Media type: E-Article Title: Relevance of Ras gene mutations in the context of the molecular heterogeneity of multiple myeloma Contributor: Intini, Daniela; Agnelli, Luca; Ciceri, Gabriella; Ronchetti, Domenica; Fabris, Sonia; Nobili, Lucia; Lambertenghi‐Deliliers, Giorgio; Lombardi, Luigia; Neri, Antonino imprint: Wiley, 2007 Published in: Hematological Oncology Language: English DOI: 10.1002/hon.801 ISSN: 0278-0232; 1099-1069 Keywords: Cancer Research ; Oncology ; Hematology ; General Medicine Origination: Footnote: Description: <jats:title>Abstract</jats:title><jats:p><jats:italic>Ras</jats:italic> gene mutations are a recurrent genetic lesion in multiple myeloma (MM). Here, we report a mutation analysis of N‐ and K‐<jats:italic>Ras</jats:italic> genes in purified plasma cell populations from a panel of 81 newly diagnosed MM patients stratified according to the most frequent genetic and molecular features associated with the neoplasia. <jats:italic>Ras</jats:italic> gene mutations, mostly involving the N‐<jats:italic>Ras</jats:italic> gene, were detected in 20% of the patients. <jats:italic>Ras</jats:italic> mutations did not correlate with the presence of chromosome 13q deletion, trisomy of chromosome 11, 1q amplification or hyperdiploidy. In addition, despite an appreciable association with tumours overexpressing Cyclin D1, <jats:italic>Ras</jats:italic> mutations did not correlate at significant levels with any of the proposed groups in the <jats:italic>TC</jats:italic> classification, based on the presence of the major IgH chromosomal translocations and expression of <jats:italic>Cyclin D</jats:italic> genes. Finally, transcription analyses revealed the presence of differentially expressed transcripts in human multiple myeloma cell lines carrying the <jats:italic>Ras</jats:italic> gene mutations but not in primary tumours. Overall, these data suggest that <jats:italic>Ras</jats:italic> gene mutations are not likely to represent a master lesion in MM but its relevance needs to be considered in the context of other genetic abnormalities. Copyright © 2006 John Wiley & Sons, Ltd.</jats:p>