INTRODUCTION: The aim of this study was to screen for cell surface markers that could discriminate CLL-type MBL from CLL or identify CLL cases likely to have stable disease. METHODS: Six color flow cytometry was performed on CLL-type MBL (n = 94) and CLL (n = 387) at diagnosis or relapse; 39 cases had poor-risk chromosomal abnormalities (17p and/or 11q deletion). Expression of 30 markers was analysed: CCR6, CD10, CD103, CD11c, CD138, CD200, CD22, CD23, CD24, CD25, CD27, CD31, CD38, CD39, CD43, CD49d, CD5, CD52, CD62L, CD63, CD79b, CD81, CD86, CD95, CXCR5, HLADR, IgD, IgG, IgM, LAIR1. RESULTS: There was no difference in expression between CLL-type MBL and CLL for the majority of markers. Differential expression was observed for several markers, mainly between MBL and CLL cases with adverse-risk chromosomal abnormalities. These differences included lower expression of CD38 (9.4-fold lower, P = 0.007) and CD49d (3.2-fold lower, P = 0.008) and higher expression of LAIR-1 (3.7-fold higher, P = 0.003), CXCR5 (1.25-fold higher, P = 0.002), and CCR6 (1.9-fold higher P < 0.001) on CLL-type MBL compared to CLL with adverse chromosomal abnormalities. CD62L (L-selectin) which mediates lymphocyte adhesion to endothelial venules of lymphoid tissue, was expressed at a significantly different level between CLL-type MBL and both CLL sub-groups, with 1.3-fold lower (P = 0.04) expression levels on the MBL cases. However, there was broad overlap in expression levels. CONCLUSIONS: CLL-type MBL is phenotypically identical to CLL for a very broad range of markers. Differential expression is predominantly related to known prognostic markers and proteins involved in homing to lymphoid tissue.
INTRODUCTION: The aim of this study was to screen for cell surface markers that could discriminate CLL-type MBL from CLL or identify CLL cases likely to have stable disease. METHODS: Six color flow cytometry was performed on CLL-type MBL (n = 94) and CLL (n = 387) at diagnosis or relapse; 39 cases had poor-risk chromosomal abnormalities (17p and/or 11q deletion). Expression of 30 markers was analysed: CCR6, CD10, CD103, CD11c, CD138, CD200, CD22, CD23, CD24, CD25, CD27, CD31, CD38, CD39, CD43, CD49d, CD5, CD52, CD62L, CD63, CD79b, CD81, CD86, CD95, CXCR5, HLADR, IgD, IgG, IgM, LAIR1. RESULTS: There was no difference in expression between CLL-type MBL and CLL for the majority of markers. Differential expression was observed for several markers, mainly between MBL and CLL cases with adverse-risk chromosomal abnormalities. These differences included lower expression of CD38 (9.4-fold lower, P = 0.007) and CD49d (3.2-fold lower, P = 0.008) and higher expression of LAIR-1 (3.7-fold higher, P = 0.003), CXCR5 (1.25-fold higher, P = 0.002), and CCR6 (1.9-fold higher P < 0.001) on CLL-type MBL compared to CLL with adverse chromosomal abnormalities. CD62L (L-selectin) which mediates lymphocyte adhesion to endothelial venules of lymphoid tissue, was expressed at a significantly different level between CLL-type MBL and both CLL sub-groups, with 1.3-fold lower (P = 0.04) expression levels on the MBL cases. However, there was broad overlap in expression levels. CONCLUSIONS: CLL-type MBL is phenotypically identical to CLL for a very broad range of markers. Differential expression is predominantly related to known prognostic markers and proteins involved in homing to lymphoid tissue.
Authors: Anneclaire J De Roos; Dana K Mirick; Kerstin L Edlefsen; Andrea Z LaCroix; Kenneth J Kopecky; Margaret M Madeleine; Larry Magpantay; Otoniel Martínez-Maza Journal: Cancer Res Date: 2012-07-30 Impact factor: 12.701
Authors: M C Lanasa; S D Allgood; S L Slager; S S Dave; C Love; G E Marti; N E Kay; C A Hanson; K G Rabe; S J Achenbach; L R Goldin; N J Camp; B K Goodman; C M Vachon; L G Spector; L Z Rassenti; J F Leis; J P Gockerman; S S Strom; T G Call; M Glenn; J R Cerhan; M C Levesque; J B Weinberg; N E Caporaso Journal: Leukemia Date: 2011-05-27 Impact factor: 11.528
Authors: Andy C Rawstron; Aloysius Ssemaganda; Ruth de Tute; Chi Doughty; Darren Newton; Anna Vardi; Paul A S Evans; Kostas Stamatopoulos; Roger G Owen; Tracy Lightfoot; Katie Wakeham; Alex Karabarinde; Gershim Asiki; Robert Newton Journal: Lancet Haematol Date: 2017-07 Impact factor: 18.959