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  1. AU="Romine, Kyle A"
  2. AU="Cunsolo, Vincenzo"
  3. AU="Ba, Aboubacar"
  4. AU="Prisca, Mirandolina"
  5. AU="Perez, Tate"
  6. AU="Bakkaloglu, Sevan"
  7. AU="Guernieri, Rebecca L"
  8. AU="Xing, Z Y"
  9. AU="Yu-Heng Cheng"
  10. AU=Freeman Richard B Jr
  11. AU="Wang, Qi-En"
  12. AU="Mallamaci, M"
  13. AU="Turk, Yael R"
  14. AU="Tinto, Monica"
  15. AU="Selvendiran, Karuppaiyah" AU="Selvendiran, Karuppaiyah"
  16. AU="Enns, Murray W"
  17. AU="Yaohua Yang" AU="Yaohua Yang"

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  1. Artikel ; Online: Rise of the Clones: Myelodysplastic Syndrome to Secondary Acute Myeloid Leukemia.

    Romine, Kyle A / van Galen, Peter

    Blood cancer discovery

    2022  Band 3, Heft 4, Seite(n) 270–272

    Abstract: Myelodysplastic syndrome (MDS) describes a family of blood disorders driven by the clonal expansion of mutated blood cells that can evolve into secondary acute myeloid leukemia (sAML). Two new studies use single-cell and deep sequencing to elucidate the ... ...

    Abstract Myelodysplastic syndrome (MDS) describes a family of blood disorders driven by the clonal expansion of mutated blood cells that can evolve into secondary acute myeloid leukemia (sAML). Two new studies use single-cell and deep sequencing to elucidate the progression of MDS to AML, revealing discrete clonal architectures and the driving role of signaling mutations.
    Mesh-Begriff(e) Clonal Evolution/genetics ; Clone Cells ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Myelodysplastic Syndromes/complications ; Neoplasms, Second Primary/genetics
    Sprache Englisch
    Erscheinungsdatum 2022-06-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Comment
    ZDB-ID 3028898-8
    ISSN 2643-3249 ; 2643-3230
    ISSN (online) 2643-3249
    ISSN 2643-3230
    DOI 10.1158/2643-3230.BCD-22-0046
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Immune cell proportions correlate with clinicogenomic features and

    Romine, Kyle A / Bottomly, Daniel / Yashar, William / Long, Nicola / Viehdorfer, Matthew / McWeeney, Shannon K / Tyner, Jeffrey W

    Frontiers in oncology

    2023  Band 13, Seite(n) 1192829

    Abstract: Introduction: The implementation of small-molecule and immunotherapies in acute myeloid leukemia (AML) has been challenging due to genetic and epigenetic variability amongst patients. There are many potential mechanisms by which immune cells could ... ...

    Abstract Introduction: The implementation of small-molecule and immunotherapies in acute myeloid leukemia (AML) has been challenging due to genetic and epigenetic variability amongst patients. There are many potential mechanisms by which immune cells could influence small-molecule or immunotherapy responses, yet, this area remains understudied.
    Methods: Here we performed cell type enrichment analysis from over 560 AML patient bone marrow and peripheral blood samples from the Beat AML dataset to describe the functional immune landscape of AML.
    Results: We identify multiple cell types that significantly correlate with AML clinical and genetic features, and we also observe significant correlations of immune cell proportions with
    Discussion: Our work, which is accessible through a new "Cell Type" module in our visualization platform (Vizome; http://vizome.org/), can be leveraged to investigate potential contributions of different immune cells on many facets of the biology of AML.
    Sprache Englisch
    Erscheinungsdatum 2023-06-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2023.1192829
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: BET inhibitors rescue anti-PD1 resistance by enhancing TCF7 accessibility in leukemia-derived terminally exhausted CD8

    Romine, Kyle A / MacPherson, Kevin / Cho, Hyun-Jun / Kosaka, Yoko / Flynn, Patrick A / Byrd, Kaelan H / Coy, Jesse L / Newman, Matthew T / Pandita, Ravina / Loo, Christopher P / Scott, Jaime / Adey, Andrew C / Lind, Evan F

    Leukemia

    2023  Band 37, Heft 3, Seite(n) 580–592

    Abstract: Many acute myeloid leukemia (AML) patients exhibit hallmarks of immune exhaustion, such as increased myeloid-derived suppressor cells, suppressive regulatory T cells and dysfunctional T cells. Similarly, we have identified the same immune-related ... ...

