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Novel spontaneous myelodysplastic syndrome mouse model
BACKGROUND: Myelodysplastic syndrome (MDS) is a group of disorders involving hemopoietic dysfunction leading to leukemia. Although recently progress has been made in identifying underlying genetic mutations, many questions still remain. Animal models of MDS have been produced by introduction of spec...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8212821/ https://www.ncbi.nlm.nih.gov/pubmed/34179724 http://dx.doi.org/10.1002/ame2.12168 |
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author | Li, Weisha Cao, Lin Li, Mengyuan Yang, Xingjiu Zhang, Wenlong Song, Zhiqi Wang, Xinpei Zhang, Lingyan Morahan, Grant Qin, Chuan Gao, Ran |
author_facet | Li, Weisha Cao, Lin Li, Mengyuan Yang, Xingjiu Zhang, Wenlong Song, Zhiqi Wang, Xinpei Zhang, Lingyan Morahan, Grant Qin, Chuan Gao, Ran |
author_sort | Li, Weisha |
collection | PubMed |
description | BACKGROUND: Myelodysplastic syndrome (MDS) is a group of disorders involving hemopoietic dysfunction leading to leukemia. Although recently progress has been made in identifying underlying genetic mutations, many questions still remain. Animal models of MDS have been produced by introduction of specific mutations. However, there is no spontaneous mouse model of MDS, and an animal model to simulate natural MDS pathogenesis is urgently needed. METHODS: In characterizing the genetically diverse mouse strains of the Collaborative Cross (CC) we observed that one, designated JUN, had abnormal hematological traits. This strain was thus further analyzed for phenotypic and pathological identification, comparing the changes in each cell population in peripheral blood and in bone marrow. RESULTS: In a specific‐pathogen free environment, mice of the JUN strain are relatively thin, with healthy appearance. However, in a conventional environment, they become lethargic, develop wrinkled yellow hair, have loose and light stools, and are prone to infections. We found that the mice were cytopenic, which was due to abnormal differentiation of multipotent bone marrow progenitor cells. These are common characteristics of MDS. CONCLUSIONS: A mouse strain, JUN, was found displaying spontaneous myelodysplastic syndrome. This strain has the advantage over existing models in that it develops MDS spontaneously and is more similar to human MDS than genetically modified mouse models. JUN mice will be an important tool for pathogenesis research of MDS and for evaluation of new drugs and treatments. |
format | Online Article Text |
id | pubmed-8212821 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82128212021-06-25 Novel spontaneous myelodysplastic syndrome mouse model Li, Weisha Cao, Lin Li, Mengyuan Yang, Xingjiu Zhang, Wenlong Song, Zhiqi Wang, Xinpei Zhang, Lingyan Morahan, Grant Qin, Chuan Gao, Ran Animal Model Exp Med Original Articles BACKGROUND: Myelodysplastic syndrome (MDS) is a group of disorders involving hemopoietic dysfunction leading to leukemia. Although recently progress has been made in identifying underlying genetic mutations, many questions still remain. Animal models of MDS have been produced by introduction of specific mutations. However, there is no spontaneous mouse model of MDS, and an animal model to simulate natural MDS pathogenesis is urgently needed. METHODS: In characterizing the genetically diverse mouse strains of the Collaborative Cross (CC) we observed that one, designated JUN, had abnormal hematological traits. This strain was thus further analyzed for phenotypic and pathological identification, comparing the changes in each cell population in peripheral blood and in bone marrow. RESULTS: In a specific‐pathogen free environment, mice of the JUN strain are relatively thin, with healthy appearance. However, in a conventional environment, they become lethargic, develop wrinkled yellow hair, have loose and light stools, and are prone to infections. We found that the mice were cytopenic, which was due to abnormal differentiation of multipotent bone marrow progenitor cells. These are common characteristics of MDS. CONCLUSIONS: A mouse strain, JUN, was found displaying spontaneous myelodysplastic syndrome. This strain has the advantage over existing models in that it develops MDS spontaneously and is more similar to human MDS than genetically modified mouse models. JUN mice will be an important tool for pathogenesis research of MDS and for evaluation of new drugs and treatments. John Wiley and Sons Inc. 2021-05-14 /pmc/articles/PMC8212821/ /pubmed/34179724 http://dx.doi.org/10.1002/ame2.12168 Text en © 2021 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Li, Weisha Cao, Lin Li, Mengyuan Yang, Xingjiu Zhang, Wenlong Song, Zhiqi Wang, Xinpei Zhang, Lingyan Morahan, Grant Qin, Chuan Gao, Ran Novel spontaneous myelodysplastic syndrome mouse model |
title | Novel spontaneous myelodysplastic syndrome mouse model |
title_full | Novel spontaneous myelodysplastic syndrome mouse model |
title_fullStr | Novel spontaneous myelodysplastic syndrome mouse model |
title_full_unstemmed | Novel spontaneous myelodysplastic syndrome mouse model |
title_short | Novel spontaneous myelodysplastic syndrome mouse model |
title_sort | novel spontaneous myelodysplastic syndrome mouse model |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8212821/ https://www.ncbi.nlm.nih.gov/pubmed/34179724 http://dx.doi.org/10.1002/ame2.12168 |
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