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  • 1
    Online Resource
    Online Resource
    Targeting UHRF1-SAP30-MXD4 axis for leukemia initiating cell eradication in myeloid leukemia
    Springer Science and Business Media LLC ; 2022
    In:  Cell Research Vol. 32, No. 12 ( 2022-10-27), p. 1105-1123
    Details
    In: Cell Research, Springer Science and Business Media LLC, Vol. 32, No. 12 ( 2022-10-27), p. 1105-1123
    Abstract: Aberrant self-renewal of leukemia initiation cells (LICs) drives aggressive acute myeloid leukemia (AML). Here, we report that UHRF1, an epigenetic regulator that recruits DNMT1 to methylate DNA, is highly expressed in AML and predicts poor prognosis. UHRF1 is required for myeloid leukemogenesis by maintaining self-renewal of LICs. Mechanistically, UHRF1 directly interacts with Sin3A-associated protein 30 (SAP30) through two critical amino acids, G572 and F573 in its SRA domain, to repress gene expression. Depletion of UHRF1 or SAP30 derepresses an important target gene, MXD4 , which encodes a MYC antagonist, and leads to suppression of leukemogenesis. Further knockdown of MXD4 can rescue the leukemogenesis by activating the MYC pathway. Lastly, we identified a UHRF1 inhibitor, UF146, and demonstrated its significant therapeutic efficacy in the myeloid leukemia PDX model. Taken together, our study reveals the mechanisms for altered epigenetic programs in AML and provides a promising targeted therapeutic strategy against AML.
    Type of Medium: Online Resource
    ISSN: 1748-7838
    URL: Article
    DOI: 10.1038/s41422-022-00735-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2082402-6
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  • 2
    Online Resource
    Online Resource
    The non-cell-autonomous function of ID1 promotes AML progression via ANGPTL7 from the microenvironment
    American Society of Hematology ; 2023
    In:  Blood Vol. 142, No. 10 ( 2023-09-07), p. 903-917
    Details
    In: Blood, American Society of Hematology, Vol. 142, No. 10 ( 2023-09-07), p. 903-917
    Abstract: The bone marrow microenvironment (BMM) can regulate leukemia stem cells (LSCs) via secreted factors. Increasing evidence suggests that dissecting the mechanisms by which the BMM maintains LSCs may lead to the development of effective therapies for the eradication of leukemia. Inhibitor of DNA binding 1 (ID1), a key transcriptional regulator in LSCs, previously identified by us, controls cytokine production in the BMM, but the role of ID1 in acute myeloid leukemia (AML) BMM remains obscure. Here, we report that ID1 is highly expressed in the BMM of patients with AML, especially in BM mesenchymal stem cells, and that the high expression of ID1 in the AML BMM is induced by BMP6, secreted from AML cells. Knocking out ID1 in mesenchymal cells significantly suppresses the proliferation of cocultured AML cells. Loss of Id1 in the BMM results in impaired AML progression in AML mouse models. Mechanistically, we found that Id1 deficiency significantly reduces SP1 protein levels in mesenchymal cells cocultured with AML cells. Using ID1-interactome analysis, we found that ID1 interacts with RNF4, an E3 ubiquitin ligase, and causes a decrease in SP1 ubiquitination. Disrupting the ID1-RNF4 interaction via truncation in mesenchymal cells significantly reduces SP1 protein levels and delays AML cell proliferation. We identify that the target of Sp1, Angptl7, is the primary differentially expression protein factor in Id1-deficient BM supernatant fluid to regulate AML progression in mice. Our study highlights the critical role of ID1 in the AML BMM and aids the development of therapeutic strategies for AML.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.2022019537
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2023
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
    Online Resource
    Online Resource
    Genomic landscape of CD34 + hematopoietic cells in myelodysplastic syndrome and gene mutation profiles as prognostic markers
    Proceedings of the National Academy of Sciences ; 2014
    In:  Proceedings of the National Academy of Sciences Vol. 111, No. 23 ( 2014-06-10), p. 8589-8594
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 111, No. 23 ( 2014-06-10), p. 8589-8594
    Abstract: Myelodysplastic syndrome (MDS) includes a group of diseases characterized by dysplasia of bone marrow myeloid lineages with ineffective hematopoiesis and frequent evolution to acute myeloid leukemia (AML). Whole-genome sequencing was performed in CD34 + hematopoietic stem/progenitor cells (HSPCs) from eight cases of refractory anemia with excess blasts (RAEB), the high-risk subtype of MDS. The nucleotide substitution patterns were found similar to those reported in AML, and mutations of 96 protein-coding genes were identified. Clonal architecture analysis revealed the presence of subclones in six of eight cases, whereas mutation detection of CD34 + versus CD34 − cells revealed heterogeneity of HSPC expansion status. With 39 marker genes belonging to eight functional categories, mutations were analyzed in 196 MDS cases including mostly RAEB ( n = 89) and refractory cytopenia with multilineage dysplasia (RCMD) ( n = 95). At least one gene mutation was detected in 91.0% of RAEB, contrary to that in RCMD (55.8%), suggesting a higher mutational burden in the former group. Gene abnormality patterns differed between MDS and AML, with mutations of activated signaling molecules and NPM1 being rare, whereas those of spliceosome more common, in MDS. Finally, gene mutation profiles also bore prognostic value in terms of overall survival and progression free survival.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1407688111
