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  1. Article ; Online: Are

    Xie, Zhuoer / Starczynowski, Daniel T

    Haematologica

    2023  Volume 108, Issue 11, Page(s) 2883–2885

    MeSH term(s) Humans ; Myelodysplastic Syndromes ; Germ-Line Mutation ; DEAD-box RNA Helicases/genetics
    Chemical Substances DDX41 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Language English
    Publishing date 2023-11-01
    Publishing country Italy
    Document type Editorial ; Comment
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2023.283416
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: HHEX expression drives AML development.

    Starczynowski, Daniel T

    Blood

    2020  Volume 136, Issue 14, Page(s) 1575–1576

    MeSH term(s) Homeodomain Proteins ; Humans ; Leukemia, Myeloid, Acute/genetics ; Repressor Proteins ; Transcription Factors
    Chemical Substances ASXL1 protein, human ; HHEX protein, human ; Homeodomain Proteins ; Repressor Proteins ; Transcription Factors
    Language English
    Publishing date 2020-10-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020007049
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  3. Article ; Online: Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS.

    Trowbridge, Jennifer J / Starczynowski, Daniel T

    The Journal of experimental medicine

    2021  Volume 218, Issue 7

    Abstract: With a growing aged population, there is an imminent need to develop new therapeutic strategies to ameliorate disorders of hematopoietic aging, including clonal hematopoiesis and myelodysplastic syndrome (MDS). Cell-intrinsic dysregulation of innate ... ...

    Abstract With a growing aged population, there is an imminent need to develop new therapeutic strategies to ameliorate disorders of hematopoietic aging, including clonal hematopoiesis and myelodysplastic syndrome (MDS). Cell-intrinsic dysregulation of innate immune- and inflammatory-related pathways as well as systemic inflammation have been implicated in hematopoietic defects associated with aging, clonal hematopoiesis, and MDS. Here, we review and discuss the role of dysregulated innate immune and inflammatory signaling that contribute to the competitive advantage and clonal dominance of preleukemic and MDS-derived hematopoietic cells. We also propose how emerging concepts will further reveal critical biology and novel therapeutic opportunities.
    MeSH term(s) Aging/immunology ; Animals ; Clonal Hematopoiesis/immunology ; Hematopoiesis/immunology ; Hematopoietic Stem Cells/immunology ; Humans ; Immunity, Innate/immunology ; Inflammation/immunology ; Myelodysplastic Syndromes/immunology ; Signal Transduction/immunology
    Language English
    Publishing date 2021-06-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20201544
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  4. Article ; Online: IRAK1 and IRAK4 as emerging therapeutic targets in hematologic malignancies.

    Bennett, Joshua / Starczynowski, Daniel T

    Current opinion in hematology

    2021  Volume 29, Issue 1, Page(s) 8–19

    Abstract: Purpose of review: Cell intrinsic and extrinsic perturbations to inflammatory signaling pathways are a hallmark of development and progression of hematologic malignancies. The interleukin 1 receptor-associated kinases (IRAKs) are a family of related ... ...

    Abstract Purpose of review: Cell intrinsic and extrinsic perturbations to inflammatory signaling pathways are a hallmark of development and progression of hematologic malignancies. The interleukin 1 receptor-associated kinases (IRAKs) are a family of related signaling intermediates (IRAK1, IRAK2, IRAK3, IRAK4) that operate at the nexus of multiple inflammatory pathways implicated in the hematologic malignancies. In this review, we explicate the oncogenic role of these kinases and review recent therapeutic advances in the dawning era of IRAK-targeted therapy.
    Recent findings: Emerging evidence places IRAK signaling at the confluence of adaptive resistance and oncogenesis in the hematologic malignancies and solid tissue tumors. Preclinical investigations nominate the IRAK kinases as targetable molecular dependencies in diverse cancers.
    Summary: IRAK-targeted therapies that have matriculated to early phase trials are yielding promising preliminary results. However, studies of IRAK kinase signaling continue to defy conventional signaling models and raise questions as to the design of optimal treatment strategies. Efforts to refine IRAK signaling mechanisms in the malignant context will inspire deliberate IRAK-targeted drug development and informed combination therapy.
    MeSH term(s) Hematologic Neoplasms/drug therapy ; Humans ; Interleukin-1 Receptor-Associated Kinases/genetics ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Signal Transduction
    Chemical Substances IRAK1 protein, human (EC 2.7.11.1) ; IRAK4 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-11-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000693
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  5. Article ; Online: IKAROS and MENIN in synergy in AML.

