Chronic lymphocytic leukaemia: clinical translations of biological features
Chronic lymphocytic leukaemia: clinical translations of biological features
The chronic lymphatic leukaemia (CLL) world was surprised to find that the disease split so neatly down the middle into those patients with unmutated immunoglobulin genes who were mainly men, had aggressive disease and were destined to die from their disease, on average at about 8 years from diagnosis, and those with mutated immunoglobulin genes who were equally distributed between the sexes, had indolent disease and usually died of something else a quarter of a century later. This discovery gave fresh impetus to the investigation into the biology of CLL. We now know more about, though we are still not certain of, the cell of origin of the disease and how it functions and fails to function. Intriguing clues about the roles of infectious agents and the functioning of the immune response have been scattered, but not quite put together. In addition, clinicians have been given a new tool for determining prognosis, though the tool is too clumsy for day-to-day use and surrogates are being sought. Treatment strategies based on the new biology are in development.
immunoglobulin-variable-region, incuded cytidine deaminase, v-h genes, class switch recombination, cell antigen receport, b-cells, CD38 expression, somatic hypermutation, germinal-centres, ZAP-70 expression
3540252797
165-185
Hamblin, T.J.
85c9639a-7cf1-4477-9267-e6d772ba66ab
2005
Hamblin, T.J.
85c9639a-7cf1-4477-9267-e6d772ba66ab
Hamblin, T.J.
(2005)
Chronic lymphocytic leukaemia: clinical translations of biological features.
Current Topics in Microbiology and Immunology, 294, .
Abstract
The chronic lymphatic leukaemia (CLL) world was surprised to find that the disease split so neatly down the middle into those patients with unmutated immunoglobulin genes who were mainly men, had aggressive disease and were destined to die from their disease, on average at about 8 years from diagnosis, and those with mutated immunoglobulin genes who were equally distributed between the sexes, had indolent disease and usually died of something else a quarter of a century later. This discovery gave fresh impetus to the investigation into the biology of CLL. We now know more about, though we are still not certain of, the cell of origin of the disease and how it functions and fails to function. Intriguing clues about the roles of infectious agents and the functioning of the immune response have been scattered, but not quite put together. In addition, clinicians have been given a new tool for determining prognosis, though the tool is too clumsy for day-to-day use and surrogates are being sought. Treatment strategies based on the new biology are in development.
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Published date: 2005
Keywords:
immunoglobulin-variable-region, incuded cytidine deaminase, v-h genes, class switch recombination, cell antigen receport, b-cells, CD38 expression, somatic hypermutation, germinal-centres, ZAP-70 expression
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Local EPrints ID: 26350
URI: http://eprints.soton.ac.uk/id/eprint/26350
ISBN: 3540252797
ISSN: 0070-217X
PURE UUID: 80629579-086b-4da8-bd99-1f2fe71ad321
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Date deposited: 21 Apr 2006
Last modified: 22 Jul 2022 20:34
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Author:
T.J. Hamblin
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