Origins of myelodysplastic syndromes after aplastic anemia

Negoro, Eiju; Nagata, Yasunobu; Clemente, Michael J.; Hosono, Naoko; Shen, Wenyi; Nazha, Aziz; Yoshizato, Tetsuichi; Hirsch, Cassandra M.; Przychodzen, Bartlomiej; Mahfouz, R.; Kuzmanovic, Teodora; Sekeres, Mikkael A.; Makishima, Hideki; Ogawa, Seishi; Maciejewski, Jaroslaw P.

doi:10.1182/blood-2017-02-767731

Cited by 53 publications

(35 citation statements)

References 12 publications

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“…After 14 weeks, the human original hematopoietic cells in mice could be checked only with ASXL1 mutations, which were then deduced as the initial mutations that lead to MDS development. In general, initial mutations were considered the founder factors that emerged before the clinical phenotypes of MDS 10,13,14 . Typical MDS symptoms appeared over time or upon the introduction of new driver gene mutations.…”

Section: Discussionmentioning

confidence: 99%

A genetic development route analysis on MDS subset carrying initial epigenetic gene mutations

Xiao

et al. 2020

Sci Rep

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Section: Discussionmentioning

confidence: 99%

A genetic development route analysis on MDS subset carrying initial epigenetic gene mutations

Xiao

et al. 2020

Sci Rep

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“…[28][29][30][31] So far, few genetic studies have focused on h-MDS, without firm conclusion. [32][33][34][35] In a recent study on patients with unexplained cytopenia, including MDS and AA, we found that mutation profiling has a high predictive value for identifying individuals with a myeloid neoplasm. [36] In particular, selected mutation patterns were proven highly specific for myeloid neoplasms with myelodysplasia, which may possibly identify bona fide MDS even in the absence of definitive morphological features, as previously acknowledged for selected cytogenetic abnormalities.…”

Section: Introductionmentioning

confidence: 87%

Clinical, histopathological and molecular characterization of hypoplastic myelodysplastic syndrome

et al. 2019

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Diagnostic criteria for hypoplastic myelodysplasic syndrome (h-MDS) have not been clearly established, making the differential diagnosis from other bone marrow failure syndromes (BMF) challenging. In this study, we aimed to delineate clinical, histopathological, and molecular features of h-MDS, based on a large and well-annotated cohort of patients with bone marrow (BM) hypocellularity. The study included 534 consecutive adult patients with hypocellular BM (278 h-MDS and 136 aplastic anemia), and 727 with normo-or hypercellular MDS (n-MDS). Comparison of clinical features of patients with h-MDS as defined by BM cellularity ≤25% (n = 204) or reduced age-adjusted cellularity (n = 74) did not reveal significant differences. We developed a diagnostic score to discriminate h-MDS from non-malignant BMF based on histological and cytological variables with the highest specificity for MDS (h-score). The information from chromosomal abnormalities and somatic mutation patterns was then integrated into a cyto-histological/genetic score (hg-score). This score was able to segregate two groups of h-MDS with a significantly different risk of blast progression (P < 0.001). The integration of cyto-histological and genetic features in adult patients with hypocellular BM facilitated segregation into two distinct groups, one with clinical and genetic features highly consistent with myeloid neoplasm, and one with features more consistent with non-malignant BMF.

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“…A better understanding of the relationship between the HSCs/LICs and their microenvironment is a key to understand the natural history of myeloid neoplasia. Even though AA is a BM failure and not a myeloid malignancy, complication in AA can lead to secondary MDS or AML [ 149 ]. Thus, evaluating qualitatively and quantitatively the composition of the bone marrow stroma during the evolution of AA to MDS and AML and dissecting the differences at different malignant stages will be highly valuable to shed light into the specific role of certain microenvironment factors in myeloid malignancies and should help adapt therapeutics treatment targeting specifically the specific cross-talk between the malignant cells and their niche [ 150 ].…”

Section: Discussionmentioning

confidence: 99%

Role of the microenvironment in myeloid malignancies

Goulard

Dosquet

Bonnet

2017

Cell. Mol. Life Sci.

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The bone marrow microenvironment (BMM) regulates the fate of hematopoietic stem cells (HSCs) in homeostatic and pathologic conditions. In myeloid malignancies, new insights into the role of the BMM and its cellular and molecular actors in the progression of the diseases have started to emerge. In this review, we will focus on describing the major players of the HSC niche and the role of the altered niche function in myeloid malignancies, more specifically focusing on the mesenchymal stroma cell compartment.

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Origins of myelodysplastic syndromes after aplastic anemia

Cited by 53 publications

References 12 publications

A genetic development route analysis on MDS subset carrying initial epigenetic gene mutations

A genetic development route analysis on MDS subset carrying initial epigenetic gene mutations

Clinical, histopathological and molecular characterization of hypoplastic myelodysplastic syndrome

Role of the microenvironment in myeloid malignancies

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