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- W2032702014 abstract "A large proportion of B‐chronic lymphocytic leukaemia (B‐CLL) cells express the anti‐apoptotic protein Bcl‐2. Basic fibroblast growth factor (bFGF) has been shown to upregulate the expression of Bcl‐2 in B‐CLL cell lines. Vascular endothelial growth factor (VEGF) has been shown to enhance the survival of endothelial cells by upregulating the expression of Bcl‐2. In the present study, we measured serum and cellular levels of bFGF and VEGF in 85 patients with CLL using a commercial quantitative sandwich enzyme immunoassay technique. Levels of Bcl‐2 were also assayed concomitantly using Western blot analysis. The mean serum level of bFGF was 53·4 pg/ml (range 0–589) and that of VEGF 459·2 pg/ml (range 33–1793). The mean cellular level of bFGF was 158·3 pg/2 × 10 5 cells (range 0·8–841) and VEGF, 42·4 pg/2 × 10 5 cells (range 0–244). A high correlation was found between serum and cellular bFGF levels ( P < 0·001), but not between the corresponding VEGF levels. Twenty‐nine of 69 patients (42%) evaluated for Bcl‐2 level, expressed it. The Bcl‐2 level was positively correlated with the serum bFGF level ( P = 0·007). However, surprisingly there was a negative correlation between Bcl‐2 expression and intracellular VEGF level ( P = 0·003). A positive correlation was also found between serum bFGF and disease follow‐up time and log white blood cell count. These findings indicate that in CLL there is a correlation between angiogenesis‐related factors and apoptosis‐related protein expression, and elevated bFGF levels may account for the elevated Bcl‐2 levels." @default.
- W2032702014 created "2016-06-24" @default.
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- W2032702014 date "2001-05-01" @default.
- W2032702014 modified "2023-10-18" @default.
- W2032702014 title "Bcl-2 expression correlates positively with serum basic fibroblast growth factor (bFGF) and negatively with cellular vascular endothelial growth factor (VEGF) in patients with chronic lymphocytic leukaemia" @default.
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- W2032702014 doi "https://doi.org/10.1046/j.1365-2141.2001.02731.x" @default.
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