Researchers from Department of Cancer Prevention reveal importance for transcriptome instability in colorectal cancer

Sveen (left) and Ňgesen, with shared first-authorship
Anita Sveen, Trude √Ögesen and co-workers at the Department of Cancer Prevention have published a paper in Genome Medicine describing transcriptome instability as a novel phenotype in colorectal cancer. This paper is the first to describe that the genome-wide amount of alternative splicing is varying in colorectal cancers. The study further shows that transcriptome instability is linked to the expression level of most splicing factors and is as well associated with patient survival.
The article is covered on the blog of BioMed Central and highlighted as Editor's pick on the journal web pages.

With 3,500 new cases in Norway each year, colorectal cancer is one of the most common types of cancer. Colorectal tumors are characterized by genomic instability, causing multiple and genome-wide genetic changes that are associated with certain risk factors and clinical features. On the RNA level, one way of causing variation is by producing structurally different transcripts via alternative splicing of pre-mRNA.

In the recent paper, Sveen et al. have used exon microarray analyses to describe great genome-wide heterogeneity in exon usage among colorectal cancers. They show that this amount of exon usage variation is associated with the expression levels of splicing factors, suggesting a potential biological rationale for such transcriptome instability. They also show that patients with a high degree of transcriptome instability have poorer survival than patients whose tumors exhibit average exon usage patterns, indicating that structural transcriptome variation may also be an important biological and clinical characteristic of colorectal cancer, analogous to genomic variation.


"Transcriptome instability in colorectal cancer identified by exon microarray analyses: Associations with splicing factor expression levels and patient survival"
Sveen A*, √Ögesen TH*, Nesbakken A, Rognum TO, Lothe RA, Skotheim RI.
Genome Medicine 2011, 3:32
*These authors contributed equally to this study

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