Abstract
VEGF , VEGFR2 and GSTM1 polymorphisms in outcome of multiple myeloma patients treated with thalidomide-based regimens
Highlights
vascular endothelial growth factor (VEGF) and its VEGF type 2 receptor (VEGFR2),[1] and hypoxiainducible factor-1 alpha (HIF-1α)[3] were described as key regulators of AG, and glutathione S-transferases mu[1] (GSTM1) and theta[1] (GSTT1) promotes AG by effecting the HIF-1α pathway.[4]
Therapeutic regimens consisted in thalidomide combined with steroids and/or chemotherapy, followed or not by autologous stem cell transplantation (ASCT)[2] (Supplementary Table S1)
Response was evaluated at the end of treatment using the International Myeloma Working Group guidelines, and classified as complete response (CR), very good partial response (VGPR), partial response (PR), stable disease (SD) or progressive disease (PD)
Summary
VEGF, VEGFR2 and GSTM1 polymorphisms in outcome of multiple myeloma patients treated with thalidomide-based regimens. In Kaplan–Meier estimates, the 60-months EFS and OS tended to be shorter in patients at ISS III (23.0 vs 25.2%, P = 0.08; 41.3 vs 56.0%, P = 0.08) At this time, both EFS and OS were shorter in patients who did not receive ASCT after chemotherapy (11.9 vs 42.4%, P o 0.0001; 34.9 vs 65.1%, P o0.0001), with VEGFR2 c.889GG (17.0 vs 43.5%, P = 0.004; 42.2 vs 62.3%, P = 0.03), VEGF c.-634GG plus VEGFR2 c.889GG (22.8 vs 50.8%, P = 0.01; 43.7 vs 85.7%, P = 0.005), VEGFR2 c.889GG plus GSTM1 present (13.6 vs 31.6%, P = 0.04; 30.7 vs 65.8%, P = 0.01), respectively (Supplementary Figure S2).
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