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1 ally corrected HSC threshold that corrects a hematopoietic disease.
2 portant field of therapeutic development for hematopoietic disease.
3 opoietic stem cell (HSC) source for treating hematopoietic disease.
4 therapeutic approach for FLT3-ITD-associated hematopoietic disease.
5 HSC) transplantation, the only cure for most hematopoietic diseases.
6 ility is a target for the treatment of these hematopoietic diseases.
7 vectors will be effective in treating human hematopoietic diseases.
8 ed into cell types that can be used to treat hematopoietic diseases.
9 major obstacle to successful gene therapy of hematopoietic diseases.
10 vivo evaluation of therapies targeting human hematopoietic diseases.
11 and for studying abnormal gene expression in hematopoietic diseases.
12 rs have been an obstacle to gene therapy for hematopoietic diseases.
13 been a major impediment to gene therapy for hematopoietic diseases.
14 iPSCs) hold great promise for modeling human hematopoietic diseases.
15 nd defects have been implicated in malignant hematopoietic diseases.
16 rtant function in blood cell homeostasis and hematopoietic diseases.
17 stinctions between RP gene mutations driving hematopoietic disease and those resulting in development
18 aftment, thereby providing a model for human hematopoietic diseases and treatments not previously ava
21 or studying the role of RAS dysregulation in hematopoietic disease in general and in discrete human d
23 th MGMTP140K has broad potential for several hematopoietic diseases including hemoglobinopathies.
24 les in JAK2 activation in the development of hematopoietic diseases including myeloproliferative neop
25 morphic RUNX2 alleles can cause CCD, whereas hematopoietic disease requires more severely inactivatin
27 rapy can potentially cure a variety of human hematopoietic diseases, such as sickle cell disease.
29 hildren with Down syndrome exhibit 2 related hematopoietic diseases: transient myeloproliferative dis
30 potential targets for treatment of numerous hematopoietic diseases using retroviral-mediated gene tr
32 to study the effects of RAS dysregulation in hematopoietic disease, we developed separate founder lin
33 5 in the abnormal activation of JAK2-induced hematopoietic diseases, we generated a stable transfecta
34 The success of retrovirus gene therapy for hematopoietic diseases will be limited both by the effic
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