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2014
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Direct-Mapping-Based MIMO-FBMC Underwater Acoustic Communication Architecture for Multimedia Signals
    MDPI AG ; 2019
    In:  Applied Sciences Vol. 10, No. 1 ( 2019-12-27), p. 233-
    Details
    In: Applied Sciences, MDPI AG, Vol. 10, No. 1 ( 2019-12-27), p. 233-
    Abstract: In this paper, a direct-mapping (DM)-based multi-input multi-output (MIMO) filter bank multi-carrier (FBMC) underwater acoustic multimedia communication architecture (UAMCA) is proposed. The proposed DM-based MIMO-FBMC UAMCA is rare and non-obvious in the underwater multimedia communication research topic. The following are integrated into the proposed UAMCA: A 2 × 2 DM transmission mechanism, a (2000, 1000) low-density parity-check code encoder, a power assignment mechanism, an object-composition petrinet mechanism, adaptive binary phase shift keying modulation and 4-offset quadrature amplitude modulation methods. The multimedia signals include voice, image, and data. The DM transmission mechanism in different spatial hardware devices transmits different multimedia packets. The proposed underwater multimedia transmission power allocation algorithm (UMTPAA) is simple, fast, and easy to implement, and the threshold transmission bit error rates (BERs) and real-time requirements for voice, image, and data signals can be achieved using the proposed UMTPAA. The BERs of the multimedia signals, data symbol error rates of the data signals, power saving ratios of the voice, image and data signals, mean square errors of the voice signals, and peak signal-to-noise ratios of the image signals, for the proposed UAMCA with a perfect channel estimation, and channel estimation errors of 5%, 10%, and 20%, respectively, were explored and demonstrated. Simulation results demonstrate that the proposed 2 × 2 DM-based MIMO-FBMC UAMCA is suitable for low power and high speed underwater multimedia sensor networks.
    Type of Medium: Online Resource
    ISSN: 2076-3417
    URL: Article
    DOI: 10.3390/app10010233
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2704225-X
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  • 5
    Online Resource
    Online Resource
    Synthesis and characterization of pyridine-containing poly(imide-siloxane)s and their adhesion to copper foil
    Wiley ; 2007
    In:  Journal of Applied Polymer Science Vol. 104, No. 4 ( 2007-05-15), p. 2561-2568
    Details
    In: Journal of Applied Polymer Science, Wiley, Vol. 104, No. 4 ( 2007-05-15), p. 2561-2568
    Type of Medium: Online Resource
    ISSN: 0021-8995 , 1097-4628
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.1002/app.v104:4
    DOI: 10.1002/(ISSN)1097-4628
    DOI: 10.1002/app.24719
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 1491105-X
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  • 6
    Online Resource
    Online Resource
    MYCN contributes to the malignant characteristics of erythroleukemia through EZH2-mediated epigenetic repression of p21
    Springer Science and Business Media LLC ; 2017
    In:  Cell Death & Disease Vol. 8, No. 10 ( 2017-10-12), p. e3126-e3126
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 8, No. 10 ( 2017-10-12), p. e3126-e3126
    Abstract: MYC proto-oncogene family including c-myc and n-myc (MYCN) are critical for normal cell development and tumorigenesis. Overexpression of c-myc causes acute erythroleukemia in vivo . However, the role of MYCN in acute erythroleukemia remains poorly understood. In this study, we found that the patients with erythroleukemia showed higher expression of MYCN than normal controls. In vitro experiments, knockdown of MYCN resulted in decreased cell proliferation, elevated autonomously cell apoptosis and increased P21-mediated cell senescence. On the contrary, overexpression of MYCN obviously promoted cell proliferation, and induced erythroid differentiation block and apoptosis resistance to cytotoxic agent. Further gene microarray and functional analysis revealed that EZH2 is a target of MYCN. Knockdown of MYCN inhibited the expression of EZH2, and then activated p21 expression through removal of H3K27me3 at the p21 promoter. Overexpression of ezh2 could antagonize the p21 activation caused by MYCN knockdown. In addition, Aurora inhibitor MLN8237 inhibited the proliferation of erythroleukemia cells through repression of MYCN/EZH2 axis, whereas it minimally affected the normal hematopoietic cells. In conclusion, MYCN contributes to the malignant characteristics of erythroleukemia through EZH2-meidated epigenetic repression of p21. MYCN may serve as a therapy target for the patients with acute erythroleukemia.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/cddis.2017.526
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2541626-1
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  • 7
    Online Resource
    Online Resource
    The use of carbon monoxide breath test to detect the effect of iron overload on erythrocyte lifespan in MDS
    Frontiers Media SA ; 2022
