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1 itution have been observed in the absence of myeloablation.
2 r-expressing cells during regeneration after myeloablation.
3 e cells efficiently rescued mice from lethal myeloablation.
4  early progenitors are crucial to compensate myeloablation.
5 nor-HSC engraftment without chemoirradiative myeloablation.
6 otential in a xenogeneic model after partial myeloablation.
7 an be beneficial in response to infection or myeloablation.
8  from hemolytic anemia, acute blood loss and myeloablation.
9 tissue regeneration models, hepatectomy, and myeloablation.
10 r proliferation after 5-fluorouracil-induced myeloablation.
11 h the same quantities of (213)Bi, had lethal myeloablation.
12  extending access to patients unsuitable for myeloablation.
13 on of endothelial-derived jagged-2 following myeloablation.
14 s enables chimeric engraftment without toxic myeloablation.
15  sufficient to cure SCD without the risks of myeloablation.
16 and was refractory to 5-fluorouracil-induced myeloablation.
17  proliferation after bacterial infection and myeloablation.
18 ith chemotherapy used for pretransplantation myeloablation.
19  cell transplantation (HSCT) with or without myeloablation.
20 regeneration and hematopoietic rebound after myeloablation.
21 nd vascular regeneration were impaired after myeloablation.
22 mal recovery of HSCs and hematopoiesis after myeloablation.
23 totoxic events and lowering the intensity of myeloablation.
24 l was consistent with that of busulfan-based myeloablation.
25 therapy and relegating its use to total body myeloablation.
26 ow is the major source of THPO protein after myeloablation.
27 pes and enhance hematopoietic recovery after myeloablation.
28 ges 13-21 years, were treated after busulfan myeloablation 4.6-7.9 years ago, with a median follow-up
29 e to doses of irradiation that cause minimal myeloablation (50 to 100 cGy) leads to very high levels
30 d be achieved with less than total recipient myeloablation (700 cGy) and that the incidence of engraf
31 topoietic stem cells (HSCs) regenerate after myeloablation, a procedure that adversely disrupts the b
32                         In a murine model of myeloablation after radiation exposure, we demonstrated
33 ment plan, such radioligand therapy-mediated myeloablation also allows one to line up patients for st
34 es but has so far been marred by threatening myeloablation and early relapses.
35 ors, such CTLs could also contribute to host myeloablation and enhance donor cell engraftment.
36         We conclude that both some degree of myeloablation and HvG tolerance are required for success
37                           After conventional myeloablation and immunoprophylaxis, the treated donor c
38 zing irradiation is used routinely to induce myeloablation and immunosuppression.
39 tokine promoting hematopoietic rebound after myeloablation and its transcripts are expressed by multi
40 etic chimerism and central tolerance with no myeloablation and no GVHD.
41 ry phase after cyclophosphamide (CP)-induced myeloablation and observed that, in the absence of CCR2,
42 crete semaphorin 3 A (SEMA3A) in response to myeloablation and SEMA3A induces p53 - mediated apoptosi
43 eral-blood lymphocytes were collected before myeloablation and served as alloantigen-presenting cells
44               This regimen combines busulfan myeloablation and six days of Colony-stimulating factor
45 c potential of PTN to improve survival after myeloablation and suggest that PTN-mediated hematopoieti
46                                              Myeloablation and syngeneic bone marrow transplantation
47 ficient clonal deletion occurs after partial myeloablation and that both donor and host ligands contr
48                      The "space" produced by myeloablation and the consequent potential for donor cel
49                               However, toxic myeloablation and the high cost of current ex vivo hemat
50 vivo HSPC transduction that does not require myeloablation and transplantation.
51 s, delayed blood cell regeneration following myeloablation, and disrupted molecular programs that pro
52 replenishment after cyclophosphamide-induced myeloablation, BCAP(-/-) mice had increased LSK prolifer
53 , in the mouse spleen after EMH induction by myeloablation, blood loss, or pregnancy.
