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  1. AU="Cotton, Anitria"
  2. AU="Bayer, Adrian E."
  3. AU="Boerke, A"
  4. AU="Brown, Guy C."
  5. AU=Ford Caleb A.
  6. AU="Hussain, Muhammad Afaq"
  7. AU="Werner Henkel"
  8. AU=Zellweger M J
  9. AU="Marasco, Michelangelo"
  10. AU="Landa-Moreno, Cinthia"
  11. AU="Kuntner, Matjaz"
  12. AU="Lemes, Robertha Mariana Rodrigues"
  13. AU="Riccioni, M E"
  14. AU="Traer, Colin J"
  15. AU="Cao, Xuejie"
  16. AU="Chen, Zishuo"
  17. AU="Kalachikov, Sergey"
  18. AU="Das, Tilak"
  19. AU="Bessat, Cécile"
  20. AU="Galina Velikova"
  21. AU="Greene, Sharrell"
  22. AU="Chen, Kallie J"
  23. AU="Schwab, Jörg O."
  24. AU="Ke Chen"
  25. AU="Hewei Liang"
  26. AU="Abreu, Cristina"
  27. AU="Mamani Ortiz, Yercin"
  28. AU="Castro, Lucíola de Fátima Albuquerque Almeida Peixoto"
  29. AU="Šimůnek, Tomáš"
  30. AU="Ong, Lizhen"
  31. AU="Chai, Chaoqing"
  32. AU="Maheswaran Kesavan"
  33. AU="Mehta, Mrunal"
  34. AU=Paredes Sergio D
  35. AU=Ghosh Nilanjan AU=Ghosh Nilanjan
  36. AU="Hofmann, Alexander"
  37. AU="Radici, Marco"
  38. AU="Noro, Fabrizia"
  39. AU="Wang, Jianzhao"
  40. AU="Divya Jeyam"
  41. AU="Wolf, Lisette"
  42. AU="Marjanovic, Nemanja Despot"
  43. AU="Jitxin, Lim"

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  1. Artikel ; Online: CBFA2T3-GLIS2-dependent pediatric acute megakaryoblastic leukemia is driven by GLIS2 and sensitive to navitoclax.

    Neault, Mathieu / Lebert-Ghali, Charles-Étienne / Fournier, Marilaine / Capdevielle, Caroline / Garfinkle, Elizabeth A R / Obermayer, Alyssa / Cotton, Anitria / Boulay, Karine / Sawchyn, Christina / St-Amand, Sarah / Nguyen, Kamy H / Assaf, Béatrice / Mercier, François E / Delisle, Jean-Sébastien / Drobetsky, Elliot A / Hulea, Laura / Shaw, Timothy I / Zuber, Johannes / Gruber, Tanja A /
    Melichar, Heather J / Mallette, Frédérick A

    Cell reports

    2023  Band 42, Heft 9, Seite(n) 113084

    Abstract: Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. Here we describe the development of CBFA2T3-GLIS2-driven mouse models of AMKL that recapitulate the phenotypic ... ...

    Abstract Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. Here we describe the development of CBFA2T3-GLIS2-driven mouse models of AMKL that recapitulate the phenotypic and transcriptional signatures of the human disease. We show that an activating Ras mutation that occurs in human AMKL increases the penetrance and decreases the latency of CBF2AT3-GLIS2-driven AMKL. CBFA2T3-GLIS2 and GLIS2 modulate similar transcriptional networks. We identify the dominant oncogenic properties of GLIS2 that trigger AMKL in cooperation with oncogenic Ras. We find that both CBFA2T3-GLIS2 and GLIS2 alter the expression of a number of BH3-only proteins, causing AMKL cell sensitivity to the BCL2 inhibitor navitoclax both in vitro and in vivo, suggesting a potential therapeutic option for pediatric patients suffering from CBFA2T3-GLIS2-driven AMKL.
    Mesh-Begriff(e) Animals ; Mice ; Child ; Humans ; Leukemia, Megakaryoblastic, Acute/drug therapy ; Leukemia, Megakaryoblastic, Acute/genetics ; Aniline Compounds ; Sulfonamides ; Oncogene Proteins, Fusion/metabolism ; Repressor Proteins
    Chemische Substanzen navitoclax (XKJ5VVK2WD) ; Aniline Compounds ; Sulfonamides ; Oncogene Proteins, Fusion ; CBFA2T3 protein, human ; Repressor Proteins ; CBFA2T3-GLIS2 fusion protein, human
    Sprache Englisch
    Erscheinungsdatum 2023-09-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.113084
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: IL-13/IL-4 signaling contributes to fibrotic progression of the myeloproliferative neoplasms.

