BACKGROUND & AIMS: A different spectrum of genetic changes including p53, c-erbB-2, c-met, adenomatous polyposis coli (APC), and deleted in colorectal cancer (DCC) is involved in gastric cancer (GC). The aim of this study was to correlate these alterations with histological subtypes, tumor stages, and Helicobacter pylori infection. METHODS: Specimens of 163 patients with GC were immunostained for p53, c-erbB-2, and c-met, and polymerase chain reaction was performed in them to determine loss of heterozygosity (LOH) of APC and DCC. RESULTS: Overexpression of p53 was more frequent in early intestinal than early diffuse GC and was noted in the stage progression of diffuse but not intestinal GC. Overexpression of c-erbB-2 occurred more commonly in intestinal GC and advanced GC of both types. Overexpression of c-met was greater in diffuse GC, particularly at advanced stage. LOH of APC was more common in intestinal GC irrespective of the stage but rarely in diffuse GC. LOH of DCC occurred primarily in advanced intestinal GC and infrequently in early GC or advanced diffuse GC. Alterations of these five genes were not correlated with H. pylori infection. CONCLUSIONS: A distinct genetic pathway exists in gastric carcinogenesis of different histological subtypes and their tumor progression, in which H. pylori infection may play an equal role or no role.
BACKGROUND & AIMS: A different spectrum of genetic changes including p53, c-erbB-2, c-met, adenomatous polyposis coli (APC), and deleted in colorectal cancer (DCC) is involved in gastric cancer (GC). The aim of this study was to correlate these alterations with histological subtypes, tumor stages, and Helicobacter pylori infection. METHODS: Specimens of 163 patients with GC were immunostained for p53, c-erbB-2, and c-met, and polymerase chain reaction was performed in them to determine loss of heterozygosity (LOH) of APC and DCC. RESULTS: Overexpression of p53 was more frequent in early intestinal than early diffuse GC and was noted in the stage progression of diffuse but not intestinal GC. Overexpression of c-erbB-2 occurred more commonly in intestinal GC and advanced GC of both types. Overexpression of c-met was greater in diffuse GC, particularly at advanced stage. LOH of APC was more common in intestinal GC irrespective of the stage but rarely in diffuse GC. LOH of DCC occurred primarily in advanced intestinal GC and infrequently in early GC or advanced diffuse GC. Alterations of these five genes were not correlated with H. pyloriinfection. CONCLUSIONS: A distinct genetic pathway exists in gastric carcinogenesis of different histological subtypes and their tumor progression, in which H. pyloriinfection may play an equal role or no role.
Authors: Jochen K Lennerz; Eunice L Kwak; Allison Ackerman; Michael Michael; Stephen B Fox; Kristin Bergethon; Gregory Y Lauwers; James G Christensen; Keith D Wilner; Daniel A Haber; Ravi Salgia; Yung-Jue Bang; Jeffrey W Clark; Benjamin J Solomon; A John Iafrate Journal: J Clin Oncol Date: 2011-10-31 Impact factor: 44.544
Authors: Stefan Kubicka; Christiane Claas; Sven Staab; Florian Kühnel; Lars Zender; Christian Trautwein; Siegfried Wagner; Karl Lenhard Rudolph; Michael Manns Journal: Dig Dis Sci Date: 2002-01 Impact factor: 3.199
Authors: Bastiaan P van Rees; Eric Caspers; Axel zur Hausen; Adriaan van den Brule; Paul Drillenburg; Marian A J Weterman; G Johan A Offerhaus Journal: Am J Pathol Date: 2002-10 Impact factor: 4.307
Authors: Tineke E Buffart; Nicole C T van Grieken; Marianne Tijssen; Jordy Coffa; Bauke Ylstra; Heike I Grabsch; Cornelis J H van de Velde; Beatriz Carvalho; Gerrit A Meijer Journal: Virchows Arch Date: 2009-08-21 Impact factor: 4.064