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1 plications for graft-versus-host disease and graft-versus-leukemia.
2 alloreactive effect might also contribute to graft-versus-leukemia.
3 cyte infusion (DLI) has been used to enhance graft-versus-leukemia activity after BMT, but the effect
4 ustrate the potential to selectively enhance graft-versus-leukemia activity by the adoptive transfer
5 These findings support a role for NK cell graft-versus-leukemia activity modulated by NK cell rece
8 amage and lethality without compromising the graft-versus-leukemia activity, which is crucial to prev
12 an improved understanding of T-cell mediated graft versus leukemia and of antiviral responses is prov
13 d-party skin graft rejection; importantly, a graft-versus-leukemia assay showed that T cell activity
15 , GVHD is not an obligatory correlate of the graft-versus-leukemia benefit or freedom from relapse af
20 vaccines represent a strategy to enhance the graft-versus-leukemia effect after allogeneic blood and
21 g the late establishment of a posttransplant graft-versus-leukemia effect and an overrepresentation o
22 ice with the advantages of possible stronger graft-versus-leukemia effect and expanding transplantati
23 outcomes, results of nonmyeloablative UCBT, graft-versus-leukemia effect and graft-versus-host disea
24 CML in chronic phase, its responsiveness to graft-versus-leukemia effect and the ability to monitor
25 ng understanding of the immunobiology of the graft-versus-leukemia effect and the immune escape mecha
26 nistered after BMT might induce or amplify a graft-versus-leukemia effect and thereby reduce the rela
27 e development of new strategies to enhance a graft-versus-leukemia effect and to decrease the inciden
29 risk of early relapse/progression before the graft-versus-leukemia effect being disproportionally lar
30 or lymphocyte transfusions indicate that the graft-versus-leukemia effect can be very powerful and to
31 at mediate graft-versus-host disease and the graft-versus-leukemia effect following stem cell transpl
33 apse risk, this analysis reveals an enhanced graft-versus-leukemia effect in acute leukemia patients
37 tation can eradicate the leukemia and that a graft-versus-leukemia effect makes a major contribution
38 tem cell transplantation (allo-HSCT) and the graft-versus-leukemia effect mediated by donor T cells,
43 monstration that an immunologically mediated graft-versus-leukemia effect plays a central role in del
45 re has been a corresponding reduction in the graft-versus-leukemia effect so that any decrease in GVH
46 D because there is no theoretical beneficial graft-versus-leukemia effect that can accompany graft-ve
49 cross the placenta and might confer a potent graft-versus-leukemia effect when cord blood (CB) is use
51 r immune reconstitution and a quite powerful graft-versus-leukemia effect with a low incidence of gra
52 ne response to these antigens may potentiate graft-versus-leukemia effect without accompanying graft-
55 nefit, the value of purging, the presence of graft-versus-leukemia effect, and the timing of transpla
56 elapse due to the lack of an immune-mediated graft-versus-leukemia effect, as occurs in the allogenei
57 al killer lymphocytes may play a role in the graft-versus-leukemia effect, attention is focusing incr
59 e immune system will allow us to improve the graft-versus-leukemia effect, improve engraftment, and d
60 inally, T-bet(-/-) T cells had a compromised graft-versus-leukemia effect, which could be essentially
76 cute myeloid leukemia (AML) and relies on a "graft-versus-leukemia" effect (GVL) where donor T lympho
78 ion for HLA-matched HCT may achieve superior graft versus leukemia effects, lower risk for relapse, a
81 as GVHD prophylaxis, Tregs potently suppress graft-versus-leukemia effects and so may be most appropr
82 teins expressed by many normal host tissues, graft-versus-leukemia effects are often accompanied by m
83 ractions between HLA-C and KIR might promote Graft-versus-Leukemia effects following transplantation.
