[1] Lee A Y, Levine M N. Venous thromboembolism and cancer: Risks and outcomes [J]. Circulation,2003,107(23 Supple 1):117-121.[2] Musallam K M, Dahdaleh F S, Shamseddine A l, et al. Incidence and prophylaxis of venous thromboembolic events in multiplemveloma patients receiving immunomodulatory therapy [J]. Tbromb Res, 2009, 123(5):679-686.[3] 杨林花.多发性骨髓瘤的凝血异常[J]. 临床血液学杂志,2012,25(7):414-417.[4] Zangari M, Tricot G, Polavaram L, et al. Survival effect of venous thromboembolism in patients with multiple myeloma treated with lenalidomide and high-dose dexamethasone [J].J Clin Oncol, 2010,28(1):132-135.[5] Smith R A, Cokkinides V, Eyre H J. American Cancer So ciety guidelines for the early detection of cancer, 2006[J].CA Cancer J Clin,2006,56(1): 11-25.[6] Shimizu K, Itoh J. A possible link between Trousseau's syndrome and tissue factor producing plasma cells [J]. Am J Hematol,2009, 84(6): 382-385.[7] 侯彦飞,杨林花,任方刚,等.组织因子微粒在多发性骨髓瘤中的表达及临床意义[J].临床血液学杂志,2014,27(7):573-576.[8] Auwerda J J, Sonneveld P, de Maat M P, et al. Prothrombotic coagulation abnormalities in patients with newly diagnosed multiple myeloma[J]. Haematologica, 2007, 92(2): 279-280.[9] 白洁,薛艳萍,许现辉,等.骨髓增殖性肿瘤患者活化蛋白C抵抗和凝血功能异常研究[J].中华血液学杂志,2011,32(3): 187-190.[10] De Lucia D, De Vita F, Orditura M, et al. Hypercoagulable state in patients with advanced gastrointestinal cancer: evidence for an acquired resistance to activated protein C [J]. Tumori,1997, 83(6):948-952.[11] Green D, Maliekel K, Sushko E, et al. Activated protein C resistance in cancer patients[J]. Haemostasis, 1997, 27(3): 112-118.[12] Haim N, Lanir N, Hoffman R, et al. Acquired activated protein C resistance is common in cancer patients and is associated with venous thromboembolism[J]. Am J Med, 2001, 110(2):91-96.[13] Zangari M, Saghafifar F, Mehta P, et al. The blood coagulation mechanism in multiple myeloma [J]. Semin Thromb Hemost,2003, 29(3):275-282.[14] Zangari M, Berno T, Zhan F, et al. Activated protein C resistance as measured by residual factor V after Russell's viper venom and activated protein C treatment analyzed as a continuous variable in multiple myeloma and normal controls[J]. Blood Coagul Fibrinolysis, 2011, 22(5): 420-423.[15] Petropoulou A D, Gerotziafas G T, Samama M M, et al. In vitro study of the hypercoagulable state in multiple myeloma patients treated or not with thalidomide [J].Thromb Res, 2008, 121(4): 493-497.[16] Bolkun L, Piszcz J, Oleksiuk J, et al. Protein Z concentration in multiple myeloma patients[J]. Thromb Res, 2011, 128(5): 401-402.[17] Barosi G, Merlini G, Billio A, et al. SIE, SIES, GITMO evidence-based guidelines on novel agents (thalidomide, bortezomib, and lenalidomide) in the treatment of multiple myeloma [J].Ann Hematol, 2012, 91(6): 875-888.[18] Moreau P, Richardson PG, Cavo M, et al. Proteasome inhibitors in multiple myeloma: 10 years later [J]. Blood, 2012, 120(5): 947-959.[19] Quach H, Kalff A, Spencer A. Lenalidomide in multiple myeloma: current status and future potential [J].Am J Hematol, 2012, 87(12): 1089-1095.[20] Gandhi A K, Kang J, Capone L, et al. Dexamethasone synergizes with lenalidomide to inhibit multiple myeloma tumor growth, but reduces lenalidomide-induced immunomodulation of T and NK cell function [J]. Curr Cancer Drug Targets, 2010, 10(2): 155-167.[21] ElAccaoui R N, Shamseddeen W A, Taher A T.Thalidomide and thrombosis a meta-analysis [J]. Thromb Haemost, 2007, 97(6): 1031-1036.[22] Görgun G, Calabrese E, Soydan E, et al. Immunomodulatory effects of lenalidomide and pomalidomide on interaction of tumor and bone marrow accessory cells in multiple myeloma[J]. Blood, 2010, 116(17): 3227-3237.[23] Bolzoni M, Stori P, Bonomini S, et al. Immunomodulatory drugs lenalidomide and pomalidomide inhibit multiple myeloma-induced osteoclast formation and the RANKL/OPG ratio in the myeloma microenviroment targeting the expression of adhesion molecules [J].Exp Hematol, 2013, 41(4): 387-397.[24] Dimopoulos M, Spencer A, Attal M, et al. Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma [J]. N Engl J Med, 2007, 357(21): 2123-2132.[25] Rajkumar S V, Jacobus S, Callander N S, et al. Lenalidomid plus high-dose dexamethasone vsersus lenalidomide plus low-dose dexmethasone as initial therapy for newly diagnosed multiple myeloma;an open-label randomized controlled trial[J].Lancet Oncol,2010,11(1): 29-37.[26] Zangari M, Fink L, Zhan F, et al. Low venous thromboembolic risk with bortezomib in multiple myeloma and potential protective effect with thalidomide/lenalidomide-based therapy: review of data from phase 3 trials and studies of novel combination regimens [J]. Clin Lymphoma Myeloma Leuk,2011,11(2): 228-236.[27] Shi D S, Smith M C, Campbell R A, et al. Proteasome function is required for platelet production [J]. J Clin Invest. 2014,124(9):3757-3766.[28] Nayak L, Shi H, Atkins G B, et al. The thromboprotective effect of bortezomib is dependent on the transcription factor Kruppel-like factor 2 (KLF2) [J]. Blood, 2014, 123(24): 3828-3831.[29] Balcik O S, Albayrak M, Uyar M E, et al. Serum thrombin activatable fibrinolysis inhibitor levels in patients with newly diagnosed multiple myeloma [J]. Blood Coaqul Fibrinolvsis, 2011, 22 (4): 260-263.[30] Dri A P, Politou M, Gialeraki A, et al. Decreased incidence of EPCR 4678G/C SNP in multiple myeloma patients with thrombosis [J]. Thromb Res,2013, 132(3): 400-401.[31] 李迎春, 张嵘,王慧涵,等.沙利度胺联合环磷酰胺和地塞米松治疗复发难治多发性骨髓瘤[J]. 中国医科大学学报,2013,42(6):564-566.[32] Palumbo A, Cavo M, Bringhen S, et al. Aspirin, warfarin, or enoxapar in thromboprophylaxis in patients with multiple myeloma treated with thalidomide:a phase Ⅲ, open-label, randomized trial [J]. J Clin Oncol, 2011, 29(8): 986-993.[33] Palumbo A,Rajkumar S V,Dimopoulos M A, et al.Prevention of thalidomide and lenalidomide-associated thrombosis in myeloma[J]. Leukemia, 2008, 22(2):414-423. |