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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1228-1232. Prepublished online as a Blood First Edition Paper on July 13, 2006; DOI 10.1182/blood-2006-05-024661. This Article Full Text (PDF) All Versions of this Article: blood-2006-05-024661v1 109/3/1228    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gonzalez-Paz, N. Articles by Fonseca, R. Search for Related Content PubMed PubMed Citation Articles by Gonzalez-Paz, N. Articles by Fonseca, R. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 22, 2006 Accepted June 20, 2006 Tumor suppressor p16 methylation in multiple myeloma: biological and clinical implications Natalia Gonzalez-Paz, Wee J Chng, Rebecca F McClure, Emily Blood, Martin M Oken, Brian Van Ness, C D James, Paul J Kurtin, Kimberly Henderson, Gregory J Ahmann, Morie Gertz, Martha Lacy, Angela Dispenzieri, Philip R Greipp, and Rafael Fonseca* Department of Hematology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA Dept. Hematology-oncology, Mayo Clinic Scottsdale, AZ, USA Laboratory Medicine and Pathology and Mayo Clinic College of Medicine, Rochester, Minnesota, USA Eastern Cooperative Oncology Group (ECOG), USA Experimental Pathology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA * Corresponding author; email: fonseca.rafael{at}mayo.edu. The biological and clinical implications of p16 gene methylation in multiple myeloma (MM) are still unclear despite previous studies. In this comprehensive study, using methylation-specific PCR (MS-PCR), we show that p16 methylation is relatively common and occurs in MGUS (n=17), SMM (n=40) and MM (n=522) at a prevalence of 24%, 28% and 34% respectively. However, p16 methylation does not appear to affect gene expression level. In a large cohort of patients with long-term follow-up information (n=439), there was no difference in overall survival between patients with or without p16 methylation. We also found no association between p16 methylation and the main cytogenetic categories, although it was more common among patients with 17p13.1 deletions (p53 locus), a genetic progression event in MM. In addition, p16 methylation have no apparent effect on the cycle as there was also no difference in the plasma cell labeling index (a direct measurement of proliferation) between patients with and without p16 methylation. Our results question a major role for p16 methylation in the oncogenesis of the PC neoplasm, and we now believe p16 methylation may be a marker for overall epigenetic changes associated with disease progression, with no obvious direct biological or clinical consequences. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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