Published online Feb 6, 2016. doi: 10.5315/wjh.v5.i1.1
Peer-review started: October 3, 2015
First decision: October 27, 2015
Revised: November 17, 2015
Accepted: December 13, 2015
Article in press: December 14, 2015
Published online: February 6, 2016
In recent years, there has been significant progress made in our understanding of the molecular genetics of myelodysplastic syndromes (MDS). Using massively parallel sequencing techniques, recurring mutations are identified in up to 80% of MDS cases, including many with a normal karyotype. The differential role of some of these mutations in the initiation and progression of MDS is starting to be elucidated. Engineering candidate genes in mice to model MDS has contributed to recent insights into this complex disease. In this review, we examine currently available mouse models, with detailed discussion of selected models. Finally, we highlight some advances made in our understanding of MDS biology, and conclude with discussions of questions that remain unanswered.
Core tip: Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic disorders. In recent years, we have witnessed a rapidly expanding catalog of MDS candidate genes. Mirroring this, there has been an increased number of candidate genes employed to model MDS. Here, we aim to review currently available mouse models of MDS, highlighting models that are robust and well-characterized phenotypically with a particular focus on models that demonstrate close resemblance to the human disease.