Soluble @entity7 (sVEGF) in adult XXXX : relationship to disease characteristics.

@entity1 @entity3052 @entity7
There is little understanding of the factors controlling the mobilization of blast cells from bone marrow to peripheral blood and tissues. The aim of this study was to evaluate the soluble hepatocyte growth factor (sHGF) and @entity7 (sVEGF) levels in newly diagnosed @entity1 with @entity3052 ( @entity3052 ) and to correlate these levels with the clinico-pathological features. Sixty-three @entity1 with @entity3052 and 15 normal controls were included in this study. The levels of sHGF and sVEGF were determined by enzyme linked immunosorbent assay at diagnosis and after remission induction chemotherapy. Our results revealed significantly increased plasma levels of sHGF and sVEGF at diagnosis when compared to both control and remission levels (P=0.000 for both). The sHGF and sVEGF levels differed between @entity3052 FAB subtypes (P=0.000). The highest concentrations were found in M5 followed by M4. SHGF and sVEGF were directly correlated with peripheral white cell counts (WBC) (r=0.836, P=0.000, r=0.718; P=0.000, respectively), but inversely correlated with blast cell distribution ratio (BCDR) (r=-0.785, P=0.000, r=-0.664, P=0.000, respectively). Moreover, both sHGF and sVEGF levels were significantly elevated in @entity3052 @entity1 with extra-medullary infiltration as compared to those without (P=0.000, 0.006, respectively). The sHGF but not sVEGF levels were significantly elevated in @entity1 who died compared to those who relapsed and to @entity1 in complete remission (P=0.02, 0.08, respectively). Logistic regression analysis revealed that the sHGF level at diagnoses is a powerful predictor of the @entity1 outcome, compared to sVEGF. IN CONCLUSION: our data support the hypothesis that angiogenic factors play a functional role in blast cell movement from the bone marrow to peripheral tissues. Assessment of sHGF at @entity3052 diagnosis is likely to be helpful in predicting @entity1 outcome and selecting optimal therapeutic regimen.
