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CD 49d associates with nodal presentation and subsequent development of lymphadenopathy in patients with chronic lymphocytic leukaemia
Author(s) -
Strati Paolo,
Parikh Sameer A.,
Chaffee Kari G,
Achenbach Sara J.,
Slager Susan L.,
Call Timothy G.,
Ding Wei,
Jelinek Diane F.,
Hanson Curtis A.,
Kay Neil E.,
Shanafelt Tait D.
Publication year - 2017
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.14647
Subject(s) - ighv@ , medicine , hazard ratio , odds ratio , confidence interval , hematology , gastroenterology , chronic lymphocytic leukemia , immunology , pathology , leukemia
Summary CD 49d is a surface integrin that is expressed on chronic lymphocytic leukaemia ( CLL ) cells, and strongly correlates with more aggressive disease. Given its association with cell‐cell adhesion and leucocyte trafficking, we hypothesized that patients with high CD 49d expression would experience a clinical course dominated by lymphadenopathy. CD 49d expression was measured by flow cytometry and considered positive if expressed by ≥30% of CLL cells. The study included 797 newly diagnosed CLL /small lymphocytic leukaemia patients; 279 (35%) were CD 49d positive. CD 49d‐positive patients were more likely to present with lymphadenopathy ( P < 0·001); a finding that persisted after adjusting for fluorescence in situ hybridisation ( FISH ) and IGHV mutation status [odds ratio ( OR ) 2·51; 95% confidence interval ( CI ) 1·64–3·83; P < 0·001]. Among CLL Rai 0 patients, CD 49d positivity was associated with shorter time to development of lymphadenopathy (3·2 years vs not reached, P < 0·01). This association was maintained after adjusting for either FISH [hazard ratio ( HR ) 2·18; 95% CI 1·25–3·81; P = 0·006) or IGHV status ( HR 2·02; 95% CI 1·11–3·69; P = 0·02) individually, but was attenuated when adjusting by both ( HR 1·72; 95% CI 0·88–3·38; P = 0·11).These data demonstrate that CD 49d‐positive CLL patients experience a disease course dominated by lymphadenopathy. These findings could have implications for therapy selection and disease monitoring.