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Serum levels of syndecan-1 in B-cell chronic lymphocytic leukemia: correlation with the extent of angiogenesis and disease-progression risk in early disease.

Abstract Syndecan-1 is a transmembrane proteoglycan generally not expressed in mature B-cell neoplasias like chronic lymphocytic leukemia (CLL). Moreover, information dealing with the evaluation of soluble syndecan-1 in CLL are lacking. We measured syndecan-1 concentrations in serum drawn at the time of diagnosis from 67 B-cell CLL patients (Binet stage A, 46; stage B, 7; stage C, 14). For this purpose a syndecan-1 enzyme-linked immunosorbent assay (ELISA, Diaclone, Besancon, France) was used. Detectable levels of syndecan-1 were found in all patients, although serum concentrations were significantly lower in CLL patients in comparison to age- and sex-matched controls (P = 0.02; Mann-Whitney test). No correlation was found with Binet clinical stages (P = 0.796), beta2-microglobulin (P = 0.923), hemoglobin level (P = 0.605), platelet count (P = 0.992) and lymphocyte doubling time (P = 0.709). Only an association with absolute peripheral blood lymphocytosis (PBL) (P = 0.01) and LDH (P = 0.05) could be detected. Serum levels of syndecan-1 did not parallel those of several angiogenic cytokines such as vascular endothelial growth factor (VEGF) (P = 0.963), basic fibroblastic growth factor (FGF-2) (P = 0.216), angiogenin (P = 0.478), metalloproteinase-9 (MMP-9) (P = 0.125) as well as bone marrow (BM) microvessel density (P = 0.110). The same applied with adhesion molecules such as CD54 (P = 0.233), CD108 (P = 0.799), CD44 (P = 0.816) and CD31 (P = 0.508). Interestingly, the inverse correlation (r = -0.4967; P = 0.03) between serum concentrations of syndecan-1 and plasma levels of stromal derived growth factor-1 (SDF-1) is in keeping with the different function, respectively, pro- and anti-apoptotic, of these molecules. In 46 Binet stage A patients, serum levels of syndecan-1 were further evaluated as a dichotomous variable with respect to progression-free survival (PFS), an end-point surrogate for overall survival in early B-cell CLL. The best separation of curves was seen with a cut-off point at the median value of syndecan-1 (i.e. 36.5 pg/ml). Median PFS was not reached in the patient group with low syndecan-1, compared to a median of 34 months observed in the remaining patients (P = 0.018; HR = 0.208; 95% CI = 0.115 - 0.816). At the multivariate analysis performed including variables significant in the univariate analysis [i.e. PBL (P = 0.03) and syndecan-1 (P = 0.01)], only syndecan-1 retained a trend of significance (P = 0.08). Despite the pro-angiogenic activity of syndecan-1 which mediates FGF-2 binding and activity, no correlation with either angiogenic cytokines or the extent of BM angiogenesis was found in CLL. The inverse correlation with plasma levels of SDF-1 suggests an involvement in the processes leading to apoptosis. Finally, our results highlight the involvement of syndecan-1 in the mechanisms of disease-progression of early CLL.
PMID
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Authors

