Stem cell concepts in myelodysplastic syndromes: lessons and challenges

Woll, Petter S.; Jacobsen, Sten Eirik W.

doi:10.1111/joim.13283

Cited by 4 publications

(5 citation statements)

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“…The clinical picture and treatment of MDS Myelodysplastic syndromes (MDSs) are a heterogeneous group of malignant diseases characterized by peripheral cytopenias and a hypercellular, dysplastic bone marrow, in most cases with a high risk of transformation into secondary AML [143][144][145][146] (Figure 8).…”

Section: Myelodysplastic Syndromes Are Malignant Diseases Of the Hema...mentioning

confidence: 99%

“…MDS is initiated by accumulation of driver mutations in HSCs capable of self-renewal and proliferation, providing growth advantage to the mutated clone 146,147 , which in turn results in a proliferative disadvantage of the normal hematopoiesis. MDS includes a group of distinct disorders subdivided by the French-American-British (FAB) and World Health Organization (WHO) classification systems 148,149 .…”

Section: Myelodysplastic Syndromes Are Malignant Diseases Of the Hema...mentioning

confidence: 99%

“…MDS stem cells reside in the Lin neg CD34 pos CD38 neg CD90 pos CD45RA neg stem cell compartment and to largely be quiescent similarly to normal HSCs 176 . Selective elimination of these quiescent stem cells could offer a therapeutic option to specifically target the disease propagating cells in MDS 146 .…”

Section: Mds Stem Cells Have Been Shown To Selectively Resist Therape...mentioning

confidence: 99%

“…The majority of the clones reacted to HLA-A2 pos cells in the presence or absence of MPL peptides, indicating cross-reactivity, but two TCRs specific for two unrelated MPL peptides were identified and selected for further studies. Malignant MDS stem cells acquire driver mutations leading to proliferative advantage and therefore outcompete normal stem cells 146,147 . MDS stem cells not only initiate the disease but are responsible for relapses after initially successful therapies, such as allo-HSCT.…”

Section: Identification Of a Tcr Recognizing Mplmentioning

confidence: 99%

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Induction of neoantigen-reactive T cells from healthy donors

et al. 2019

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Section: Myelodysplastic Syndromes Are Malignant Diseases Of the Hema...mentioning

confidence: 99%

Section: Myelodysplastic Syndromes Are Malignant Diseases Of the Hema...mentioning

confidence: 99%

Section: Mds Stem Cells Have Been Shown To Selectively Resist Therape...mentioning

confidence: 99%

Section: Identification Of a Tcr Recognizing Mplmentioning

confidence: 99%

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Induction of neoantigen-reactive T cells from healthy donors

et al. 2019

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“…The basic prospect of using these cells is to repair tissue injuries and to restore tissue degeneration when it becomes unresponsive to traditional treatment options. Despite the restricted differentiation potential, MSCs remain valuable resources of cell-based therapies in metabolic diseases, disorders of the immune system, and cancer and blood disorders [2][3][4][5]. MSCs' transplantation has been used in conditions of severe skin burns and showed the impressive repair of the affected lesions [6].…”

Section: Introductionmentioning

confidence: 99%

Optimizing the Adipogenic Induction Protocol Using Rosiglitazone Improves the Physiological Parameters and Differentiation Capacity of Adipose Tissue-Derived Mesenchymal Stem Cells for Horses, Sheep, Dogs, Murines, and Humans

Heimann,

Elashry,

Klymiuk

et al. 2023

Animals

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The investigation of adipose tissue-derived mesenchymal stem cells (ASCs) has received considerable interest in regenerative medicine. A nontoxic adipogenic induction protocol valid for cells of different mammalian species has not been described. This study aims to establish an adipogenic differentiation protocol suitable for horses, sheep, dogs, murines, and human cells. An optimized rosiglitazone protocol, consisting of 5% fetal calf serum in Dulbecco’s Modified Eagle’s Medium, 10 μg/mL insulin, 0.55 μg/mL transferrin, 6.8 ng sodium selenite, 1 μM dexamethasone, and 1–5 μM of rosiglitazone, is compared to the 3-isobutyl-1-methylxantine (IBMX) protocol, where rosiglitazone was replaced with 0.5 mM IBMX and 0.2 mM indomethacin. Cell viability, cytotoxicity, a morphometric analysis of the lipid, and the expression of adipogenic markers for 14 days were assessed. The data revealed that using 5 µM of rosiglitazone promotes the adipogenic differentiation capacity in horse, sheep, and dog cells compared to IBMX induction. Meanwhile, marked reductions in the cell viability and cell number with the IBMX protocol were detected, and rosiglitazone increased the cell number and lipid droplet size, prevented apoptosis, and upregulated FABP-4 and Leptin expression in the cells of most of the species. Our data revealed that the rosiglitazone protocol improves the adipogenesis of ASCs, together with having less toxicity, and should be considered for cell reproducibility and clinical applications targeting obesity.

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