Evidently, overexpression of naturally occurring cytokine receptor alternate isoforms are observed in multiple myeloid diseases such as myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), and polycythemia vera (PV).
Evidently, overexpression of naturally occurring cytokine receptor alternate isoforms are observed in multiple myeloid diseases such as myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), and polycythemia vera (PV).
Our meta-analysis suggested that SF3B1 has no impact on OS of patients with MDS, however, an adequately designed prospective study with a large number of patients with different type of SF3B1 mutations is needed to confirm these results.
We observed significantly diminished expression of AKAP12 in MDS samples. miR-144 directly bound to AKAP12 3'UTR and reduced its expression in hematopoietic cells.
We observed significantly diminished expression of AKAP12 in MDS samples. miR-144 directly bound to AKAP12 3'UTR and reduced its expression in hematopoietic cells.
GATA2 and RUNX1 deficiency is not associated with host susceptibility to DNA damage, and therefore, conventional treatment strategies for MDS and AML can be used.
RUNX1 deficiency has a highly variable phenotype, and MDS can occur in childhood and later in adulthood within the same families, making annual surveillance with marrow examination burdensome; however, such strategies should be discussed with affected persons, allowing an informed choice.
Correction to: The prognostic value of serum erythropoietin in patients with lower-risk myelodysplastic syndromes: a review of the literature and expert opinion.
Internal Next Generation Sequencing (NGS) database with targeted genetic profiling of >4000 tumor cases was queried to locate cases of MDS with BCL6 Corepressor protein (<i>BCOR</i>) mutations only (pBCOR) and cBCOR (comutated epigenetic modulators: <i>TET2</i>, <i>ASXL1</i>, <i>DNMT3A</i>, <i>EZH2</i>, <i>IDH2</i>, <i>IDH1</i>, <i>BCORL1</i>, <i>ATRX</i>).
The detection of SF mutations demonstrates the importance of splicing abnormalities in the hematopoiesis of MDS and AML patients given the fact that abnormal splicing regulates the function of several transcriptional factors (<i>PU.1, RUNX1,</i> etc.) crucial in hematopoietic function.
These suggested that MDSCs might be the donor of Gal-9, and TIM3/Gal-9 pathway might be involved in CD8<sup>+</sup> T cells exhaustion in MDS, and that TIM3/Gal-9 pathway inhibitor might be the promising candidate for target therapy of MDS in the future.
Expression of Notch1, EOMES (associated with perforin and granzyme B secretion), p-mTOR and p-AKT (associated with cell proliferation) was decreased in CD8<sup>+</sup> T cells from MDS after co-culture with excess exogenous Gal-9.
Expression of Notch1, EOMES (associated with perforin and granzyme B secretion), p-mTOR and p-AKT (associated with cell proliferation) was decreased in CD8<sup>+</sup> T cells from MDS after co-culture with excess exogenous Gal-9.
Expression of Notch1, EOMES (associated with perforin and granzyme B secretion), p-mTOR and p-AKT (associated with cell proliferation) was decreased in CD8<sup>+</sup> T cells from MDS after co-culture with excess exogenous Gal-9.
Expression of Notch1, EOMES (associated with perforin and granzyme B secretion), p-mTOR and p-AKT (associated with cell proliferation) was decreased in CD8<sup>+</sup> T cells from MDS after co-culture with excess exogenous Gal-9.
Expression of Notch1, EOMES (associated with perforin and granzyme B secretion), p-mTOR and p-AKT (associated with cell proliferation) was decreased in CD8<sup>+</sup> T cells from MDS after co-culture with excess exogenous Gal-9.