DOI . ORG {
}
We began analyzing https://link.springer.com/article/10.1007/s00018-019-03084-7, but it redirected us to https://link.springer.com/article/10.1007/s00018-019-03084-7. The analysis below is for the second page.
Title[redir]:
The role of ASXL1 in hematopoiesis and myeloid malignancies | Cellular and Molecular Life Sciences
Description:
Recent high-throughput genome-wide sequencing studies have identified recurrent somatic mutations in myeloid neoplasms. An epigenetic regulator, Additional sex combs-like 1 (ASXL1), is one of the most frequently mutated genes in all subtypes of myeloid malignancies. ASXL1 mutations are also frequently detected in clonal hematopoiesis, which is associated with an increased risk of mortality. Therefore, it is important to understand how ASXL1 mutations contribute to clonal expansion and myeloid transformation in hematopoietic cells. Studies using ASXL1-depleted human hematopoietic cells and Asxl1 knockout mice have shown that deletion of wild-type ASXL1 protein leads to impaired hematopoiesis and accelerates myeloid malignancies via loss of interaction with polycomb repressive complex 2 proteins. On the other hand, ASXL1 mutations in myeloid neoplasms typically occur near the last exon and result in the expression of C-terminally truncated mutant ASXL1 protein. Biological studies and biochemical analyses of this variant have shed light on its dominant-negative and gain-of-function features in myeloid transformation via a variety of epigenetic changes. Based on these results, it would be possible to establish novel promising therapeutic strategies for myeloid malignancies harboring ASXL1 mutations by blocking interactions between ASXL1 and associating epigenetic regulators. Here, we summarize the clinical implications of ASXL1 mutations, the role of wild-type ASXL1 in normal hematopoiesis, and oncogenic functions of mutant ASXL1 in myeloid neoplasms.
Title[redir]:
The role of ASXL1 in hematopoiesis and myeloid malignancies | Cellular and Molecular Life Sciences
Description:
Recent high-throughput genome-wide sequencing studies have identified recurrent somatic mutations in myeloid neoplasms. An epigenetic regulator, Additional sex combs-like 1 (ASXL1), is one of the most frequently mutated genes in all subtypes of myeloid malignancies. ASXL1 mutations are also frequently detected in clonal hematopoiesis, which is associated with an increased risk of mortality. Therefore, it is important to understand how ASXL1 mutations contribute to clonal expansion and myeloid transformation in hematopoietic cells. Studies using ASXL1-depleted human hematopoietic cells and Asxl1 knockout mice have shown that deletion of wild-type ASXL1 protein leads to impaired hematopoiesis and accelerates myeloid malignancies via loss of interaction with polycomb repressive complex 2 proteins. On the other hand, ASXL1 mutations in myeloid neoplasms typically occur near the last exon and result in the expression of C-terminally truncated mutant ASXL1 protein. Biological studies and biochemical analyses of this variant have shed light on its dominant-negative and gain-of-function features in myeloid transformation via a variety of epigenetic changes. Based on these results, it would be possible to establish novel promising therapeutic strategies for myeloid malignancies harboring ASXL1 mutations by blocking interactions between ASXL1 and associating epigenetic regulators. Here, we summarize the clinical implications of ASXL1 mutations, the role of wild-type ASXL1 in normal hematopoiesis, and oncogenic functions of mutant ASXL1 in myeloid neoplasms.