84 g the beneficial graft-versus-tumor (GVT) or graft-versus-leukemia effects from graft-versus-host dis
86 DR15 on graft-versus-host disease (GVHD) and graft-versus-leukemia effects in HLA-matched allogeneic
87 ells was associated with decreased cGVHD and graft-versus-leukemia effects in recipients of allogenei
88 relapse-free survival, it commonly reflects graft-versus-leukemia effects mediated by donor T cells
89 ecipients was strikingly advantageous in the graft-versus-leukemia effects of delayed donor lymphocyt
90 of allogeneic cells and they rely largely on graft-versus-leukemia effects rather than high-dose cyto
92 minant cytotoxic subset after BMT, mediating graft-versus-leukemia effects while limiting inflammatio
94 d fludarabine, relying almost exclusively on graft-versus-leukemia effects, can result in long-term r
95 al in a mouse model of aGVHD while retaining graft-versus-leukemia effects, unveiling a novel therape
105 K) cells can enhance engraftment and mediate graft-versus-leukemia following allogeneic hematopoietic
106 cells, providing a basis for separating the graft-versus-leukemia from graft-versus-host reactions.
108 Strategies to control GVHD while maintaining graft versus leukemia (GVL) include herpes simplex virus
110 To confirm that the role of TNF-alpha in graft versus leukemia (GVL) was due to effects on donor
111 H) disease (GVHD) is usually associated with graft versus leukemia (GVL), GVL can occur in the absenc
113 st DDX3Y have the potential to contribute to graft-versus-leukemia (GVL) activity after female into m
114 sus-host disease (GVHD) while preserving the graft-versus-leukemia (GVL) activity of donor T cells.
115 adicate chemorefractory leukemia through the graft-versus-leukemia (GVL) activity of donor T cells.
116 Caspase-11 deficiency does not decrease the graft-versus-leukemia (GVL) activity, which is essential
121 onor APCs were not required for CD8-mediated graft-versus-leukemia (GVL) against a mouse model of chr
125 selectively depleted transplants to evaluate graft-versus-leukemia (GVL) and survival are warranted.
126 d leukemia (CML) is exquisitely sensitive to graft-versus-leukemia (GVL) because patients relapsing a
127 We postulate that ibrutinib augments the graft-versus-leukemia (GVL) benefit through a T-cell-med
129 d Wilms tumor antigen (WT1) contributes to a graft-versus-leukemia (GVL) effect after allogeneic stem
130 FTY slightly impaired but did not abrogate a graft-versus-leukemia (GVL) effect against C1498, a myel
131 esidual leukemia and prevent relapse via the graft-versus-leukemia (GVL) effect and are critical for
133 ed by Y-chromosome genes may contribute to a graft-versus-leukemia (GVL) effect and to graft-versus-h
139 on primary human AML cells and enhanced the graft-versus-leukemia (GVL) effect in human xenograft mo
140 long-term survival without compromising the graft-versus-leukemia (GVL) effect in lymphocytic and my
141 , we investigated whether IL-18 can maintain graft-versus-leukemia (GVL) effect in this context.
142 host disease (GVHD) with preservation of the graft-versus-leukemia (GVL) effect is a crucial step to
143 rsus-host disease (GVHD) without loss of the graft-versus-leukemia (GVL) effect is the holy grail of
144 curing hematologic malignancies is due to a graft-versus-leukemia (GVL) effect mediated by donor T c
147 current understanding of the biology of the graft-versus-leukemia (GVL) effect still lags behind tha
148 HSCT) commonly results from the failure of a graft-versus-leukemia (GVL) effect to eradicate minimal
149 eneic BM transplantation (BMT) relies on the graft-versus-leukemia (GVL) effect to eradicate residual
150 poietic cell transplantation, leveraging the graft-versus-leukemia (GvL) effect to restore immune con
151 we address various maneuvers to optimize the graft-versus-leukemia (GVL) effect while preventing graf
152 nctionally defined T-cell subsets mediated a graft-versus-leukemia (GVL) effect with reduced graft-ve
153 age between GVHD toxicity and the beneficial graft-versus-leukemia (GVL) effect, as well as the impai
156 resumed that allogeneic T cells mediate this graft-versus-leukemia (GVL) effect, the influence of DLI
167 ic T-lymphocyte (CTL) activity and preserved graft-versus-leukemia (GVL) effects after allogeneic BMT
