4.4 Article

Additional genetic abnormalities significantly worsen poor prognosis associated with 1q21 amplification in multiple myeloma patients

期刊

HEMATOLOGICAL ONCOLOGY
卷 31, 期 1, 页码 41-48

出版社

WILEY
DOI: 10.1002/hon.2018

关键词

Multiple myeloma; 1q21 amplification; prognosis

资金

  1. Foundation for Polish Science [NN402287236]

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We investigated the prognostic value of amp(1q21) alone and in combination with other abnormalities in newly diagnosed myeloma patients. The study group consisted of 104 patients treated with various induction regimens, mostly thalidomide based (87 patients). Amp(1q21) was detected in 49 (47.1%) of patients; in 26 (25.0%) cases, it was combined with del(13q14), in 7 (6.7%) with del(17p13) and in 15 (14.4%) with t(4;14)(p16;q32). The response rate was significantly better in amp(1q21)-negative than in amp(1q21)-positive patients (74.5% vs 55.1%, p=0.025; complete response 18.2% vs 4.1%, p=0.024). The median progression-free survival (PFS) was 33.9months in patients without amp(1q21) and 10.3months with this aberration (p=0.002). The presence of additional abnormalities resulted in significantly shortened PFS when compared with patients with isolated amp(1q21): coexisting del(13q14) resulted in 7.8 vs 29.0months of PFS (p=0.024) and del(17p13) resulted in 4.0 vs 24.9months of PFS (p=0.034). The presence of amp(1q21) significantly influenced overall survival (OS) as well as PFS resulting in the median OS of 26.6 vs 62.4months (p=0.018) in patients without amp(1q21). The presence of additional genetic abnormalities significantly affected OS when compared with patients carrying isolated amp(1q21): for del(13q14) 18.9 vs 58.4months (p=0.004) and for del(17p13) 12.0 vs 46.5months (p=0.036). On multivariate analysis amp(1q21), del(13q14) and del(17p13) were found to be an independent adverse predictors of shorter PFS and OS. Our results showed that the presence of amp(1q21) was associated with poor prognosis. Moreover additional genetic abnormalities made PFS and OS further shortened. Copyright (c) 2012 John Wiley & Sons, Ltd.

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