Chronic lymphocytic leukaemia
Chronic lymphocytic leukaemia
Chronic lymphocytic leukaemia is the commonest form of leukaemia in Europe and North America, and mainly, though not exclusively, affects older individuals. It has a very variable course, with survival ranging from months to decades. Major progress has been made in identification of molecular and cellular markers that could predict disease progression in patients with chronic lymphocytic leukaemia. In particular, the mutational profile of immunoglobulin genes and some cytogenetic abnormalities are important predictors of prognosis. However, these advances have raised new questions about the biology, prognosis, and management of chronic lymphocytic leukaemia, some of which are addressed here. In particular, we discuss how better understanding of the function of the B-cell receptor, the nature of genetic lesions, and the balance between proliferation and apoptosis have affected our ability to assess prognosis and to manage chronic lymphocytic leukaemia. Available treatments generally induce remission, although nearly all patients relapse, and chronic lymphocytic leukaemia remains an incurable disease. Advances in molecular biology have enhanced our understanding of the pathophysiology of the disease and, together with development of new therapeutic agents, have made management of chronic lymphocytic leukaemia more rational and more effective than previously. Unfortunately, we know of no way that chronic lymphocytic leukaemia can be prevented. Early detection is practised widely, but seemingly makes no difference to the patient's eventual outcome.
high-dose methylprednisolone, minimal residual disease, disease, time, individuals, survival, induced cytidine deaminase, fludarabine plus cyclophosphamide, variable-region mutations, b-cell-receptor, development, progression-free survival, apoptosis, genes, phase-iii trial, identification, heavy-chain gene, gene, management, gene mutational status, b cell, proliferation
1017-1029
Dighiero, G.
147b3a7a-3601-41e6-8bcc-01bee55a90ba
Hamblin, T.J.
85c9639a-7cf1-4477-9267-e6d772ba66ab
2008
Dighiero, G.
147b3a7a-3601-41e6-8bcc-01bee55a90ba
Hamblin, T.J.
85c9639a-7cf1-4477-9267-e6d772ba66ab
Abstract
Chronic lymphocytic leukaemia is the commonest form of leukaemia in Europe and North America, and mainly, though not exclusively, affects older individuals. It has a very variable course, with survival ranging from months to decades. Major progress has been made in identification of molecular and cellular markers that could predict disease progression in patients with chronic lymphocytic leukaemia. In particular, the mutational profile of immunoglobulin genes and some cytogenetic abnormalities are important predictors of prognosis. However, these advances have raised new questions about the biology, prognosis, and management of chronic lymphocytic leukaemia, some of which are addressed here. In particular, we discuss how better understanding of the function of the B-cell receptor, the nature of genetic lesions, and the balance between proliferation and apoptosis have affected our ability to assess prognosis and to manage chronic lymphocytic leukaemia. Available treatments generally induce remission, although nearly all patients relapse, and chronic lymphocytic leukaemia remains an incurable disease. Advances in molecular biology have enhanced our understanding of the pathophysiology of the disease and, together with development of new therapeutic agents, have made management of chronic lymphocytic leukaemia more rational and more effective than previously. Unfortunately, we know of no way that chronic lymphocytic leukaemia can be prevented. Early detection is practised widely, but seemingly makes no difference to the patient's eventual outcome.
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Published date: 2008
Keywords:
high-dose methylprednisolone, minimal residual disease, disease, time, individuals, survival, induced cytidine deaminase, fludarabine plus cyclophosphamide, variable-region mutations, b-cell-receptor, development, progression-free survival, apoptosis, genes, phase-iii trial, identification, heavy-chain gene, gene, management, gene mutational status, b cell, proliferation
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Cancer Sciences
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Local EPrints ID: 62723
URI: http://eprints.soton.ac.uk/id/eprint/62723
ISSN: 0140-6736
PURE UUID: 82382b80-3d57-48f0-9fcb-e40665ba5de2
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Date deposited: 05 Sep 2008
Last modified: 15 Mar 2024 11:32
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Author:
G. Dighiero
Author:
T.J. Hamblin
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