PMID- 12647807
OWN - NLM
STAT- MEDLINE
DCOM- 20030922
LR  - 20170419
IS  - 0213-3911 (Print)
IS  - 0213-3911 (Linking)
VI  - 18
IP  - 2
DP  - 2003 Apr
TI  - Dynamics of lineage-restricted mixed chimerism following sex-mismatched 
      allogeneic bone marrow transplantation.
PG  - 557-74
LID - 10.14670/HH-18.557 [doi]
AB  - Scant knowledge is available about the dynamics of lineage-specific mixed 
      chimerism (Ch) following bone marrow transplantation (BMT). This review is 
      focused on findings derived from bone marrow (BM) biopsies in patients with 
      chronic myeloid leukemia (CML) including a sex-mismatched host/donor 
      constellation. Appropriate techniques involved immunophenotyping by monoclonal 
      antibodies to identify the various cell lineages, dual color fluorescence in situ 
      hybridization (FISH) with x- and y-chromosome-specific DNA-probes and a proper 
      detection system for a simultaneous labeling of the bcr/abl locus. A significant 
      degree of Ch with more than 20% host CD34+ progenitors was found in the early and 
      late (up to 200 days after BMT) posttransplant period. However, only 10% of these 
      cells harbored the bcr/abl translocation gene. This result fits well with 
      corresponding molecular biological findings of so-called minimal residual 
      disease. Conversion of Ch evolved during leukemic relapse with 90% host 
      progenitors of which 50% revealed the bcr/abl locus. A Ch of nucleated erythroid 
      percursors (5%) and CD68+ macrophages (8%) was expressed to a significantly lower 
      degree. The slightly increased frequency found in CD61+ megakaryocytes (16%) was 
      probably due to the polyploid state of these cells. Similar to the CD34+ 
      progenitor cells abrupt changes from donor to host type was associated with an 
      insidious transformation into recurrent leukemia. The CD34+ endothelial cells 
      showed a minor degree of Ch, because donor-derived elements ranged from 18% to 
      25%. Leukemic relapse was characterized by an almost complete conversion of the 
      endothelial cells to a host type. These findings point towards a CD34+ progenitor 
      cell origin of the (leukemic) endothelial cell layer and suggests that their 
      dysfunction may contribute to an expansion of the neoplastic clone.
FAU - Thiele, J
AU  - Thiele J
AD  - Institute of Pathology, University of Cologne, Cologne, Germany. 
      j.thiele@uni-koeln.de
FAU - Wickenhauser, C
AU  - Wickenhauser C
FAU - Kvasnicka, H M
AU  - Kvasnicka HM
FAU - Varus, E
AU  - Varus E
FAU - Beelen, D W
AU  - Beelen DW
FAU - Schaefer, U W
AU  - Schaefer UW
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Spain
TA  - Histol Histopathol
JT  - Histology and histopathology
JID - 8609357
RN  - 0 (Antigens, CD34)
SB  - IM
MH  - Animals
MH  - Antigens, CD34/immunology
MH  - Bone Marrow Transplantation/*physiology
MH  - Cell Lineage
MH  - Chimera/*genetics
MH  - Female
MH  - Humans
MH  - Leukemia/*therapy
MH  - Male
MH  - Megakaryocytes/physiology
MH  - Neoplasm Recurrence, Local
MH  - Stem Cells
RF  - 121
EDAT- 2003/03/22 04:00
MHDA- 2003/09/23 05:00
CRDT- 2003/03/22 04:00
PHST- 2003/03/22 04:00 [pubmed]
PHST- 2003/09/23 05:00 [medline]
PHST- 2003/03/22 04:00 [entrez]
AID - 10.14670/HH-18.557 [doi]
PST - ppublish
SO  - Histol Histopathol. 2003 Apr;18(2):557-74. doi: 10.14670/HH-18.557.