    Melo-Cardenas, Johanna / Bezavada, Lavanya / Crawford, Jeremy Chase / Gurbuxani, Sandeep / Cotton, Anitria / Kang, Guolian / Gossett, Jeffrey / Marinaccio, Christian / Weinberg, Rona / Hoffman, Ronald / Migliaccio, Anna Rita / Zheng, Yan / Derecka, Marta / Rinaldi, Ciro R / Crispino, John D

    Blood

    2022  Band 140, Heft 26, Seite(n) 2805–2817

    Abstract: Myelofibrosis (MF) is a disease associated with high unmet medical needs because allogeneic stem cell transplantation is not an option for most patients, and JAK inhibitors are generally effective for only 2 to 3 years and do not delay disease ... ...

    Abstract Myelofibrosis (MF) is a disease associated with high unmet medical needs because allogeneic stem cell transplantation is not an option for most patients, and JAK inhibitors are generally effective for only 2 to 3 years and do not delay disease progression. MF is characterized by dysplastic megakaryocytic hyperplasia and progression to fulminant disease, which is associated with progressively increasing marrow fibrosis. Despite evidence that the inflammatory milieu in MF contributes to disease progression, the specific factors that promote megakaryocyte growth are poorly understood. Here, we analyzed changes in the cytokine profiles of MF mouse models before and after the development of fibrosis, coupled with the analysis of bone marrow populations using single-cell RNA sequencing. We found high interleukin 13 (IL-13) levels in the bone marrow of MF mice. IL-13 promoted the growth of mutant megakaryocytes and induced surface expression of transforming growth factor β and collagen biosynthesis. Similarly, analysis of samples from patients with MF revealed elevated levels of IL-13 in the plasma and increased IL-13 receptor expression in marrow megakaryocytes. In vivo, IL-13 overexpression promoted disease progression, whereas reducing IL-13/IL-4 signaling reduced several features of the disease, including fibrosis. Finally, we observed an increase in the number of marrow T cells and mast cells, which are known sources of IL-13. Together, our data demonstrate that IL-13 is involved in disease progression in MF and that inhibition of the IL-13/IL-4 signaling pathway might serve as a novel therapeutic target to treat MF.
    Mesh-Begriff(e) Mice ; Animals ; Interleukin-13/therapeutic use ; Interleukin-4 ; Neoplasms/complications ; Myeloproliferative Disorders/complications ; Primary Myelofibrosis/genetics ; Signal Transduction/genetics ; Fibrosis ; Disease Progression
    Chemische Substanzen Interleukin-13 ; Interleukin-4 (207137-56-2)
    Sprache Englisch
    Erscheinungsdatum 2022-11-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022017326
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Proteasome inhibition targets the KMT2A transcriptional complex in acute lymphoblastic leukemia.

    Kamens, Jennifer L / Nance, Stephanie / Koss, Cary / Xu, Beisi / Cotton, Anitria / Lam, Jeannie W / Garfinkle, Elizabeth A R / Nallagatla, Pratima / Smith, Amelia M R / Mitchell, Sharnise / Ma, Jing / Currier, Duane / Wright, William C / Kavdia, Kanisha / Pagala, Vishwajeeth R / Kim, Wonil / Wallace, LaShanale M / Cho, Ji-Hoon / Fan, Yiping /
    Seth, Aman / Twarog, Nathaniel / Choi, John K / Obeng, Esther A / Hatley, Mark E / Metzger, Monika L / Inaba, Hiroto / Jeha, Sima / Rubnitz, Jeffrey E / Peng, Junmin / Chen, Taosheng / Shelat, Anang A / Guy, R Kiplin / Gruber, Tanja A

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 809

    Abstract: Rearrangments in Histone-lysine-N-methyltransferase 2A (KMT2Ar) are associated with pediatric, adult and therapy-induced acute leukemias. Infants with KMT2Ar acute lymphoblastic leukemia (ALL) have a poor prognosis with an event-free-survival of 38%. ... ...

