ライフサイエンスコーパス: myeloablation

1 on of endothelial-derived jagged-2 following myeloablation.

2 otential in a xenogeneic model after partial myeloablation.

3 from hemolytic anemia, acute blood loss and myeloablation.

4 tissue regeneration models, hepatectomy, and myeloablation.

5 r proliferation after 5-fluorouracil-induced myeloablation.

6 h the same quantities of (213)Bi, had lethal myeloablation.

7 extending access to patients unsuitable for myeloablation.

8 s enables chimeric engraftment without toxic myeloablation.

9 sufficient to cure SCD without the risks of myeloablation.

10 early progenitors are crucial to compensate myeloablation.

11 nor-HSC engraftment without chemoirradiative myeloablation.

12 e to doses of irradiation that cause minimal myeloablation (50 to 100 cGy) leads to very high levels

13 d be achieved with less than total recipient myeloablation (700 cGy) and that the incidence of engraf

14 In a murine model of myeloablation after radiation exposure, we demonstrated

15 ors, such CTLs could also contribute to host myeloablation and enhance donor cell engraftment.

16 We conclude that both some degree of myeloablation and HvG tolerance are required for success

17 After conventional myeloablation and immunoprophylaxis, the treated donor c

18 zing irradiation is used routinely to induce myeloablation and immunosuppression.

19 etic chimerism and central tolerance with no myeloablation and no GVHD.

20 ry phase after cyclophosphamide (CP)-induced myeloablation and observed that, in the absence of CCR2,

21 eral-blood lymphocytes were collected before myeloablation and served as alloantigen-presenting cells

22 c potential of PTN to improve survival after myeloablation and suggest that PTN-mediated hematopoieti

23 Myeloablation and syngeneic bone marrow transplantation

24 ficient clonal deletion occurs after partial myeloablation and that both donor and host ligands contr

25 The "space" produced by myeloablation and the consequent potential for donor cel

26 vivo HSPC transduction that does not require myeloablation and transplantation.

27 replenishment after cyclophosphamide-induced myeloablation, BCAP(-/-) mice had increased LSK prolifer

28 , in the mouse spleen after EMH induction by myeloablation, blood loss, or pregnancy.

29 ells to reconstitute hematopoiesis following myeloablation, bone marrow (BM) transplantation was perf

30 Using a novel minimal myeloablation-bone marrow chimera approach, we visualize

31 However, myeloablation can cause severe complications and even mo

32 allogeneic bone marrow transplantation after myeloablation can prevent experimental autoimmunity and

33 ducing hematolymphoid microchimerism without myeloablation could confer the ability to resist mercuri

34 All patients underwent myeloablation followed by HSCT.

35 Despite myeloablation, host CD4+ T cells having a regulatory phe

36 ely used to reconstitute hematopoiesis after myeloablation; however, transplantation efficacy and mul

37 Because therapy (myeloablation, immunotherapy, or differentiation) for MR

38 ow tolerant allogeneic engraftment devoid of myeloablation in neonatal normal and mutant mice with ly

39 his observation raises concern for potential myeloablation in patients with AML treated with CD123-re

40 ins to be clarified to what extent recipient myeloablation is fundamental in the establishment of don

41 tion for gene therapy studies where complete myeloablation is not desirable and partial replacement o

42 otection, mice were subjected to irradiative myeloablation, marrow reconstitution, and then stroke fo

43 able AML therapy, suggest that CART123-based myeloablation may be used as a novel conditioning regime

44 Importantly, despite myeloablation of circulating leukocytes following TBI, t

45 Profound lymphodepletion, by myeloablation or by genetic means, focused the nonspecif

46 ietic stem cells without the requirement for myeloablation or immunosuppression.

47 se findings, during cyclophosphamide-induced myeloablation or specific monocyte depletion, BCAP(-/-)

48 l tolerance can be reliably achieved without myeloablation or T cell depletion of the host.

49 steady-state hematopoiesis, HSC response to myeloablation, or for rapid expansion of HSCs through in

50 t that rare hematopoietic stem cells survive myeloablation that can eventually repopulate irradiated

51 A rapid induction regimen enables myeloablation to be given much earlier, which might cont

52 ML, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis, indicating that

53 The concept that myeloablation to open space was a prerequisite for marro

54 Myeloablation was given a median of 55 days earlier in p

55 or Csf2rb-gene-corrected macrophages without myeloablation was safe and well-tolerated and that one a

56 t since, even in the absence of HvG, partial myeloablation was still required.

57 t not from nonautoimmune patients undergoing myeloablation, where they were efficiently removed by ma

58 on is an effective cell therapy but requires myeloablation, which increases infection risk and mortal

59 ficiency delays hematopoietic recovery after myeloablation with 5-fluorouracil (5-FU).

60 gens can be achieved using partial recipient myeloablation with 500 cGy total-body irradiation (TBI)

61 ansplantation in most patients with MMM, (2) myeloablation with busulfan was associated with acceptab

62 All patients received conventional myeloablation with busulfan/cyclophosphamide (BuCy) and

63 ed erythropoiesis with blood transfusions or myeloablation with chemotherapeutic drugs.

64 All patients experienced expected myeloablation with engraftment of platelets (> or = 20 K

65 e sufficient to achieve myelosuppression and myeloablation with less nonhematologic toxicity compared

66 Twenty-one patients then underwent myeloablation with oral busulfan (16 mg/kg) and PBSC tra

67 he primary tumour was attempted, followed by myeloablation (with 200 mg/m2 of melphalan) and haemopoi