    Abstract Many acute myeloid leukemia (AML) patients exhibit hallmarks of immune exhaustion, such as increased myeloid-derived suppressor cells, suppressive regulatory T cells and dysfunctional T cells. Similarly, we have identified the same immune-related features, including exhausted CD8
    Mesh-Begriff(e) Animals ; Mice ; CD8-Positive T-Lymphocytes ; Leukemia, Myeloid, Acute/metabolism ; T-Lymphocytes, Regulatory
    Chemische Substanzen Pdcd1 protein, mouse ; Hnf1a protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2023-01-21
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 807030-1
    ISSN 1476-5551 ; 0887-6924
    ISSN (online) 1476-5551
    ISSN 0887-6924
    DOI 10.1038/s41375-023-01808-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Secondary fusion proteins as a mechanism of BCR::ABL1 kinase-independent resistance in chronic myeloid leukaemia.

    Barnes, Evan J / Eide, Christopher A / Kaempf, Andy / Bottomly, Daniel / Romine, Kyle A / Wilmot, Beth / Saunders, Dominick / McWeeney, Shannon K / Tognon, Cristina E / Druker, Brian J

    British journal of haematology

    2022  Band 200, Heft 3, Seite(n) 323–328

    Abstract: Drug resistance in chronic myeloid leukaemia (CML) may occur via mutations in the causative BCR::ABL1 fusion or BCR::ABL1-independent mechanisms. We analysed 48 patients with BCR::ABL1-independent resistance for the presence of secondary fusion genes by ... ...

    Abstract Drug resistance in chronic myeloid leukaemia (CML) may occur via mutations in the causative BCR::ABL1 fusion or BCR::ABL1-independent mechanisms. We analysed 48 patients with BCR::ABL1-independent resistance for the presence of secondary fusion genes by RNA sequencing. We identified 10 of the most frequently detected secondary fusions in 21 patients. Validation studies, cell line models, gene expression analysis and drug screening revealed differences with respect to proliferation rate, differentiation and drug sensitivity. Notably, expression of RUNX1::MECOM led to resistance to ABL1 tyrosine kinase inhibitors in vitro. These results suggest secondary fusions contribute to BCR::ABL1-independent resistance and may be amenable to combined therapies.
    Mesh-Begriff(e) Humans ; Fusion Proteins, bcr-abl/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Mutation ; Cell Line ; Drug Resistance, Neoplasm/genetics
    Chemische Substanzen Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Protein Kinase Inhibitors
    Sprache Englisch
    Erscheinungsdatum 2022-10-20
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.18515
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Acute myeloid leukemia-induced T-cell suppression can be reversed by inhibition of the MAPK pathway.

    Moshofsky, Kaycee B / Cho, Hyun J / Wu, Guanming / Romine, Kyle A / Newman, Matthew T / Kosaka, Yoko / McWeeney, Shannon K / Lind, Evan F

    Blood advances

    2019  Band 3, Heft 20, Seite(n) 3038–3051

    Abstract: Acute myeloid leukemia (AML) remains difficult to treat due to mutational heterogeneity and the development of resistance to therapy. Targeted agents, such as MEK inhibitors, may be incorporated into treatment; however, the impact of MEK inhibitors on ... ...