    Abstract Rearrangments in Histone-lysine-N-methyltransferase 2A (KMT2Ar) are associated with pediatric, adult and therapy-induced acute leukemias. Infants with KMT2Ar acute lymphoblastic leukemia (ALL) have a poor prognosis with an event-free-survival of 38%. Herein we evaluate 1116 FDA approved compounds in primary KMT2Ar infant ALL specimens and identify a sensitivity to proteasome inhibition. Upon exposure to this class of agents, cells demonstrate a depletion of histone H2B monoubiquitination (H2Bub1) and histone H3 lysine 79 dimethylation (H3K79me2) at KMT2A target genes in addition to a downregulation of the KMT2A gene expression signature, providing evidence that it targets the KMT2A transcriptional complex and alters the epigenome. A cohort of relapsed/refractory KMT2Ar patients treated with this approach on a compassionate basis had an overall response rate of 90%. In conclusion, we report on a high throughput drug screen in primary pediatric leukemia specimens whose results translate into clinically meaningful responses. This innovative treatment approach is now being evaluated in a multi-institutional upfront trial for infants with newly diagnosed ALL.
    Mesh-Begriff(e) Infant ; Adult ; Humans ; Child ; Proteasome Endopeptidase Complex/genetics ; Lysine/genetics ; Myeloid-Lymphoid Leukemia Protein/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Transcriptome
    Chemische Substanzen Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Lysine (K3Z4F929H6) ; Myeloid-Lymphoid Leukemia Protein (149025-06-9)
    Sprache Englisch
    Erscheinungsdatum 2023-02-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36370-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Author Correction: Proteasome inhibition targets the KMT2A transcriptional complex in acute lymphoblastic leukemia.

    Kamens, Jennifer L / Nance, Stephanie / Koss, Cary / Xu, Beisi / Cotton, Anitria / Lam, Jeannie W / Garfinkle, Elizabeth A R / Nallagatla, Pratima / Smith, Amelia M R / Mitchell, Sharnise / Ma, Jing / Currier, Duane / Wright, William C / Kavdia, Kanisha / Pagala, Vishwajeeth R / Kim, Wonil / Wallace, LaShanale M / Cho, Ji-Hoon / Fan, Yiping /
    Seth, Aman / Twarog, Nathaniel / Choi, John K / Obeng, Esther A / Hatley, Mark E / Metzger, Monika L / Inaba, Hiroto / Jeha, Sima / Rubnitz, Jeffrey E / Peng, Junmin / Chen, Taosheng / Shelat, Anang A / Guy, R Kiplin / Gruber, Tanja A

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 1297

    Sprache Englisch
    Erscheinungsdatum 2023-03-09
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-37141-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: A high-throughput screen indicates gemcitabine and JAK inhibitors may be useful for treating pediatric AML.

    Drenberg, Christina D / Shelat, Anang / Dang, Jinjun / Cotton, Anitria / Orwick, Shelley J / Li, Mengyu / Jeon, Jae Yoon / Fu, Qiang / Buelow, Daelynn R / Pioso, Marissa / Hu, Shuiying / Inaba, Hiroto / Ribeiro, Raul C / Rubnitz, Jeffrey E / Gruber, Tanja A / Guy, R Kiplin / Baker, Sharyn D

    Nature communications

    2019  Band 10, Heft 1, Seite(n) 2189

    Abstract: Improvement in survival has been achieved for children and adolescents with AML but is largely attributed to enhanced supportive care as opposed to the development of better treatment regimens. High risk subtypes continue to have poor outcomes with event ...

    Abstract Improvement in survival has been achieved for children and adolescents with AML but is largely attributed to enhanced supportive care as opposed to the development of better treatment regimens. High risk subtypes continue to have poor outcomes with event free survival rates <40% despite the use of high intensity chemotherapy in combination with hematopoietic stem cell transplant. Here we combine high-throughput screening, intracellular accumulation assays, and in vivo efficacy studies to identify therapeutic strategies for pediatric AML. We report therapeutics not currently used to treat AML, gemcitabine and cabazitaxel, have broad anti-leukemic activity across subtypes and are more effective relative to the AML standard of care, cytarabine, both in vitro and in vivo. JAK inhibitors are selective for acute megakaryoblastic leukemia and significantly prolong survival in multiple preclinical models. Our approach provides advances in the development of treatment strategies for pediatric AML.
    Mesh-Begriff(e) Adult ; Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Bone Marrow/pathology ; Bone Marrow/radiation effects ; Bone Marrow Transplantation ; Cell Line, Tumor ; Child ; Child, Preschool ; Cytarabine/pharmacology ; Cytarabine/therapeutic use ; Deoxycytidine/analogs & derivatives ; Deoxycytidine/pharmacology ; Deoxycytidine/therapeutic use ; Disease-Free Survival ; Female ; High-Throughput Screening Assays/methods ; Humans ; Infant ; Janus Kinase Inhibitors/pharmacology ; Janus Kinase Inhibitors/therapeutic use ; Leukemia, Experimental/drug therapy ; Leukemia, Experimental/etiology ; Leukemia, Experimental/mortality ; Leukemia, Experimental/pathology ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/mortality ; Leukemia, Myeloid, Acute/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Taxoids/pharmacology ; Taxoids/therapeutic use ; Whole-Body Irradiation/adverse effects ; Xenograft Model Antitumor Assays ; Young Adult ; Gemcitabine
    Chemische Substanzen Janus Kinase Inhibitors ; Taxoids ; Cytarabine (04079A1RDZ) ; Deoxycytidine (0W860991D6) ; cabazitaxel (51F690397J) ; Gemcitabine
    Sprache Englisch
    Erscheinungsdatum 2019-05-16
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-019-09917-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Menin inhibitor MI-3454 induces remission in MLL1-rearranged and NPM1-mutated models of leukemia.

