Utilisation example:Detection of angiogenesis activators and inhibitors as A predictor of response to therapy with autologous transplantation

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Klin Onkol 2008; 21(Suppl 1): 270-271.

Angiogenesis is involved in the development and progression of multiple myeloma (MM.) Role of angiogenesis activators in myeloma seems to be confi rmen but role of angiogenesis inhibitors in MM remains very unclear. The aim of this study was to evaluate the role of VEGF, HGF, bFGF, thrombospondin, endostatin, and angiostatin peripheral plasma (PP) and bone marrow plasma (BM)
levels in a group of patients with MM who underwent autologous stem cell transplant (ASCT) and their infl uence on treatment response. Patients were divided into three groups according to treatment response: group A) 43 patients who achieved at least very good partial response (VGPR); group B) 35 patients who achieved partial response (PR) ; group C) 14 patients who did not achieved even
PR. HGF concentration at the time of diagnosis in both PP and BM is signifi cantly lower at group A (PP-median=472 pg/L; 95%IS 417-823pg/L. BM-median= 886 pg/L; 95%IS 928-2111pg/L) than at group B (PP-median=623 pg/L; 95%IS 493-990pg/L;/p= 0,025/. BM-median= 1165 pg/L; 95%IS 1140-2656pg/L/;p= 0,001/ ) and group C (PP-median=1870 pg/L; 95%IS 522-4971pg/L;/p= 0,001/.
BM-median= 2605 pg/L; 95%IS 1328-5355pg/L/;p= 0,001/ ). Thrombospondin concentration at the time of diagnosis only in BM not in PP is signifi cantly lower at group C (BM-median= 188 pg/L; 95%IS 38-678pg/L) than at group B (BM-median= 303 pg/L; 95%IS 249-705p/L/;p= 0,036) and group A (BM-median= 351pg/L; 95%IS 437-916pg/L/;p= 0,001/. VEGF, bFGF, endostatin and
angiostatin concentrations at diagnosis time did not differ signifi cantly in PP and BM in patiensts with VGPR, PR and no response. Our results confi rmed that key angiogenesis activators in MM is HGF. If the treatment is successful low levels of HGF occurs only. There is important fi nding that thrombospondin in BM is higher in patients with successful treatment. It means, that angiogenesis is
more inhibited in patients with VGPR than in other.