The University of Southampton
University of Southampton Institutional Repository

Chronic lymphocytic leukaemia

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
0140-6736
1017-1029
Dighiero, G.
147b3a7a-3601-41e6-8bcc-01bee55a90ba
Hamblin, T.J.
85c9639a-7cf1-4477-9267-e6d772ba66ab
Dighiero, G.
147b3a7a-3601-41e6-8bcc-01bee55a90ba
Hamblin, T.J.
85c9639a-7cf1-4477-9267-e6d772ba66ab

Dighiero, G. and Hamblin, T.J. (2008) Chronic lymphocytic leukaemia. The Lancet, 371 (9617), 1017-1029. (doi:10.1016/S0140-6736(08)60456-0).

Record type: Article

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.

This record has no associated files available for download.

More information

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
Organisations: Cancer Sciences

Identifiers

Local EPrints ID: 62723
URI: http://eprints.soton.ac.uk/id/eprint/62723
ISSN: 0140-6736
PURE UUID: 82382b80-3d57-48f0-9fcb-e40665ba5de2

Catalogue record

Date deposited: 05 Sep 2008
Last modified: 15 Aug 2024 17:11

Export record

Altmetrics

Contributors

Author: G. Dighiero
Author: T.J. Hamblin

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×