PMID- 23510414
OWN - NLM
STAT- MEDLINE
DCOM- 20130904
LR  - 20211021
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 81
IP  - 4
DP  - 2013 Apr
TI  - Dissecting graft-versus-leukemia from graft-versus-host-disease using novel 
      strategies.
PG  - 183-93
LID - 10.1111/tan.12090 [doi]
AB  - The intrinsic anti-leukemic effect of allogeneic hematopoietic cell 
      transplantation (HCT) is dependent on genetic disparity between donor and 
      recipient, intimately associated with graft-versus-host disease (GVHD), and 
      mediated by lymphocytes contained in or derived from the donor hematopoietic cell 
      graft. Three decades of intense effort have not identified clinical strategies 
      that can reliably separate the graft-versus-leukemia (GVL) effect from the 
      alloimmune reaction that drives clinical GVHD. For patients who require HCT and 
      for whom two or more human leukocyte antigen (HLA)-A, -B, -C, and -DRB1-matched 
      donor candidates can be identified, consideration of donor and recipient genotype 
      at additional genetic loci both within and outside the major histocompatibility 
      complex may offer the possibility of selecting the donor [candidate(s)] that 
      poses the lowest probability of GVHD and the highest probability of a potent GVL 
      effect. Strategies for engineering conventional donor lymphocyte infusion also 
      hold promise for prevention or improved treatment of post-transplant relapse. The 
      brightest prospects for selectively enhancing the anti-leukemic efficacy of 
      allogeneic HCT, however, are likely to be interventions that are designed to 
      enhance specific antitumor immunity via vaccination or adoptive cell transfer, 
      rather than those that attempt to exploit donor alloreactivity against the host. 
      Adoptive transfer of donor-derived T cells genetically modified for 
      tumor-specific reactivity, in particular, has the potential to transform the 
      practice of allogeneic HCT by selectively enhancing antitumor immunity without 
      causing GVHD.
CI  - (c) 2013 John Wiley & Sons A/S.
FAU - Warren, E H
AU  - Warren EH
AD  - Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 
      98109-1024, USA. ehwarren@u.washington.edu
FAU - Deeg, H J
AU  - Deeg HJ
LA  - eng
GR  - P01 AI033484/AI/NIAID NIH HHS/United States
GR  - R01 HL105914/HL/NHLBI NIH HHS/United States
GR  - AI033484/AI/NIAID NIH HHS/United States
GR  - HL105914/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA Antigens)
SB  - IM
MH  - Chromosome Mapping
MH  - Genetic Loci/*immunology
MH  - Graft vs Host Disease/*prevention & control
MH  - *Graft vs Leukemia Effect
MH  - HLA Antigens/immunology
MH  - *Hematopoietic Stem Cell Transplantation
MH  - Histocompatibility
MH  - Humans
MH  - *Immunotherapy, Adoptive
MH  - Leukemia/immunology/pathology/*therapy
MH  - T-Lymphocytes/immunology/transplantation
MH  - Tissue Donors
MH  - Transplantation, Homologous
PMC - PMC3645301
MID - NIHMS447774
COIS- Conflict of Interests The authors have declared no conflicting interests.
EDAT- 2013/03/21 06:00
MHDA- 2013/09/05 06:00
PMCR- 2014/04/01
CRDT- 2013/03/21 06:00
PHST- 2013/03/21 06:00 [entrez]
PHST- 2013/03/21 06:00 [pubmed]
PHST- 2013/09/05 06:00 [medline]
PHST- 2014/04/01 00:00 [pmc-release]
AID - 10.1111/tan.12090 [doi]
PST - ppublish
SO  - Tissue Antigens. 2013 Apr;81(4):183-93. doi: 10.1111/tan.12090.