168 rs than their cycling counterparts; however, graft-versus-leukemia (GVL) effects after allogeneic ste
171 oles in graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) effects following bone marro
172 tively prevents GVHD while preserving strong graft-versus-leukemia (GVL) effects in allogeneic and xe
174 teroid-refractory GVHD, without compromising graft-versus-leukemia (GVL) effects in multiple mouse mo
175 intensive chemoradiotherapy and from potent graft-versus-leukemia (GVL) effects mediated by donor im
176 donor leukocyte infusions (DLIs) can induce graft-versus-leukemia (GVL) effects without graft-versus
177 ure patients with high-risk leukemia through graft-versus-leukemia (GVL) effects, the process by whic
185 mediate graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) is a fundamental question in
186 tion of a profound donor lymphocyte-mediated graft-versus-leukemia (GVL) or graft-versus-tumor (GVT)
188 lant donor have been used to induce a direct graft-versus-leukemia (GVL) reaction in patients with re
190 Donor leukocyte infusion (DLI) can induce graft-versus-leukemia (GvL) reactions in patients with c
194 , recognize and eliminate leukemic cells via graft-versus-leukemia (GVL) reactivity, and transfer of
195 nor lymphocyte infusion (DLI) can experience graft-versus-leukemia (GVL) reactivity, with a lower ris
198 ith ipilimumab can reinvigorate an effective graft-versus-leukemia (GVL) response, we integrated tran
200 ucidate the antigenic basis of the effective graft-versus-leukemia (GvL) responses associated with DL
201 -) T cells were capable of generating robust graft-versus-leukemia (GVL) responses in vivo, as well a
202 e (GVHD) but do not contribute to beneficial graft-versus-leukemia (GVL) responses, as reported by Ga
204 tiating graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL), and separation of GVL from
208 t tissues or sites of leukemic infiltration (graft-versus-leukemia [GVL]) is likely mediated by chemo
209 a good response against the malignant cells (graft-versus-leukemia [GVL]), it also leads to the devel
212 mphocytes (DLI) has the potential to restore graft-versus-leukemia immunologic surveillance; however,
216 ogic malignancies due to the well-recognized graft-versus-leukemia/lymphoma (GVL) effect that is medi
217 tempting to capture this approach to achieve graft-versus-leukemia/lymphoma (GVL) effects without GVH
218 onstitution and reduce donor T-cell-mediated graft-versus-leukemia/lymphoma (GVL) effects, derived fr
220 l transplantation (HSCT), but the potency of graft-versus-leukemia mediated by naturally reconstituti
221 ic system, we have proposed that the desired graft-versus-leukemia or graft-versus-lymphoma effect ca
222 is necessary to predict its contribution to graft-versus-leukemia reactions and to eventually use KI
223 tem-cell transplantation can induce curative graft-versus-leukemia reactions in patients with hematol
224 immune conditions and cancer, as well as for graft-versus-leukemia reactions in settings of allogenei
226 sulting in nonspecific graft-versus-host and graft-versus-leukemia reactions, there is also the possi
227 To identify immunological targets of the graft-versus-leukemia response (GVL) after DLI, we used
228 iller-cell receptors may explain the loss of graft-versus-leukemia response and extramedullary AML re
229 e is to devise strategies for separating the graft-versus-leukemia response from graft-versus-host di
233 are targets of graft-versus-host disease and graft-versus-leukemia responses after allogeneic human l
235 ation, IRX4204-treated recipients maintained graft-versus-leukemia responses against both leukemia an
236 currently known regarding the association of graft-versus-leukemia responses and graft-versus-host di
238 tinib balanced graft-versus-host disease and graft-versus-leukemia responses in delayed donor lymphoc
240 dox whereby GVH-reactive T cells can mediate graft-versus-leukemia responses without inducing GVHD in
241 re the main targets of graft-versus-host and graft-versus-leukemia responses, we tested the hypothesi
242 ed to increase our understanding of GVHD and graft-versus-leukemia responses, which will greatly impr