    Abstract Acute myeloid leukemia (AML) remains difficult to treat due to mutational heterogeneity and the development of resistance to therapy. Targeted agents, such as MEK inhibitors, may be incorporated into treatment; however, the impact of MEK inhibitors on the immune microenvironment in AML is not well understood. A greater understanding of the implications of MEK inhibition on immune responses may lead to a greater understanding of immune evasion and more rational combinations with immunotherapies. This study describes the impact of trametinib on both T cells and AML blast cells by using an immunosuppressive mouse model of AML and primary patient samples. We also used a large AML database of functional drug screens to understand characteristics of trametinib-sensitive samples. In the mouse model, trametinib increased T-cell viability and restored T-cell proliferation. Importantly, we report greater proliferation in the CD8+CD44+ effector subpopulation and impaired activation of CD8+CD62L+ naive cells. Transcriptome analysis revealed that trametinib-sensitive samples have an inflammatory gene expression profile, and we also observed increased programmed cell death ligand 1 (PD-L1) expression on trametinib-sensitive samples. Finally, we found that trametinib consistently reduced PD-L1 and PD-L2 expression in a dose-dependent manner on the myeloid population. Altogether, our data present greater insight into the impact of trametinib on the immune microenvironment and characteristics of trametinib-sensitive patient samples.
    Mesh-Begriff(e) Animals ; Antineoplastic Agents/pharmacology ; Biomarkers ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Gene Expression Profiling/methods ; Humans ; Immunomodulation/drug effects ; Immunophenotyping ; Leukemia, Myeloid, Acute/etiology ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Lymphocyte Activation/immunology ; MAP Kinase Signaling System/drug effects ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Xenograft Model Antitumor Assays ; ras Proteins/genetics ; ras Proteins/metabolism
    Chemische Substanzen Antineoplastic Agents ; Biomarkers ; ras Proteins (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2019-10-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2019000574
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Monocytic differentiation and AHR signaling as Primary Nodes of BET Inhibitor Response in Acute Myeloid Leukemia.

    Romine, Kyle A / Nechiporuk, Tamilla / Bottomly, Daniel / Jeng, Sophia / McWeeney, Shannon K / Kaempf, Andy / Corces, M Ryan / Majeti, Ravindra / Tyner, Jeffrey W

    Cancer discovery

    2021  

    Abstract: To understand mechanisms of response to BET inhibitors (BETi), we mined the Beat AML functional genomic dataset and performed genome-wide CRISPR screens on BETi- sensitive and BETi- resistant AML cells. Both strategies revealed regulators of monocytic ... ...

    Abstract To understand mechanisms of response to BET inhibitors (BETi), we mined the Beat AML functional genomic dataset and performed genome-wide CRISPR screens on BETi- sensitive and BETi- resistant AML cells. Both strategies revealed regulators of monocytic differentiation, SPI1, JUNB, FOS, and aryl-hydrocarbon receptor signaling (AHR/ARNT), as determinants of BETi response. AHR activation synergized with BETi while inhibition antagonized BETi-mediated cytotoxicity. Consistent with BETi sensitivity dependence on monocytic differentiation, ex vivo sensitivity to BETi in primary AML patient samples correlated with higher expression of monocytic markers CSF1R, LILRs, and VCAN. In addition, HL-60 cell line differentiation enhanced its sensitivity to BETi. Further, screens to rescue BETi sensitivity identified BCL2 and CDK6 as druggable vulnerabilities. Finally, monocytic AML patient samples refractory to venetoclax ex vivo were significantly more sensitive to combined BETi + venetoclax. Together, our work highlights mechanisms that could predict BETi response and identifies combination strategies to overcome resistance.
    Sprache Englisch
    Erscheinungsdatum 2021-07-01
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2643-3230.BCD-21-0012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Monocytic differentiation and AHR signaling as Primary Nodes of BET Inhibitor Response in Acute Myeloid Leukemia.

    Romine, Kyle A / Nechiporuk, Tamilla / Bottomly, Daniel / Jeng, Sophia / McWeeney, Shannon K / Kaempf, Andy / Corces, M Ryan / Majeti, Ravindra / Tyner, Jeffrey W

    Blood cancer discovery

    2021  Band 2, Heft 5, Seite(n) 518–531

    Abstract: To understand mechanisms of response to BET inhibitors (BETi), we mined the Beat AML functional genomic dataset and performed genome-wide CRISPR screens on BETi- sensitive and BETi- resistant AML cells. Both strategies revealed regulators of monocytic ... ...

    Abstract To understand mechanisms of response to BET inhibitors (BETi), we mined the Beat AML functional genomic dataset and performed genome-wide CRISPR screens on BETi- sensitive and BETi- resistant AML cells. Both strategies revealed regulators of monocytic differentiation, SPI1, JUNB, FOS, and aryl-hydrocarbon receptor signaling (AHR/ARNT), as determinants of BETi response. AHR activation synergized with BETi while inhibition antagonized BETi-mediated cytotoxicity. Consistent with BETi sensitivity dependence on monocytic differentiation,
    Mesh-Begriff(e) Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; HL-60 Cells ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Signal Transduction
    Chemische Substanzen Antineoplastic Agents
    Sprache Englisch
    Erscheinungsdatum 2021-07-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3028898-8
    ISSN 2643-3249 ; 2643-3230
    ISSN (online) 2643-3249
    ISSN 2643-3230
    DOI 10.1158/2643-3230.BCD-21-0012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Integrative analysis of drug response and clinical outcome in acute myeloid leukemia.

