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CSE1L, DIDO1 and RBM39 in colorectal adenoma to carcinoma progression
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2012 (English)In: Cellular Oncology, ISSN 1570-5870, E-ISSN 2211-3436, Vol. 35, no 4, 293-300 p.Article in journal (Refereed) Published
Abstract [en]

Background Gain of chromosome 20q is an important factor in the progression from colorectal adenomas to carcinomas. Genes that drive 20q gain are expected to show correlation of mRNA and protein expression levels with 20q DNA copy number status while functionally influencing cancer processes. CSE1L, DIDO1 and RBM39 are located on the 20q amplicon and affect processes such as cell viability and anchorage-independent growth in colorectal cancer. This study aimed to investigate whether CSE1L, DIDO1 and RBM39 may drive 20q amplification.

Methods Protein expression levels were examined by immunohistochemical evaluation of tissue microarrays containing a series of colorectal adenoma and carcinoma samples, which were characterized by genome-wide (microarray-based) DNA and mRNA profiling.

Results CSE1L, DIDO1 and RBM39 mRNA expression levels correlated with chromosome 20q DNA copy number status. CSE1L protein expression was not associated with 20q gain, although its expression was increased in carcinomas compared to adenomas. DIDO1 and RBM39 protein expression was quite strong in the majority of tumors irrespective of 20q DNA copy number status.

Conclusion The lack of correlation between protein expression levels and 20q DNA copy number status implies that CSE1L, DIDO1 and RBM39 are merely passengers rather than drivers of chromosome 20q gain in colorectal adenoma-to-carcinoma progression.

Place, publisher, year, edition, pages
2012. Vol. 35, no 4, 293-300 p.
Keyword [en]
Colorectal adenoma-to-carcinoma progression, Chromosome 20q gain, CSE1L, DIDO1, RBM39, Driver genes
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-181415DOI: 10.1007/s13402-012-0088-2ISI: 000306950400006OAI: oai:DiVA.org:uu-181415DiVA: diva2:557592
Available from: 2012-09-28 Created: 2012-09-24 Last updated: 2012-09-28Bibliographically approved

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