    Jones, LaQuita M / Starczynowski, Daniel T

    Nature cancer

    2022  Volume 3, Issue 5, Page(s) 528–529

    MeSH term(s) Humans ; Leukemia, Myeloid, Acute ; Transcription Factors
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2022-05-24
    Publishing country England
    Document type Journal Article ; Comment
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-022-00387-w
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  6. Article ; Online: In vivo ablation of NFκB cascade effectors alleviates disease burden in myeloproliferative neoplasms.

    Laranjeira, Angelo Brunelli Albertoni / Kong, Tim / Snyder, Steven C / Fulbright, Mary C / Fisher, Daniel A C / Starczynowski, Daniel T / Oh, Stephen T

    Blood

    2024  

    Abstract: Hyperactivation of the NFκB cascade propagates oncogenic signaling and pro-inflammation, which together augments disease burden in myeloproliferative neoplasms (MPNs). Here, we systematically ablate NFκB signaling effectors to identify core dependencies ... ...

    Abstract Hyperactivation of the NFκB cascade propagates oncogenic signaling and pro-inflammation, which together augments disease burden in myeloproliferative neoplasms (MPNs). Here, we systematically ablate NFκB signaling effectors to identify core dependencies using a series of primary samples and syngeneic and patient-derived xenograft (PDX) mouse models. Conditional knockout of Rela attenuated Jak2V617F and MPLW515L-driven onset of polycythemia vera and myelofibrosis disease hallmarks, respectively. In PDXs, RELA-knockout diminished leukemic engraftment and bone marrow fibrosis while extending survival. Knock-out of upstream effector Myd88 also alleviated disease burden; conversely, perturbation of negative regulator miR-146a microRNA induced earlier lethality and exacerbated disease. Perturbation of NFκB effectors further skewed the abundance and distribution of hematopoietic multipotent progenitors. Finally, pharmacological targeting of interleukin-1 receptor-associated kinase 4 (IRAK4) with inhibitor CA-4948 suppressed disease burden and inflammatory cytokines specifically in MPN without inducing toxicity in non-diseased models. These findings highlight vulnerabilities in MPN that are exploitable with emerging therapeutic approaches.
    Language English
    Publishing date 2024-03-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2023022804
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  7. Article ; Online: Errant innate immune signaling in del(5q) MDS.

    Starczynowski, Daniel T

    Blood

    2014  Volume 124, Issue 5, Page(s) 669–671

    Abstract: In this issue of Blood, Keerthivasan et al have identified that the deletion of mDia1, a chromosome 5q gene, contributes to myelodysplastic syndromes (MDSs) by increasing innate immune signaling in granulocytes. ...

    Abstract In this issue of Blood, Keerthivasan et al have identified that the deletion of mDia1, a chromosome 5q gene, contributes to myelodysplastic syndromes (MDSs) by increasing innate immune signaling in granulocytes.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Carrier Proteins/metabolism ; Chromosome Deletion ; Chromosomes, Human, Pair 5 ; Female ; Formins ; Gene Expression Regulation ; Granulocytes/metabolism ; Heterozygote ; Humans ; Immunity, Innate ; Lipopolysaccharide Receptors/biosynthesis ; Male ; Myelodysplastic Syndromes/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Carrier Proteins ; DIAPH1 protein, human ; Diap1 protein, mouse ; Formins ; Lipopolysaccharide Receptors
    Language English
    Publishing date 2014-07-31
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2014-06-581728
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  8. Article ; Online: TIFA and TIFAB: FHA-domain proteins involved in inflammation, hematopoiesis, and disease.

    Niederkorn, Madeline / Agarwal, Puneet / Starczynowski, Daniel T

    Experimental hematology

    2020  Volume 90, Page(s) 18–29

    Abstract: Forkhead-associated (FHA) domain-containing proteins are widely expressed across eubacteria and in eukaryotes. FHA domains contain phosphopeptide recognition motifs, which operate in a variety of phosphorylation-dependent and -independent biological ... ...