    Klossowski, Szymon / Miao, Hongzhi / Kempinska, Katarzyna / Wu, Tao / Purohit, Trupta / Kim, EunGi / Linhares, Brian M / Chen, Dong / Jih, Gloria / Perkey, Eric / Huang, Huang / He, Miao / Wen, Bo / Wang, Yi / Yu, Ke / Lee, Stanley Chun-Wei / Danet-Desnoyers, Gwenn / Trotman, Winifred / Kandarpa, Malathi /
    Cotton, Anitria / Abdel-Wahab, Omar / Lei, Hongwei / Dou, Yali / Guzman, Monica / Peterson, Luke / Gruber, Tanja / Choi, Sarah / Sun, Duxin / Ren, Pingda / Li, Lian-Sheng / Liu, Yi / Burrows, Francis / Maillard, Ivan / Cierpicki, Tomasz / Grembecka, Jolanta

    The Journal of clinical investigation

    2019  Band 130, Heft 2, Seite(n) 981–997

    Abstract: The protein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or with mutations in the nucleophosmin 1 (NPM1) gene. As a step toward clinical translation of ...

    Abstract The protein-protein interaction between menin and mixed lineage leukemia 1 (MLL1) plays a critical role in acute leukemias with translocations of the MLL1 gene or with mutations in the nucleophosmin 1 (NPM1) gene. As a step toward clinical translation of menin-MLL1 inhibitors, we report development of MI-3454, a highly potent and orally bioavailable inhibitor of the menin-MLL1 interaction. MI-3454 profoundly inhibited proliferation and induced differentiation in acute leukemia cells and primary patient samples with MLL1 translocations or NPM1 mutations. When applied as a single agent, MI-3454 induced complete remission or regression of leukemia in mouse models of MLL1-rearranged or NPM1-mutated leukemia, including patient-derived xenograft models, through downregulation of key genes involved in leukemogenesis. We also identified MEIS1 as a potential pharmacodynamic biomarker of treatment response with MI-3454 in leukemia, and demonstrated that this compound is well tolerated and did not impair normal hematopoiesis in mice. Overall, this study demonstrates, for the first time to our knowledge, profound activity of the menin-MLL1 inhibitor as a single agent in clinically relevant PDX models of leukemia. These data provide a strong rationale for clinical translation of MI-3454 or its analogs for leukemia patients with MLL1 rearrangements or NPM1 mutations.
    Mesh-Begriff(e) Antineoplastic Agents/pharmacology ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Humans ; K562 Cells ; Leukemia/drug therapy ; Leukemia/genetics ; Leukemia/metabolism ; Leukemia/pathology ; Mutation ; Myeloid Ecotropic Viral Integration Site 1 Protein/genetics ; Myeloid Ecotropic Viral Integration Site 1 Protein/metabolism ; Myeloid-Lymphoid Leukemia Protein/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Neoplasms, Experimental/drug therapy ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/pathology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Nucleophosmin ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Remission Induction ; U937 Cells
    Chemische Substanzen Antineoplastic Agents ; KMT2A protein, human ; MEIS1 protein, human ; MEN1 protein, human ; Myeloid Ecotropic Viral Integration Site 1 Protein ; NPM1 protein, human ; Npm1 protein, mouse ; Nuclear Proteins ; Proto-Oncogene Proteins ; Nucleophosmin (117896-08-9) ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
    Sprache Englisch
    Erscheinungsdatum 2019-12-17
    Erscheinungsland United States
    Dokumenttyp 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.
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI129126
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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