AMACR amplification and overexpression in primary imatinib-naive gastrointestinal stromal tumors: a driver of cell proliferation indicating adverse prognosis.

ABSTRACT: Non-random gains of chromosome 5p have been observed in clinically aggressive gastrointestinal stromal tumors, whereas the driving oncogenes on 5p remain to be characterized. We used an integrative genomic and functional approach to identify amplified oncogenes on 5p and to evaluate the relevance of AMACR amplification at 5p13.3 and its overexpression in gastrointestinal stromal tumors. Thirty-seven tumor samples, imatinib-sensitive GIST882 cell line, and imatinib-resistant GIST48 cell line were analyzed for DNA imbalances using array-based genomic profiling. Forty-one fresh tumor samples of various risk categories were enriched for pure tumor cells by laser capture microdissection and quantified for AMACR mRNA expression. AMACR-specific fluorescence in situ hybridization and immunohistoch

SUBMITTER: Li CF 

PROVIDER: S-EPMC4294386 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature