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Updated: Jul 29, 2026

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
Published on: October 19, 2014
Chronic lymphocytic leukaemia: clinical translations of biological features
1Department of Haematology, Royal Bournemouth Hospital, UK. terjoha@aol.com
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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