54 ells to reconstitute hematopoiesis following myeloablation, bone marrow (BM) transplantation was perf
55                        Using a novel minimal myeloablation-bone marrow chimera approach, we visualize
56 eneration after irradiation or chemotherapy (myeloablation), but little is known about how this is re
57 Cs as well as impaired B lymphopoiesis after myeloablation, but not in the steady state.
58                                     However, myeloablation can cause severe complications and even mo
59 allogeneic bone marrow transplantation after myeloablation can prevent experimental autoimmunity and
60 uch as infections and cytotoxic drug-induced myeloablation, cause molecular, cellular and metabolic c
61 ducing hematolymphoid microchimerism without myeloablation could confer the ability to resist mercuri
62     Hepatitis was associated with absence of myeloablation during conditioning, split chimerism, and
63                       All patients underwent myeloablation followed by HSCT.
64                                      Despite myeloablation, host CD4+ T cells having a regulatory phe
65 ely used to reconstitute hematopoiesis after myeloablation; however, transplantation efficacy and mul
66                             Because therapy (myeloablation, immunotherapy, or differentiation) for MR
67 ow tolerant allogeneic engraftment devoid of myeloablation in neonatal normal and mutant mice with ly
68 his observation raises concern for potential myeloablation in patients with AML treated with CD123-re
69 ins to be clarified to what extent recipient myeloablation is fundamental in the establishment of don
70 tion for gene therapy studies where complete myeloablation is not desirable and partial replacement o
71 otection, mice were subjected to irradiative myeloablation, marrow reconstitution, and then stroke fo
72 able AML therapy, suggest that CART123-based myeloablation may be used as a novel conditioning regime
73                         Importantly, despite myeloablation of circulating leukocytes following TBI, t
74                 Profound lymphodepletion, by myeloablation or by genetic means, focused the nonspecif
75 ietic stem cells without the requirement for myeloablation or immunosuppression.
76 se findings, during cyclophosphamide-induced myeloablation or specific monocyte depletion, BCAP(-/-)
77 l tolerance can be reliably achieved without myeloablation or T cell depletion of the host.
78  steady-state hematopoiesis, HSC response to myeloablation, or for rapid expansion of HSCs through in
79 gave rise to, increased NGF production after myeloablation, promoting nerve sprouting in the bone mar
80                           However, the toxic myeloablation required for allogeneic HCT can cause seri
81          Treatment with exa-cel, preceded by myeloablation, resulted in transfusion independence in 9
82 t that rare hematopoietic stem cells survive myeloablation that can eventually repopulate irradiated
83 itive HSCs were robustly activated by severe myeloablation, they did not contribute to the regenerati
84            A rapid induction regimen enables myeloablation to be given much earlier, which might cont
85 ML, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis, indicating that
86                             The concept that myeloablation to open space was a prerequisite for marro
87                             After undergoing myeloablation, two patients - one with TDT and the other
88                                              Myeloablation was given a median of 55 days earlier in p
89 or Csf2rb-gene-corrected macrophages without myeloablation was safe and well-tolerated and that one a
90 t since, even in the absence of HvG, partial myeloablation was still required.
91 t not from nonautoimmune patients undergoing myeloablation, where they were efficiently removed by ma
92 on is an effective cell therapy but requires myeloablation, which increases infection risk and mortal
93 ell transplantation (HSCT) in the absence of myeloablation, which leads to donor T cell engraftment,
94 ficiency delays hematopoietic recovery after myeloablation with 5-fluorouracil (5-FU).
95 gens can be achieved using partial recipient myeloablation with 500 cGy total-body irradiation (TBI)
96                           Patients underwent myeloablation with busulfan (with doses adjusted on the
97 ansplantation in most patients with MMM, (2) myeloablation with busulfan was associated with acceptab
98           All patients received conventional myeloablation with busulfan/cyclophosphamide (BuCy) and
99 ed erythropoiesis with blood transfusions or myeloablation with chemotherapeutic drugs.
100            All patients experienced expected myeloablation with engraftment of platelets (> or = 20 K
101 e sufficient to achieve myelosuppression and myeloablation with less nonhematologic toxicity compared
102           Twenty-one patients then underwent myeloablation with oral busulfan (16 mg/kg) and PBSC tra
103 he primary tumour was attempted, followed by myeloablation (with 200 mg/m2 of melphalan) and haemopoi

 
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