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Use of Hematopoietic Stem Cell Transplantation to Assess the Origin of Myelodysplastic Syndrome
Published on: October 3, 2018
The Apc(min) mouse has altered hematopoietic stem cell function and provides a model for MPD/MDS.
Steven W Lane1, Stephen M Sykes, Fatima Al-Shahrour
1Department of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Steven.lane@childrens.harvard.edu
Blood
|March 4, 2010
Summary
Loss of Apc function in mice leads to myeloid disorders by impairing hematopoietic stem cells (HSCs). This suggests Apc
Area of Science:
- Hematology
- Oncology
- Stem Cell Biology
Background:
- Adenomatous polyposis coli (Apc) is a tumor suppressor regulating Wnt signaling.
- Loss of Apc function causes intestinal polyposis and is linked to chromosome 5q deletions in myelodysplastic syndrome (MDS).
Purpose of the Study:
- To investigate the role of Apc haploinsufficiency in hematopoietic stem cell (HSC) function and MDS development.
- To determine if Apc loss-of-function contributes to MDS phenotypes.
Main Methods:
- Analysis of the hematopoietic system in Apc(min) mice with a loss-of-function allele.
- Assessment of long-term HSC repopulation potential and serial transplantation.
- Evaluation of MDS/myeloproliferative phenotypes in Apc(min) mice.
Main Results:
- Apc(min) mice showed enhanced HSC repopulation but impaired secondary recipient engraftment due to loss of HSC quiescence.
- Apc(min) mice developed MDS/myeloproliferative disease.
- Wnt activation via Apc haploinsufficiency caused insidious HSC dysfunction evident in serial transplantation.
Conclusions:
- Apc loss-of-function contributes to MDS phenotypes.
- Wnt pathway activation for HSC expansion requires careful consideration due to potential HSC dysfunction.
- Cell extrinsic factors may play a role in myeloid disease development.