Mayor MeshTerms

Gene Expression Regulation, Leukemic

Neovascularization, Pathologic

Keywords
Journal Title leukemia & lymphoma
Publication Year Start




PMID- 16840194
OWN - NLM
STAT- MEDLINE
DA  - 20060714
DCOM- 20070925
LR  - 20071115
IS  - 1042-8194 (Print)
IS  - 1026-8022 (Linking)
VI  - 47
IP  - 6
DP  - 2006 Jun
TI  - Serum levels of syndecan-1 in B-cell chronic lymphocytic leukemia: correlation
      with the extent of angiogenesis and disease-progression risk in early disease.
PG  - 1034-40
AB  - Syndecan-1 is a transmembrane proteoglycan generally not expressed in mature
      B-cell neoplasias like chronic lymphocytic leukemia (CLL). Moreover, information 
      dealing with the evaluation of soluble syndecan-1 in CLL are lacking. We measured
      syndecan-1 concentrations in serum drawn at the time of diagnosis from 67 B-cell 
      CLL patients (Binet stage A, 46; stage B, 7; stage C, 14). For this purpose a
      syndecan-1 enzyme-linked immunosorbent assay (ELISA, Diaclone, Besancon, France) 
      was used. Detectable levels of syndecan-1 were found in all patients, although
      serum concentrations were significantly lower in CLL patients in comparison to
      age- and sex-matched controls (P = 0.02; Mann-Whitney test). No correlation was
      found with Binet clinical stages (P = 0.796), beta2-microglobulin (P = 0.923),
      hemoglobin level (P = 0.605), platelet count (P = 0.992) and lymphocyte doubling 
      time (P = 0.709). Only an association with absolute peripheral blood
      lymphocytosis (PBL) (P = 0.01) and LDH (P = 0.05) could be detected. Serum levels
      of syndecan-1 did not parallel those of several angiogenic cytokines such as
      vascular endothelial growth factor (VEGF) (P = 0.963), basic fibroblastic growth 
      factor (FGF-2) (P = 0.216), angiogenin (P = 0.478), metalloproteinase-9 (MMP-9)
      (P = 0.125) as well as bone marrow (BM) microvessel density (P = 0.110). The same
      applied with adhesion molecules such as CD54 (P = 0.233), CD108 (P = 0.799), CD44
      (P = 0.816) and CD31 (P = 0.508). Interestingly, the inverse correlation (r =
      -0.4967; P = 0.03) between serum concentrations of syndecan-1 and plasma levels
      of stromal derived growth factor-1 (SDF-1) is in keeping with the different
      function, respectively, pro- and anti-apoptotic, of these molecules. In 46 Binet 
      stage A patients, serum levels of syndecan-1 were further evaluated as a
      dichotomous variable with respect to progression-free survival (PFS), an
      end-point surrogate for overall survival in early B-cell CLL. The best separation
      of curves was seen with a cut-off point at the median value of syndecan-1 (i.e.
      36.5 pg/ml). Median PFS was not reached in the patient group with low syndecan-1,
      compared to a median of 34 months observed in the remaining patients (P = 0.018; 
      HR = 0.208; 95% CI = 0.115 - 0.816). At the multivariate analysis performed
      including variables significant in the univariate analysis [i.e. PBL (P = 0.03)
      and syndecan-1 (P = 0.01)], only syndecan-1 retained a trend of significance (P =
      0.08). Despite the pro-angiogenic activity of syndecan-1 which mediates FGF-2
      binding and activity, no correlation with either angiogenic cytokines or the
      extent of BM angiogenesis was found in CLL. The inverse correlation with plasma
      levels of SDF-1 suggests an involvement in the processes leading to apoptosis.
      Finally, our results highlight the involvement of syndecan-1 in the mechanisms of
      disease-progression of early CLL.
FAU - Molica, Stefano
AU  - Molica S
AD  - Medical Oncology, Azienda Ospedaliera Pugliese-Ciaccio, Catanzaro, Italy.
      [email protected]
FAU - Vitelli, Gaetano
AU  - Vitelli G
FAU - Mirabelli, Rosanna
AU  - Mirabelli R
FAU - Digiesu, Giovanna
AU  - Digiesu G
FAU - Giannarelli, Diana
AU  - Giannarelli D
FAU - Cuneo, Antonio
AU  - Cuneo A
FAU - Ribatti, Domenico
AU  - Ribatti D
FAU - Vacca, Angelo
AU  - Vacca A
LA  - eng
PT  - Journal Article
PL  - England
TA  - Leuk Lymphoma
JT  - Leukemia & lymphoma
JID - 9007422
RN  - 0 (Syndecan-1)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Bone Marrow Cells/metabolism
MH  - Disease Progression
MH  - Disease-Free Survival
MH  - Female
MH  - *Gene Expression Regulation, Leukemic
MH  - Humans
MH  - Karyotyping
MH  - Leukemia, Lymphocytic, Chronic, B-Cell/*blood
MH  - Male
MH  - Middle Aged
MH  - *Neovascularization, Pathologic
MH  - Syndecan-1/*blood
EDAT- 2006/07/15 09:00
MHDA- 2007/09/26 09:00
CRDT- 2006/07/15 09:00
AID - V9X82Q1342V77840 [pii]
AID - 10.1080/10428190500470358 [doi]
PST - ppublish
SO  - Leuk Lymphoma. 2006 Jun;47(6):1034-40.