循发育异常-腺癌序列,18q和17p的缺失比5q缺失更早发生。食管腺癌中17p和18q的等位基因缺失可识别预后不良的患者。