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骨髓增生异常综合征最新研究进展:第56届美国血液学会年会报道 被引量:3

Recent progress of myelodysplastic syndrome: reports from the 56th American Society of Hematology annual meeting
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摘要 骨髓增生异常综合征(MDS)是一组起源于造血干/祖细胞水平损伤而产生的获得性克隆性疾病,以无效造血和易转化为急性白血病为特点。第56届美国血液学会(ASH)年会报道了大量MDS的相关发病机制及对患者预后、指导用药意义的研究,并就不同MDS的药物治疗及造血干细胞移植等方面做了详尽报道。 The myelodysplastic syndromes (MDS), which are characterized by the presence of ineffective hematopoiesis and an increased risk of transformation to acute myeloid leukemia (AML), are a group of clonal disorders deriving from damage of the hematopoietic stem/progenitor cells. In the 56th American Society of Hematology (ASH) annual meeting, lots of new discoveries about the pathogenesis of MDS and the role of the pathogenesis in the clinical outcomes and treatment were introduced. There were also many developments in the treatment of MDS including drug therapies and Hematopoietic stem cell tranplantation (HSCT) reported in the meeting.
作者 刘平 陈宝安
出处 《白血病.淋巴瘤》 CAS 2015年第1期43-45,共3页 Journal of Leukemia & Lymphoma
关键词 骨髓增生异常综合征 发病机制 治疗 美国血液学会年会 Myelodysplastic syndromes Pathogenesis Treatment American Society of Hematology annual meeting
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参考文献11

  • 1Daichi I, Hirotaka M, Hsin-an H, et al. SETBPI mutations drive leukemic transformation in ASXLl-mutated MDS[C/OLJII 56th ASH Annual Meeting, San Francisco ,2014: Abstract 525.
  • 2Jeffrey CL,Joanna W, Rawa I, et al. Loss of miR-143 and miR-145 inhibits hematopoietic stem cell self-renewal through dysregulated TGF 13 signaling[C/OLJ II 56th ASH Annual Meeting, San Frandsco, 2014: Abstract 527.
  • 3Mathew AC, Raoul T, Theresa F, et al. A study of high dose lenalidomide induction and low dose lenalidomide maintenance for patients with hypomethylating agent refractory MDS[C/OLJ II 56th ASH Annual Meeting, San Francisco,2014:Abstract 1931.
  • 4Amma B, YanG, Sanjay M, et al. miRNA predictors of response to DNA methyltransferase inhibitors[C/OLJ II 56th ASH Annual Meeting, San Francisco, 2014: Abstract 1913.
  • 5Erika AE, Karl-Heinz H, Bjoern R, et al. Novel therapeutic approach to improve hematopoiesis by targeting myeloid derived suppressor cells with a humanized anti-CD33 antibody[C/OLJ II 56th ASH Annual Meeting, San Francisco, 2014: Abstract 4597.
  • 6Mathew AC, Raoul T, Theresa F, et al. A study of high dose lenalidomide induction and low dose lenalidomide maintenance f'lT patients with hypomethylating agent refractory MDS[C/OLJ II 561ft ASH Annual Meeting, San Francisco, 2014: Abstract 1931.
  • 7Courtney DD, Naval D, EliasJ, et al. A final report: phase I I II study of sequential azacitidine and lenalidomide in patients with bigher-risk myelodysplastic syndrome ( MDS ) and acute myeloid leukemia (AML)[C/OLJ II 56th ASH Annual Meeting, San Francisco, 2014: Abstract 164.
  • 8Charikleia K, Thorsten B, Gregory L, et al. Long-term outcome of lower-risk MDS patients after immunosuppressive therapy ( 1ST) with anti-thymocyte globulin (ATG) +1- cyclosporin A (CsA)[C/OLJII 56th ASH Annual Meeting, San Francisco, 2014: Abstract 1921.
  • 9Guillermo G, Ellen KR, Katherine W, et al. First clinical results of a randomized phase 2 dose-response study of SGI-llO, a novel subcutaneous (SC) hypomethylating agent (HMA) ,in 102 patients with intermediate ( lnt ) or high risk (HR) myelodysplastic syndromes (MDS) or chronic myelomonocytic leukemia ( CMML )[C/OLJII 56th ASH Annual Meeting, San Francisco, 2014: Abstract 529.
  • 10Guillermo G, Pierre F, Aref A, et al. Overall survival and subgroup analysis from a randomized phase ill study of intravenous rigosenib versus best supportive care (BSC) in patients (pts) with higher?risk myelodysplastic syndrome ( HR - MDS ) after failure of hypomethylating agents (HMAs)[C/OLJ II 56th ASH Annual Meeting, San Francisco, 2014: Abstract 163.

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