Analysis of Expression Profile of Gene Encoding Proteins of Signal Cascades Activated by Insulin-like Growth Factors in Colorectal Cancer

The aim of the study is to analyse gene typing with the use of the microarray technique (HG-U133A, Affymetrix), differentiating colorectal cancer tissues from tissues assessed histopathologically as healthy ones among a panel of 93 mRNA of gene encoding proteins involved in the activation of cellula...

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Bibliographic Details
Published in:International journal of immunopathology and pharmacology 2011-07, Vol.24 (3), p.781-787
Main Authors: Nowakowska-Zajdel, E., Mazurek, U., Ziółko, E., Niedworok, E., Fatyga, E., Kokot, T., Muc-Wierzgoń, M.
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Body Mass Index
Colorectal Neoplasms - genetics
Female
Gene Expression Profiling
Humans
Insulin-Like Growth Factor I - genetics
Insulin-Like Growth Factor II - genetics
Male
Microarray Analysis
Middle Aged
Neoplasm Staging
Receptor, IGF Type 1 - genetics
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
Sex Characteristics
Signal Transduction - genetics
Somatomedins - genetics
Transcriptome
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Summary:The aim of the study is to analyse gene typing with the use of the microarray technique (HG-U133A, Affymetrix), differentiating colorectal cancer tissues from tissues assessed histopathologically as healthy ones among a panel of 93 mRNA of gene encoding proteins involved in the activation of cellular signal transduction pathways by insulin-like growth factors. The study was conducted on a group of 8 colorectal cancer patients. Frozen tumor and healthy specimens from the patients were used in molecular tests. Transcript IGF2 differentiated cancer from healthy tissue. Among the genes participating in the cascade of signal transfer in cells activated by IGF, GRB10, PIK3R3, PIK3R1, and IRSI were qualified as differentiating transcripts. IRSI indicated over-expression in tumour. Transcript SMAD2 showed a significant changed in tumour samples (increased expression).
ISSN:0394-6320
2058-7384
DOI:10.1177/039463201102400324