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11 - Multiple myeloma: management of de novo disease to include HDT

from Section 3 - Myeloma: clinical entities

Published online by Cambridge University Press:  18 December 2013

Stephen A. Schey
Affiliation:
Department of Haematology, King’s College Hospital, London
Kwee L. Yong
Affiliation:
Department of Haematology, University College Hospital, London
Robert Marcus
Affiliation:
Department of Haematology, King’s College Hospital, London
Kenneth C. Anderson
Affiliation:
Dana-Farber Cancer Institute, Boston
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Summary

Introduction

Treatment strategies of de novo symptomatic multiple myeloma (MM) are mainly related to age and comorbidity. Patients <65 years of age without major organ dysfunction (renal, liver, heart and lung) are eligible for intensive chemotherapy and ASCT[1]. The goal of this approach is to obtain a durable complete remission and long-term disease control. A reduced-intensity conditioning regimen followed by ASCT may be also used in patients aged 65–70, or younger patients with pre-existing comorbidities[2]. Patients older than 65 and those who are ineligible for transplantation are candidates for melphalan–prednisone (MP)-based chemotherapy in combination with the new drugs thalidomide, bortezomib and lenalidomide [2].

Risk stratification in multiple myeloma

Multiple myeloma is a heterogeneous disease with variable clinical presentation and prognosis with a survival outcome that ranges from one year in a patient with aggressive disease to ten years in a patient with indolent disease presentation. Evaluation of prognostic factors and risk stratification is important to define appropriate treatment strategies. There is consensus that the current risk stratification is applicable to newly diagnosed patients: a report of the International Myeloma Workshop consensus panel suggested the following parameters: serum beta2 microglobulin and albumin (ISS stage), cytogenetic translocation determined by fluorescent in situ hybridization (FISH) analysis [t(4;14), t(14;16), del(17p)], LDH, immunoglobulin type IgA and histology of plasmablastic disease. Additional analyses for risk stratification are conventional cytogenetics, gene expression profiling, labeling index, MRI/PET scan and DNA copy number alterations by CGH/SNP array[3]. There is a general agreement that risk stratification should be a global stratification and that the risk factors will change in the future with introduction of novel agents and combination therapies.

Type
Chapter
Information
Myeloma
Pathology, Diagnosis, and Treatment
, pp. 134 - 143
Publisher: Cambridge University Press
Print publication year: 2013

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