    Bottomly, Daniel / Long, Nicola / Schultz, Anna Reister / Kurtz, Stephen E / Tognon, Cristina E / Johnson, Kara / Abel, Melissa / Agarwal, Anupriya / Avaylon, Sammantha / Benton, Erik / Blucher, Aurora / Borate, Uma / Braun, Theodore P / Brown, Jordana / Bryant, Jade / Burke, Russell / Carlos, Amy / Chang, Bill H / Cho, Hyun Jun /
    Christy, Stephen / Coblentz, Cody / Cohen, Aaron M / d'Almeida, Amanda / Cook, Rachel / Danilov, Alexey / Dao, Kim-Hien T / Degnin, Michie / Dibb, James / Eide, Christopher A / English, Isabel / Hagler, Stuart / Harrelson, Heath / Henson, Rachel / Ho, Hibery / Joshi, Sunil K / Junio, Brian / Kaempf, Andy / Kosaka, Yoko / Laderas, Ted / Lawhead, Matt / Lee, Hyunjung / Leonard, Jessica T / Lin, Chenwei / Lind, Evan F / Liu, Selina Qiuying / Lo, Pierrette / Loriaux, Marc M / Luty, Samuel / Maxson, Julia E / Macey, Tara / Martinez, Jacqueline / Minnier, Jessica / Monteblanco, Andrea / Mori, Motomi / Morrow, Quinlan / Nelson, Dylan / Ramsdill, Justin / Rofelty, Angela / Rogers, Alexandra / Romine, Kyle A / Ryabinin, Peter / Saultz, Jennifer N / Sampson, David A / Savage, Samantha L / Schuff, Robert / Searles, Robert / Smith, Rebecca L / Spurgeon, Stephen E / Sweeney, Tyler / Swords, Ronan T / Thapa, Aashis / Thiel-Klare, Karina / Traer, Elie / Wagner, Jake / Wilmot, Beth / Wolf, Joelle / Wu, Guanming / Yates, Amy / Zhang, Haijiao / Cogle, Christopher R / Collins, Robert H / Deininger, Michael W / Hourigan, Christopher S / Jordan, Craig T / Lin, Tara L / Martinez, Micaela E / Pallapati, Rachel R / Pollyea, Daniel A / Pomicter, Anthony D / Watts, Justin M / Weir, Scott J / Druker, Brian J / McWeeney, Shannon K / Tyner, Jeffrey W

    Cancer cell

    2022  Band 40, Heft 8, Seite(n) 850–864.e9

    Abstract: Acute myeloid leukemia (AML) is a cancer of myeloid-lineage cells with limited therapeutic options. We previously combined ex vivo drug sensitivity with genomic, transcriptomic, and clinical annotations for a large cohort of AML patients, which ... ...

    Abstract Acute myeloid leukemia (AML) is a cancer of myeloid-lineage cells with limited therapeutic options. We previously combined ex vivo drug sensitivity with genomic, transcriptomic, and clinical annotations for a large cohort of AML patients, which facilitated discovery of functional genomic correlates. Here, we present a dataset that has been harmonized with our initial report to yield a cumulative cohort of 805 patients (942 specimens). We show strong cross-cohort concordance and identify features of drug response. Further, deconvoluting transcriptomic data shows that drug sensitivity is governed broadly by AML cell differentiation state, sometimes conditionally affecting other correlates of response. Finally, modeling of clinical outcome reveals a single gene, PEAR1, to be among the strongest predictors of patient survival, especially for young patients. Collectively, this report expands a large functional genomic resource, offers avenues for mechanistic exploration and drug development, and reveals tools for predicting outcome in AML.
    Mesh-Begriff(e) Cell Differentiation ; Cohort Studies ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Receptors, Cell Surface/genetics ; Transcriptome
    Chemische Substanzen PEAR1 protein, human ; Receptors, Cell Surface
    Sprache Englisch
    Erscheinungsdatum 2022-07-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2022.07.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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