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Analysis of Intratumoral Heterogeneity in Myelodysplastic Syndromes with Isolated del(5q) Using a Single Cell Approach
Review

Myelodysplasia Syndrome, Clonal Hematopoiesis and Cardiovascular Disease

1
Division of Immunometabolism, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
2
Department of Anatomy and Physiology, University of Melbourne, Parkville, Melbourne, VIC 3010, Australia
3
Walter and Eliza Hall Institute of Medical Research, 1 G Royal Parade, Parkville, Melbourne, VIC 3052, Australia
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Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3052, Australia
5
Department of Diabetes, Department of Immunology, Monash University, Clayton, VIC 3004, Australia
6
Baker Department of Cardiometabolic Health, University of Melbourne, Melbourne, VIC 3052, Australia
*
Author to whom correspondence should be addressed.
Academic Editor: Adriano Venditti
Cancers 2021, 13(8), 1968; https://doi.org/10.3390/cancers13081968
Received: 18 March 2021 / Revised: 12 April 2021 / Accepted: 14 April 2021 / Published: 19 April 2021
(This article belongs to the Special Issue Recent Advances in Myelodysplastic Syndrome)
The development of blood cancers is a complex process that involves the acquisition of specific blood disorders that precede cancer. These blood disorders are often driven by the accumulation of genetic abnormalities, which are discussed in this review. Likewise, predicting the rate of progression of these diseases is difficult, but it appears to be linked to which specific gene mutations are present in blood cells. In this review, we discuss a variety of genetic abnormalities that drive blood cancer, conditions that precede clinical symptoms of blood cancer, and how alterations in these genes change blood cell function. Additionally, we discuss the novel links between blood cancer development and heart disease.
The development of myelodysplasia syndromes (MDS) is multiphasic and can be driven by a plethora of genetic mutations and/or abnormalities. MDS is characterized by a hematopoietic differentiation block, evidenced by increased immature hematopoietic cells, termed blast cells and decreased mature circulating leukocytes in at least one lineage (i.e., cytopenia). Clonal hematopoiesis of indeterminate potential (CHIP) is a recently described phenomenon preceding MDS development that is driven by somatic mutations in hemopoietic stem cells (HSCs). These mutant HSCs have a competitive advantage over healthy cells, resulting in an expansion of these clonal mutated leukocytes. In this review, we discuss the multiphasic development of MDS, the common mutations found in both MDS and CHIP, how a loss-of-function in these CHIP-related genes can alter HSC function and leukocyte development and the potential disease outcomes that can occur with dysfunctional HSCs. In particular, we discuss the novel connections between MDS development and cardiovascular disease. View Full-Text
Keywords: myelodysplasia syndrome; clonal hematopoiesis and indeterminate potential (CHIP); DNMT3A; TET2; P53; ASXL1; JAK2; hematopoietic stem cell (HSC); cardiovascular disease myelodysplasia syndrome; clonal hematopoiesis and indeterminate potential (CHIP); DNMT3A; TET2; P53; ASXL1; JAK2; hematopoietic stem cell (HSC); cardiovascular disease
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MDPI and ACS Style

Veiga, C.B.; Lawrence, E.M.; Murphy, A.J.; Herold, M.J.; Dragoljevic, D. Myelodysplasia Syndrome, Clonal Hematopoiesis and Cardiovascular Disease. Cancers 2021, 13, 1968. https://doi.org/10.3390/cancers13081968

AMA Style

Veiga CB, Lawrence EM, Murphy AJ, Herold MJ, Dragoljevic D. Myelodysplasia Syndrome, Clonal Hematopoiesis and Cardiovascular Disease. Cancers. 2021; 13(8):1968. https://doi.org/10.3390/cancers13081968

Chicago/Turabian Style

Veiga, Camilla B., Erin M. Lawrence, Andrew J. Murphy, Marco J. Herold, and Dragana Dragoljevic. 2021. "Myelodysplasia Syndrome, Clonal Hematopoiesis and Cardiovascular Disease" Cancers 13, no. 8: 1968. https://doi.org/10.3390/cancers13081968

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