    Abstract Forkhead-associated (FHA) domain-containing proteins are widely expressed across eubacteria and in eukaryotes. FHA domains contain phosphopeptide recognition motifs, which operate in a variety of phosphorylation-dependent and -independent biological processes, including the DNA damage response, signal transduction, and regulation of the cell cycle. More recently, two FHA domain-containing proteins were discovered in mammalian cells as tumor necrosis factor receptor-associated factor (TRAF)-interacting proteins: TIFA and TIFAB. TIFA and TIFAB are important modifiers of the innate immune signaling through their regulation of TRAF proteins. Recent studies have also revealed distinct roles for TIFA and TIFAB in the context of immune cell function, chronic inflammation, hematopoiesis, and hematologic disorders. Collectively, these studies indicate the important role of TIFA- and TIFAB-dependent signaling in hematopoietic cells and their dysregulation in several human diseases. In this review, we summarize the molecular mechanisms and biological role of these FHA-domain homologues, placing them into the context of human disease.
    MeSH term(s) Adaptor Proteins, Signal Transducing/immunology ; Animals ; Hematologic Diseases/immunology ; Hematopoiesis/immunology ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Intracellular Signaling Peptides and Proteins/immunology ; Signal Transduction/immunology
    Chemical Substances Adaptor Proteins, Signal Transducing ; Intracellular Signaling Peptides and Proteins ; TIFA protein, human ; Tifab protein, human
    Language English
    Publishing date 2020-09-07
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 185107-x
    ISSN 1873-2399 ; 0531-5573 ; 0301-472X
    ISSN (online) 1873-2399
    ISSN 0531-5573 ; 0301-472X
    DOI 10.1016/j.exphem.2020.08.010
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  9. Article ; Online: GMP-ing to Spatial Conclusions about Emergency and Leukemic Myelopoiesis.

    Niederkorn, Madeline / Starczynowski, Daniel T

    Cell stem cell

    2017  Volume 20, Issue 5, Page(s) 579–581

    Abstract: Hematopoietic stem cells (HSCs) in the bone marrow (BM) form mature blood cells of all lineages through expansion of lineage-biased progenitors. In a recent issue of Nature, Hérault et al. (2017) uncover a unique spatiotemporal mechanism of granulocyte- ... ...

    Abstract Hematopoietic stem cells (HSCs) in the bone marrow (BM) form mature blood cells of all lineages through expansion of lineage-biased progenitors. In a recent issue of Nature, Hérault et al. (2017) uncover a unique spatiotemporal mechanism of granulocyte-macrophage progenitors (GMPs) employed in emergency hematopoiesis that is also hijacked in leukemia.
    Language English
    Publishing date 2017-05-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2017.04.005
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  10. Article ; Online: Nuclear deubiquitination in the spotlight: the multifaceted nature of USP7 biology in disease.

    Rawat, Radhika / Starczynowski, Daniel T / Ntziachristos, Panagiotis

    Current opinion in cell biology

    2019  Volume 58, Page(s) 85–94

    Abstract: Ubiquitination is a versatile and tightly regulated post-translational protein modification with many distinct outcomes affecting protein stability, localization, interactions, and activity. Ubiquitin chain linkages anchored on substrates can be further ... ...

    Abstract Ubiquitination is a versatile and tightly regulated post-translational protein modification with many distinct outcomes affecting protein stability, localization, interactions, and activity. Ubiquitin chain linkages anchored on substrates can be further modified by additional post-translational modifications, including phosphorylation and SUMOylation. Deubiquitinases (DUBs) reverse these ubiquitin marks with matched levels of precision. Over hundred known DUBs regulate a wide variety of cellular events. In this review, we focus on ubiquitin-specific protease 7 (USP7, also known as herpesvirus-associated ubiquitin-specific protease, or HAUSP) as one of the best studied, disease-associated DUBs. By highlighting the functions of USP7, particularly in the nucleus, and the emergence of the newest generation of USP7 inhibitors, we illustrate the importance of individual DUBs in the nucleus, and the therapeutic prospects of DUB targeting in human disease.
    MeSH term(s) Animals ; Apoptosis ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Phosphorylation ; Proteolysis ; Ubiquitin-Specific Peptidase 7/antagonists & inhibitors ; Ubiquitin-Specific Peptidase 7/metabolism ; Ubiquitination
    Chemical Substances USP7 protein, human (EC 3.4.19.12) ; Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12)
    Language English
    Publishing date 2019-03-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1026381-0
    ISSN 1879-0410 ; 0955-0674
    ISSN (online) 1879-0410
    ISSN 0955-0674
    DOI 10.1016/j.ceb.2019.02.008
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