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P53 缺失可能驱动多发性骨髓瘤的临床演变和治疗反应。

P53 deletion may drive the clinical evolution and treatment response in multiple myeloma.

机构信息

Servicio de Hematología, Hospital Universitario, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.

出版信息

Eur J Haematol. 2010 Apr;84(4):359-61. doi: 10.1111/j.1600-0609.2009.01399.x. Epub 2009 Dec 14.

Abstract

We report a patient with multiple myeloma presenting with a paraspinal plasmacytoma with a marked dissociation between the response obtained in bone marrow (BM) infiltration and that achieved in soft tissue masses. While a complete remission was reached and maintained in BM, extramedullary plasmacytomas were refractory to every line of treatment. Genetic analysis identified the presence of t(4;14) and RB deletion in myeloma cells of both origins. However, a P53 deletion was only detected in plasma cells from extramedullary plasmacytomas. This finding suggests that P53 deletion has a role in the lack of treatment response of extramedullary plasmacytomas.

摘要

我们报告了一例多发性骨髓瘤患者,其脊柱旁浆细胞瘤的骨髓浸润和软组织肿块的缓解程度明显分离。虽然骨髓完全缓解并维持,但髓外浆细胞瘤对每一线治疗均耐药。基因分析发现两种起源的骨髓瘤细胞均存在 t(4;14)和 RB 缺失。然而,仅在外髓浆细胞瘤的浆细胞中检测到 P53 缺失。这一发现表明 P53 缺失在外髓浆细胞瘤缺乏治疗反应中起作用。

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