Publication: Dynamics of lineage-restricted
mixed chimerism following sex-mismatched
allogeneic bone marrow transplantation
Authors
Thiele, J. ; Wickenhauser, C. ; Kvasnicka, H.M. ; Varus, E. ; Beelen, D.W. ; Schaefer, U.W.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
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-chromosomespecific
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
molecularbiological 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.
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