abstract
Hematopoietic reconstitution, following bone marrow or stem cell transplantation, requires a microenvironment niche
capable of supporting both immature progenitors and stem cells with the capacity to differentiate and expand.Melphalan and VP-16 induced damage of HOB suggests vulnerability of this critical niche
to therapeutic agents frequently utilized in pre-transplant regimens and suggests that dose escalated chemotherapy may
contribute to post-transplantation hematopoietic deficits by damaging structural components of this supportive niche.This increase was
coincident with reduced HOB capacity to support immature B lineage cell chemotaxis and adherence.