INTRODUCTION: The adenomatous polyposis coli (APC) gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It has been shown to be involved in genetic instability and to be down-regulated in several human carcinomas. The chromosome locus of APC, 5q21-22, is frequently deleted in gastric cancers (GCs). The functional impact of such regions needs to be extensively investigated in large amount of clinical samples. PATIENTS AND MATERIALS: Case-matched tissues of GC and adjacent normal epithelium (n = 141) were included in this study. Quantitative PCR was carried out to examine the copy number as well as mRNA expression of APC gene in gastric malignancies. RESULTS: Our results showed that copy number deletions of APC were present in a relatively high percentage (25.9%, 34 out of 131) of gastric cancer samples. There was a correlation between APC deletion and tumor progression (p < 0.01) as well as gene expression (p < 0.05) in collected GC samples. On the other hand, mRNA levels of APC were also impaired in GC samples with unaltered copy numbers. CONCLUSION: Sporadic GCs exhibit different mechanisms of APC regulation.
INTRODUCTION: The adenomatous polyposis coli (APC) gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It has been shown to be involved in genetic instability and to be down-regulated in several humancarcinomas. The chromosome locus of APC, 5q21-22, is frequently deleted in gastric cancers (GCs). The functional impact of such regions needs to be extensively investigated in large amount of clinical samples. PATIENTS AND MATERIALS: Case-matched tissues of GC and adjacent normal epithelium (n = 141) were included in this study. Quantitative PCR was carried out to examine the copy number as well as mRNA expression of APC gene in gastric malignancies. RESULTS: Our results showed that copy number deletions of APC were present in a relatively high percentage (25.9%, 34 out of 131) of gastric cancer samples. There was a correlation between APC deletion and tumor progression (p < 0.01) as well as gene expression (p < 0.05) in collected GC samples. On the other hand, mRNA levels of APC were also impaired in GC samples with unaltered copy numbers. CONCLUSION: Sporadic GCs exhibit different mechanisms of APC regulation.
Authors: J Sanz-Ortega; J Sanz-Esponera; T Caldes; E Gomez de la Concha; M E Sobel; M J Merino Journal: Pathol Res Pract Date: 1996-12 Impact factor: 3.250
Authors: B Yu; Y Shao; P Li; J Zhang; Q Zhong; H Yang; X Hu; B Chen; X Peng; Q Wu; Y Chen; M Guan; J Wan; W Zhang Journal: Br J Dermatol Date: 2010-11 Impact factor: 9.302
Authors: K L Neufeld; D A Nix; H Bogerd; Y Kang; M C Beckerle; B R Cullen; R L White Journal: Proc Natl Acad Sci U S A Date: 2000-10-24 Impact factor: 11.205
Authors: Winnie S Liang; David W Craig; John Carpten; Mitesh J Borad; Michael J Demeure; Glen J Weiss; Tyler Izatt; Shripad Sinari; Alexis Christoforides; Jessica Aldrich; Ahmet Kurdoglu; Michael Barrett; Lori Phillips; Hollie Benson; Waibhav Tembe; Esteban Braggio; Jeffrey A Kiefer; Christophe Legendre; Richard Posner; Galen H Hostetter; Angela Baker; Jan B Egan; Haiyong Han; Douglas Lake; Edward C Stites; Ramesh K Ramanathan; Rafael Fonseca; A Keith Stewart; Daniel Von Hoff Journal: PLoS One Date: 2012-10-10 Impact factor: 3.240