实验描述
GIST is considered to invariably arise through gain-of-function KIT or PDGFRA mutation of the interstitial cells of Cajal (ICC). However, the genetic basis of the malignant progression of GIST is poorly understood. We analysed the expression levels of 54,613 probe sets in 32 surgical samples of untreated GIST of the stomach and small intestine with GeneChip Human Genome U133 Plus 2.0 arrays. Experiment Overall Design: Total RNA was extracted from 32 fresh frozen tumour specimens. We analysed the global gene exprssion profiles of these GIST cases in order to clarify the genomic basis behind the malignant progression of this tumor
参考文献
Distinct gene expression-defined classes of gastrointestinal stromal tumor
Yamaguchi U, Nakayama R, Honda K, Ichikawa H, Hasegawa T, Shitashige M, Ono M, Shoji A, Sakuma T, Kuwabara H, Shimada Y, Sasako M, Shimoda T, Kawai A, Hirohashi S, Yamada T.
PMID: 18757323
芯片平台
A-AFFY-44
Affymetrix GeneChip Human Genome U133 Plus 2.0 [HG-U133_Plus_2](32 例)
样本属性
Age
34 years, 40 years, 41 years, 47 years, 50 years, 51 years, 52 years, 54 years, 55 years, 56 years, 58 years, 61 years, 63 years, 64 years, 68 years, 69 years, 71 years, 72 years, 76 years, 77 years, 81 years, 82 years
Disease State
gastrointestinal stromal tumor
Genotype
KIT mutation: Exon 11, KIT mutation: Exon 9, KIT mutation: wildtype
OrganismPart
small intestine, stomach
TumorSize
10 centimetre, 11 centimetre, 12 centimetre, 13 centimetre, 17 centimetre, 18 centimetre, 19 centimetre, 20 centimetre, 21 centimetre, 25 centimetre, 3 centimetre, 38 centimetre, 4 centimetre, 5 centimetre, 6 centimetre, 7 centimetre, 8 centimetre