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Keywords {🔍}
pubmed, article, google, scholar, cas, asxl, mutations, central, myeloid, leukemia, cell, hematopoiesis, blood, gene, acute, myelodysplastic, patients, clinical, chronic, tet, nat, malignancies, neoplasms, additional, clonal, syndromes, myelomonocytic, zhang, med, sex, prognostic, wang, inoue, bap, histone, leukaemia, cancer, genet, hematol, chen, research, role, somatic, loss, polycomb, mutation, engl, oncol, idh, genetic,
Topics {✒️}
month download article/chapter susumu goyama & toshio kitamura acute myeloid leukaemia malignant myeloid diseases vega-rubin-de-celis chronic myelomonocytic leukaemia prc2-mediated gene repression /runx1-runx1t1 chromosomal translocations full article pdf age-related clonal hematopoiesis micol jb hox gene silencing e2f1-responsive gene expression accelerate myeloid malignancy mast-cell diseases abdel-wahab therapy-related clonal hematopoiesis blast-phase myeloproliferative neoplasms blood-cancer risk inferred exome sequencing reveals bohring-opitz syndrome acute myeloid leukemia post-polycythemia vera myelofibrosis drosophila hox genes myelodysplastic syndrome patients acute myeloid leukemias promote myeloid leukaemogenesis article asada mds/mpn aid scientific research asxl1-mutated mds privacy choices/manage cookies accelerates myeloid malignancies high-risk group lin cc malignant pleural mesothelioma wild-type asxl1 asxl1 truncating protein chronic myelomonocytic leukemia asxl1–bap1 complex nuclear deubiquitinase bap1 additional sex combs additional sex combs chronic myelogenous leukemia bmc cancer 10 detectable protein levels advanced systemic mastocytosis article cellular tumor suppressor bap1 myelodysplastic syndrome
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headline:The role of ASXL1 in hematopoiesis and myeloid malignancies
description:Recent high-throughput genome-wide sequencing studies have identified recurrent somatic mutations in myeloid neoplasms. An epigenetic regulator, Additional sex combs-like 1 (ASXL1), is one of the most frequently mutated genes in all subtypes of myeloid malignancies. ASXL1 mutations are also frequently detected in clonal hematopoiesis, which is associated with an increased risk of mortality. Therefore, it is important to understand how ASXL1 mutations contribute to clonal expansion and myeloid transformation in hematopoietic cells. Studies using ASXL1-depleted human hematopoietic cells and Asxl1 knockout mice have shown that deletion of wild-type ASXL1 protein leads to impaired hematopoiesis and accelerates myeloid malignancies via loss of interaction with polycomb repressive complex 2 proteins. On the other hand, ASXL1 mutations in myeloid neoplasms typically occur near the last exon and result in the expression of C-terminally truncated mutant ASXL1 protein. Biological studies and biochemical analyses of this variant have shed light on its dominant-negative and gain-of-function features in myeloid transformation via a variety of epigenetic changes. Based on these results, it would be possible to establish novel promising therapeutic strategies for myeloid malignancies harboring ASXL1 mutations by blocking interactions between ASXL1 and associating epigenetic regulators. Here, we summarize the clinical implications of ASXL1 mutations, the role of wild-type ASXL1 in normal hematopoiesis, and oncogenic functions of mutant ASXL1 in myeloid neoplasms.
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headline:The role of ASXL1 in hematopoiesis and myeloid malignancies
description:Recent high-throughput genome-wide sequencing studies have identified recurrent somatic mutations in myeloid neoplasms. An epigenetic regulator, Additional sex combs-like 1 (ASXL1), is one of the most frequently mutated genes in all subtypes of myeloid malignancies. ASXL1 mutations are also frequently detected in clonal hematopoiesis, which is associated with an increased risk of mortality. Therefore, it is important to understand how ASXL1 mutations contribute to clonal expansion and myeloid transformation in hematopoietic cells. Studies using ASXL1-depleted human hematopoietic cells and Asxl1 knockout mice have shown that deletion of wild-type ASXL1 protein leads to impaired hematopoiesis and accelerates myeloid malignancies via loss of interaction with polycomb repressive complex 2 proteins. On the other hand, ASXL1 mutations in myeloid neoplasms typically occur near the last exon and result in the expression of C-terminally truncated mutant ASXL1 protein. Biological studies and biochemical analyses of this variant have shed light on its dominant-negative and gain-of-function features in myeloid transformation via a variety of epigenetic changes. Based on these results, it would be possible to establish novel promising therapeutic strategies for myeloid malignancies harboring ASXL1 mutations by blocking interactions between ASXL1 and associating epigenetic regulators. Here, we summarize the clinical implications of ASXL1 mutations, the role of wild-type ASXL1 in normal hematopoiesis, and oncogenic functions of mutant ASXL1 in myeloid neoplasms.
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