Author/Authors :
Carrasco، نويسنده , , Daniel R. and Tonon، نويسنده , , Giovanni and Huang، نويسنده , , Yongsheng and Zhang، نويسنده , , Yunyu and Sinha، نويسنده , , Raktim and Feng، نويسنده , , Bin and Stewart، نويسنده , , James P. and Zhan، نويسنده , , Fenghuang and Khatry، نويسنده , , Deepak and Protopopova، نويسنده , , Marina and Protopopov، نويسنده , , Alexei and Sukhdeo، نويسنده , , Kumar and Hanamura، نويسنده , , Ichiro and Stephens، نويسنده , , Owen and Barlogie، نويسنده , , Bart and Anderson، نويسنده , , Kenneth C. and Chin، نويسنده , , Lynda and Shaughnessy Jr.، نويسنده , , John D. and Brennan، نويسنده , , Cameron and DePinho، نويسنده , , Ronald A.، نويسنده ,
Abstract :
Summary
ntify genetic events underlying the genesis and progression of multiple myeloma (MM), we conducted a high-resolution analysis of recurrent copy number alterations (CNAs) and expression profiles in a collection of MM cell lines and outcome-annotated clinical specimens. Attesting to the molecular heterogeneity of MM, unsupervised classification using nonnegative matrix factorization (NMF) designed for array comparative genomic hybridization (aCGH) analysis uncovered distinct genomic subtypes. Additionally, we defined 87 discrete minimal common regions (MCRs) within recurrent and highly focal CNAs. Further integration with expression data generated a refined list of MM gene candidates residing within these MCRs, thereby providing a genomic framework for dissection of disease pathogenesis, improved clinical management, and initiation of targeted drug discovery for specific MM patients.
