What can we learn from leukemia as for the process of lineage commitment in hematopoiesis?

Abstract:

:Most contemporary models of hematopoiesis assume lineage fidelity of early progenitor cells. Along with this concept normal hematopoietic cells and the majority of leukemias express exclusively myeloid or lymphoid specific antigens. On the other hand, growing evidence exists challenging the lineage fidelity model. Chronic myeloid leukemia (CML) in the blast crisis may switch to acute lymphoblastic leukemia (ALL) and as a result of the chemotherapy ALL may converse to acute myeloid leukemia (AML). Furthermore, a substantial portion of leukemia cases, named acute mixed-lineage leukemia (AMLL), show simultaneous expression of both myeloid and lymphoid antigens. Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements, correlating with myeloid-lymphoid immunophenotype in AMLL, support the hypothesis of lineage infidelity of early progenitor cells, rather than the aberrant antigen expression. Based on a detailed characterization of AMLL we present a modified model of a "common myeloid/lymphoid progenitor cell". This hypothetical very early hematopoietic progenitor cell shows a transient expression of myeloid and B- or T-lymphoid antigen and may also have rearranged its Ig and/or TCR genes. Subsequently, myeloid or lymphoid markers are downregulated and the hematopoietic cell enters either myeloid, T-lymphoid or B-lymphoid differentiation pathway.

journal_name

Int Rev Immunol

authors

Schmidt CA,Przybylski GK

doi

10.3109/08830180109056725

subject

Has Abstract

pub_date

2001-02-01 00:00:00

pages

107-15

issue

1

eissn

0883-0185

issn

1563-5244

pii

I341E001022

journal_volume

20

pub_type

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