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沙利度胺治疗难治性复发性多发性骨髓瘤的临床和实验研究 被引量:1

Oinical and experimental study fw thalidomide to treat refratory and replased multiple myeloma
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摘要 目的 观察沙利度胺治疗难治性、复发性多发性骨髓瘤(MM)的疗效和毒副反应,并从IL-6、sIL-R水平探索沙利度胺治疗多发性骨髓瘤有效的可能机制。方法 用随机分组的方法观察和比较沙利度胺组和VIDM对照组的部分缓解(PR)率、总有效率、达到PR所需的时间;用双抗夹心法ELISA检测沙利度胺组治疗前后MM患者血清IL-6、sIL-6R的变化情况。结果 沙利度胺组的PR率和总有效率为50.0%、69.2%,分别高于对照组的40.9%、59.1%(P<0.05);达到PR所需的中位时间沙利度胺组为69 d,明显长于VIDM组的46 d(P<0.05)。沙利度胺组治疗后MM患者血清IL-6、sIL-6R的水平分别为180.3±101.3 ng/L、178.2±56.9 μg/L,均明显低于治疗前的564.8±319.4 μg/L、253.5±130.5 ng/L(P<0.05)。结论 沙利度胺是一种有效且副作用小的治疗难治性、复发性多发性骨髓瘤的药物,无严重不良反应。它可能还通过减少MM患者IL-6、sIL-R水平发挥抗瘤作用。 Objective To observe results,toxicity and adverse effects for thalidomide in treating refratory and replased multiple myeloma (MM), and to explore efficacious mechanism for thalidomide to treat refratory and replased MM from IL-SIL-6R. Methods Part remission (PR) rate, total response rate, the days reaching PR were observed.The levels of serum IL^sIL-6R before and after treated by thalidomide were measured by with filling double antibody EL1SA. Results PR rate and total response rate of thalidomide group were 50.0% ,69.2%, which were higher than 40.9% ,59.9% of control,respectively (P < 0.05) .The average days reaching PR were 69 in thalidomide group, which was longer than 46 in VIDM group( P < 0.05). The level of serum IL-6, sIL- R after treated by thalidomide were 180. 3 ± 101. 3 ng/L, 178. 2 ± 56. 9 ug/L. They were all lower than 564. 8 ± 319.4 ng/L,253.5± 130.5 ug/L before treated by thalidomide(P<0.05).Conclusion Thalidomide is effective and safe drug to refractory and replased MM. It has little serious toxicity and adverse effect. It plays an antitumor regimen maybe through decreasing level of serum IL-6,sIL-6R.
出处 《中国肿瘤临床与康复》 2003年第2期120-123,共4页 Chinese Journal of Clinical Oncology and Rehabilitation
关键词 沙利度胺 治疗 难治性 复发性 多发性 骨髓瘤 疗效 毒副反应 IL-6 sIL-R Myeloma, multiple/ drug therpy Thalidomide
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  • 1王学文,杨天楹.难治性和复发性骨髓瘤的治疗进展[J].国外医学(输血及血液学分册),1993,16(1):35-37. 被引量:11
  • 2Kneller A, Raanani P, Handan l,et al. Therapy with thalidomide in refractory multiple myeloma patient--the revival of an old drug[J].Br J Haematol,2000, 108:391-392.
  • 3Dufie BG, Salmon SE. A clinical staging system for multiple myeloma correlation of measured myeloma cell mess with presenting clinical features response to treatment and survival[J]. Cancer, 1975,36:842-854.
  • 4Giles FJ. Refractory multiple myeloma:recent advances in therapy[ J ].Hematol Pathol, 1995,9:121-140.
  • 5Singhal S, Mehta J, Desikan R, et al. Antiumor activity of thalidomide in refractory multiple myeloma [ J ]. N Engl J Meal, 1999, 341 : 1565-1571.
  • 6Yiwu H, Audrey H, Omar J, et al. Current drug therapy for nmltiple myeloma[ J ]. Drugs, 1999,57 ( 4 ) : 485-506.
  • 7Ogata A, Chauhan D, Tenh G, et al. Interleukin 6 triggers cell growth via the ras dependent mitogen-activated protein kinase cascade[J]. J Immunol, 1997,159:2212-2221.

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  • 1Preston SL, Alison MR, Forbes SJ, et al. The new stem cell biology: something for everyone[J]. Mol Pathol, 2003,56 (2) :86-96.
  • 2Solchaga LA, Penick K, Porter JD, et al. FGF-2 enhances the mitogenic and chondrogenic potential of human adult bone marrow-derived mesenchymal stem cells[J]. J Cell Physiol, 2005,203(2) : 398-409.
  • 3Hecht M, Heider U, Kaiser M, et al. Osteoblasts promote migration and invasion of myeloma cells through upregulation of matrix metalloproteinases, urokinase plasminogen activator, hepatocyte growth factor and activation of p38 MAPK[J]. Br J Haematol, 2007,138(4) : 446-458.
  • 4Vacca A, Ribatti D, Presta M, et al. Bone marrow neovascu- larization, plasma cell angiogenic potential, and matrix metalloproteinase-2 secretion parallel progression of human multiple myeloma[J]. Blood, 1999,93 (9) : 3064-3073.
  • 5Birkedal-Hansen H. Role of matrix metalloproteinases in human periodontal diseases [J]. J Periodontol, 1993, 64 (5 Suppl) :474-484.
  • 6Rafei M, Hsieh J, Fortier S, et al. Mesenchymal stromal cell-derived CCL2 suppresses plasma cell immunoglobulin production via STAT3 inactivation and PAX5 induction [J]. Blood,2008,112(13) :4991-4998.
  • 7Dvorak P, Dvorakova D, Hampl A. Fibroblast growth factor signaling in embryonic and cancer stem cells[J]. FEBS Lett, 2006,580(12) :2869-2874.
  • 8Solchaga LA, Penick K, Porter JD, et al. FGF-2 enhances the mitogenic and chondrogenic potential of human adult bone marrow-derived mesenchymal stem cells[J]. J Cell Physiol, 2005,203(2) :398-409.
  • 9Go MJ, Takenaka C, Ohgushi H. Forced expression of Sox2 or Nanog in human bone marrow derived mesenchymal stem cells maintains their expansion and differentiation capabilities [J]. Exp Cell Res,2008,314(5) : 1147-1154.
  • 10Hill PA, Murphy G, Docherty AJ, et al. The effects of selec- tive inhibitors of matrix metalloproteinases(MMPs) on bone resorption and the identification of MMPs and TIMP-1 in isolated osteoclasts [J]. J Cell Sci, 1994, 107 (Ptll): 3055- 3064.

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