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Lineage promiscuity in hemopoietic differentiation and leukemia
Blood
|January 1, 1986
Summary
Leukemic cells sometimes express markers from different cell types. This phenomenon, termed lineage infidelity, may not be aberrant programming but a relic of normal progenitor cell gene expression.
Area of Science:
- Hematopoiesis
- Cancer Biology
- Molecular Genetics
Background:
- Leukemic cells occasionally coexpress markers from distinct cell lineages, challenging traditional views of lineage fidelity.
- Previous interpretations suggested aberrant genetic programming or "lineage infidelity" in leukemia.
Purpose of the Study:
- To re-evaluate the phenomenon of lineage infidelity in leukemia.
- To propose an alternative explanation for observed marker coexpression in leukemic cells.
Main Methods:
- Critical review of existing reports on marker coexpression in leukemia.
- Analysis of specific examples such as Ig heavy-chain and T cell receptor gene expression.
- Consideration of terminal deoxynucleotidyl transferase expression in leukemic myeloblasts.
Main Results:
- Some reported instances of lineage infidelity may be due to technical artifacts.
- Genuine cases of marker coexpression in leukemia are observed and require explanation.
- Aberrant gene expression occurs but lacks consistent regularity for general significance.
Conclusions:
- Apparent lineage infidelity in leukemia may represent a preserved transient phase of gene expression promiscuity from normal multipotential progenitors.
- This phenomenon is likely a relic in leukemic cells arrested during maturation, not necessarily aberrant genetic programming.
- The proposed explanation offers insights into hematopoietic differentiation and generates testable predictions.