    In:  Frontiers in Oncology Vol. 12 ( 2022-11-29)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 12 ( 2022-11-29)
    Abstract: To investigate the effect of iron overload (IO) on red blood cell (RBC) lifespan in MDS patients with the use of carbon monoxide breath test Methods The red blood cell lifespan of 93 patients with myelodysplastic syndrome (MDS) and 22 healthy volunteers in the control group were measured by alveolar gas carbon monoxide (CO) assay, with the detection of liver iron concentration, iron metabolism index, erythropoietin (EPO) concentration, peripheral blood inflammatory cytokines, etc. The MDS patients were divided into the severe IO group, mild IO group and non IO group according to liver iron concentration. The effect of IO on RBC lifespan was analyzed in MDS patients. Results The RBC lifespan of MDS patients in the severe IO group was significantly lower than that in the mild IO group (p & lt;0.05), while the RBC life span in the mild IO group was significantly lower than that in the non IO group (p & lt;0.05). The expression of inflammatory cytokines in the severe IO group was significantly higher than that of the mild and non IO groups. After receiving iron removal treatment(ICT), the expression of inflammatory cytokines was decreased significantly, and the RBC lifespan was significantly prolonged (p & lt;0.05).Besides, liver iron concentration was significantly positively correlated with EPO concentration, while EPO concentration was significantly negatively correlated with RBC lifespan, especially in the MDS-RS subgroup. The RBC lifespan in the EPO & gt;1000 group was significantly lower than that in the EPO & lt;1000 group. Conclusion IO can shorten RBC lifespan in MDS patients, which may be result from the increase of endogenous EPO and the over-expression of inflammatory cytokines. After ICT, the ineffective hematopoiesis caused by increased EPO may reduced and the decrease of inflammatory cytokine may significantly prolong the RBC lifespan in MDS patients.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    DOI: 10.3389/fonc.2022.1058482
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2649216-7
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  • 8
    Online Resource
    Online Resource
    Primary lymphoma of bone: a case report and review of the literature
    Springer Science and Business Media LLC ; 2011
    In:  Medical Oncology Vol. 28, No. 1 ( 2011-03), p. 202-206
    Details
    In: Medical Oncology, Springer Science and Business Media LLC, Vol. 28, No. 1 ( 2011-03), p. 202-206
    Type of Medium: Online Resource
    ISSN: 1357-0560 , 1559-131X
    URL: Article
    DOI: 10.1007/s12032-009-9405-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 1201189-7
    detail.hit.zdb_id: 605563-1
    detail.hit.zdb_id: 2008172-8
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  • 9
    Online Resource
    Online Resource
    Rigosertib as a selective anti-tumor agent can ameliorate multiple dysregulated signaling transduction pathways in high-grade myelodysplastic syndrome
    Springer Science and Business Media LLC ; 2014
    In:  Scientific Reports Vol. 4, No. 1 ( 2014-12-04)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 4, No. 1 ( 2014-12-04)
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep07310
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2014
    detail.hit.zdb_id: 2615211-3
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  • 10
    Online Resource
    Online Resource
    Table_2.xlsx
    Frontiers Media SA ; 2021
    In:  Frontiers in Oncology Vol. 10 ( 2021-1-13)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 10 ( 2021-1-13)
    Abstract: Despite the improvements in prognostication of the revised International Prognostic Scoring System (IPSS-R) in myelodysplastic syndrome (MDS), there remain a portion of patients with lower risk (low/intermediate risk, LR) but poor prognostics. This study aimed to evaluate the relative contribution of mutational status when added to the IPSS-R, for estimating overall survival (OS) and progression-free survival (PFS) in patients with LR-MDS. We retrospectively analyzed clinical and laboratory variables of 328 patients diagnosed with MDS according to the FAB criteria. Twenty-nine-gene NGS assay was applied to bone marrow samples obtained at diagnosis. 233 (71.04%) patients were classified as LR-MDS. Univariate analysis showed association between inferior outcome (OS and PFS) and presence of JAK2 (p = 0.0177, p = 0.0002), RUNX1 (p = 0.0250, p = 0.0387), and U2AF1 (p = 0.0227, p = 0.7995) mutations. Multivariable survival analysis revealed JAK2 (p & lt; 0.0001) and RUNX1 (p = 0.0215) mutations were independently prognostic for PFS in LR-MDS. Interestingly, bone marrow blast & gt;1.5% could further predict disease progression of patients with LR-MDS (HR 8.06, 95%CI 2.95–22.04, p & lt; 0.0001). Incorporation of JAK2 , RUNX1 mutation and bone marrow blast in the IPSS-R can improve risk stratification in patients with LR-MDS. In summary, our result provided new risk factors for LR-MDS prognostics to identify candidates for early therapeutic intervention.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2020.610525
    DOI: 10.3389/fonc.2020.610525.s001
    DOI: 10.3389/fonc.2020.610525.s002
    DOI: 10.3389/fonc.2020.610525.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2649216-7
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