Gastroenterology · 2001
Genetic differences between adenocarcinomas arising in Barrett's esophagus and gastric mucosa.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
El-Rifai W, Frierson H F, Moskaluk C A, Harper J C, Petroni G R, Bissonette E A, Jones D R, Knuutila S, Powell S M
Аннотация
BACKGROUND & AIMS: Barrett adenocarcinoma (BA+) and gastric adenocarcinoma comprise a related group of neoplasms that nevertheless have some distinct clinicopathologic characteristics. This study aimed at defining critical molecular abnormalities that may underlie differences between BA+ and gastric adenocarcinomas.
METHODS: We used comparative genomic hybridization for the analyses of 34 xenografts of adenocarcinomas that arose from esophageal or gastric origin.
RESULTS: All tumors, except one, exhibited DNA copy number alterations. Losses in 4q and 14q and gains at 2p and 17q were more frequent in proximal (esophageal, gastroesophageal junction [GEJ], and cardia) tumors than in distal (body and antrum) tumors (P <or= 0.050). These changes were significantly higher in BA+ compared with distal tumors (P <or= 0.040). In addition, losses in 5q and gains at 20q were significantly higher in BA+ than in distal cancers (P <or= 0.040). Losses in 5q and 8p and gains at 2q, 6p, 12p, and 20q were significantly more frequent in BA+ tumors (P <or= 0.050) than in GEJ and cardiac tumors without associated Barrett's esophagus. Additionally, losses in 14q, which were common in proximal tumors, were more often seen in BA+ (P = 0.100) than in other proximal tumors.
CONCLUSIONS: Although these adenocarcinomas share some common genetic alterations, the differences in the DNA copy numbers in BA+ cases suggest that unique genetic alterations may be involved in these cancers' development.
METHODS: We used comparative genomic hybridization for the analyses of 34 xenografts of adenocarcinomas that arose from esophageal or gastric origin.
RESULTS: All tumors, except one, exhibited DNA copy number alterations. Losses in 4q and 14q and gains at 2p and 17q were more frequent in proximal (esophageal, gastroesophageal junction [GEJ], and cardia) tumors than in distal (body and antrum) tumors (P <or= 0.050). These changes were significantly higher in BA+ compared with distal tumors (P <or= 0.040). In addition, losses in 5q and gains at 20q were significantly higher in BA+ than in distal cancers (P <or= 0.040). Losses in 5q and 8p and gains at 2q, 6p, 12p, and 20q were significantly more frequent in BA+ tumors (P <or= 0.050) than in GEJ and cardiac tumors without associated Barrett's esophagus. Additionally, losses in 14q, which were common in proximal tumors, were more often seen in BA+ (P = 0.100) than in other proximal tumors.
CONCLUSIONS: Although these adenocarcinomas share some common genetic alterations, the differences in the DNA copy numbers in BA+ cases suggest that unique genetic alterations may be involved in these cancers' development.