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  1. AU="Benjamin L. Ebert"
  2. AU="Loeuillet, Laurence"
  3. AU="Le Noir De Carlan, Marine"
  4. AU="Braakhuis, A J"
  5. AU="Daoud, Chaudhry"
  6. AU="Allameh, S.F." AU="Allameh, S.F."
  7. AU="Liu, Pengyu"
  8. AU=Geller Stephen A. AU=Geller Stephen A.
  9. AU="Guenounou, Sarah"
  10. AU="Noto, Jennifer M"
  11. AU="Lan, Li"
  12. AU="De Panfilis, Simone"
  13. AU="Barnestein, R"
  14. AU="Grafton, R. Quentin"
  15. AU="Lee, Cin-Ty Aeolus"
  16. AU="Tahmasbi, Fateme"
  17. AU="Marmolejo-Ramos, Fernando"
  18. AU="Michel, Christoph M"
  19. AU="Drury, Ashleigh"
  20. AU="Besson, François"
  21. AU="Lee, Seong-Min"
  22. AU=Fath Mohsen Karami AU=Fath Mohsen Karami
  23. AU="Isabel, P."
  24. AU="Melniker, Larry"
  25. AU="Wagner, Marlies"
  26. AU="Karina A. Dow"
  27. AU="Prieto, A. Fernández"
  28. AU=Arnaout Omar AU=Arnaout Omar
  29. AU="Holden, Joseph M."
  30. AU="Balcells, Ll"
  31. AU="Ho, Raymond W"
  32. AU="Richardson, Marcy"
  33. AU="Stephanie Fischinger"
  34. AU="Wilkinson, Michelle J"

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  1. Artikel: Doubling Down on Mutant RAS Can MEK or Break Leukemia

    Tothova, Zuzana / Benjamin L. Ebert

    Cell. 2017 Feb. 23, v. 168, no. 5

    2017  

    Abstract: Targeting of the RAS pathway has long been a critical therapeutic challenge in oncology. Burgess et al. examine how the relative expression of mutant and wild-type KRAS modulates clonal fitness and sensitivity to MEK inhibitors in a model of KrasG12D ... ...

    Abstract Targeting of the RAS pathway has long been a critical therapeutic challenge in oncology. Burgess et al. examine how the relative expression of mutant and wild-type KRAS modulates clonal fitness and sensitivity to MEK inhibitors in a model of KrasG12D mutant acute myeloid leukemia and propose its use as a predictive biomarker.
    Schlagwörter biomarkers ; models ; mutants ; myeloid leukemia
    Sprache Englisch
    Erscheinungsverlauf 2017-0223
    Umfang p. 749-750.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2017.02.013
    Datenquelle NAL Katalog (AGRICOLA)

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  2. Artikel ; Online: Obesity-induced inflammation exacerbates clonal hematopoiesis

    Santhosh Kumar Pasupuleti / Baskar Ramdas / Sarah S. Burns / Lakshmi Reddy Palam / Rahul Kanumuri / Ramesh Kumar / Taruni Reddy Pandhiri / Utpal P. Dave / Nanda Kumar Yellapu / Xinyu Zhou / Chi Zhang / George E. Sandusky / Zhi Yu / Michael C. Honigberg / Alexander G. Bick / Gabriel K. Griffin / Abhishek Niroula / Benjamin L. Ebert / Sophie Paczesny /
    Pradeep Natarajan / Reuben Kapur

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Band 11

    Abstract: Characterized by the accumulation of somatic mutations in blood cell lineages, clonal hematopoiesis of indeterminate potential (CHIP) is frequent in aging and involves the expansion of mutated hematopoietic stem and progenitor cells (HSC/Ps) that leads ... ...

    Abstract Characterized by the accumulation of somatic mutations in blood cell lineages, clonal hematopoiesis of indeterminate potential (CHIP) is frequent in aging and involves the expansion of mutated hematopoietic stem and progenitor cells (HSC/Ps) that leads to an increased risk of hematologic malignancy. However, the risk factors that contribute to CHIP-associated clonal hematopoiesis (CH) are poorly understood. Obesity induces a proinflammatory state and fatty bone marrow (FBM), which may influence CHIP-associated pathologies. We analyzed exome sequencing and clinical data for 47,466 individuals with validated CHIP in the UK Biobank. CHIP was present in 5.8% of the study population and was associated with a significant increase in the waist-to-hip ratio (WHR). Mouse models of obesity and CHIP driven by heterozygosity of Tet2, Dnmt3a, Asxl1, and Jak2 resulted in exacerbated expansion of mutant HSC/Ps due in part to excessive inflammation. Our results show that obesity is highly associated with CHIP and that a proinflammatory state could potentiate the progression of CHIP to more significant hematologic neoplasia. The calcium channel blockers nifedipine and SKF-96365, either alone or in combination with metformin, MCC950, or anakinra (IL-1 receptor antagonist), suppressed the growth of mutant CHIP cells and partially restored normal hematopoiesis. Targeting CHIP-mutant cells with these drugs could be a potential therapeutic approach to treat CH and its associated abnormalities in individuals with obesity.
    Schlagwörter Hematology ; Inflammation ; Medicine ; R
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2023-06-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Intergenerational epigenetic inheritance of cancer susceptibility in mammals

    Bluma J Lesch / Zuzana Tothova / Elizabeth A Morgan / Zhicong Liao / Roderick T Bronson / Benjamin L Ebert / David C Page

    eLife, Vol

    2019  Band 8

    Abstract: Susceptibility to cancer is heritable, but much of this heritability remains unexplained. Some ‘missing’ heritability may be mediated by epigenetic changes in the parental germ line that do not involve transmission of genetic variants from parent to ... ...

    Abstract Susceptibility to cancer is heritable, but much of this heritability remains unexplained. Some ‘missing’ heritability may be mediated by epigenetic changes in the parental germ line that do not involve transmission of genetic variants from parent to offspring. We report that deletion of the chromatin regulator Kdm6a (Utx) in the paternal germ line results in elevated tumor incidence in genetically wild type mice. This effect increases following passage through two successive generations of Kdm6a male germline deletion, but is lost following passage through a wild type germ line. The H3K27me3 mark is redistributed in sperm of Kdm6a mutants, and we define approximately 200 H3K27me3-marked regions that exhibit increased DNA methylation, both in sperm of Kdm6a mutants and in somatic tissue of progeny. Hypermethylated regions in enhancers may alter regulation of genes involved in cancer initiation or progression. Epigenetic changes in male gametes may therefore impact cancer susceptibility in adult offspring.
    Schlagwörter epigenetics ; transgenerational inheritance ; histone modification ; gametes ; spermatogenesis ; cancer ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2019-04-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Rapid and deep-scale ubiquitylation profiling for biology and translational research

    Namrata D. Udeshi / Deepak C. Mani / Shankha Satpathy / Shaunt Fereshetian / Jessica A. Gasser / Tanya Svinkina / Meagan E. Olive / Benjamin L. Ebert / Philipp Mertins / Steven A. Carr

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 11

    Abstract: Comprehensive protein ubiquitylation profiling by mass spectrometry typically requires large sample amounts, limiting its applicability to tissue samples. Here, the authors present an optimized proteomics method that enables multiplexed ubiquitylome ... ...

    Abstract Comprehensive protein ubiquitylation profiling by mass spectrometry typically requires large sample amounts, limiting its applicability to tissue samples. Here, the authors present an optimized proteomics method that enables multiplexed ubiquitylome analysis of cells and tumor tissue samples.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Genetic modification of inflammation- and clonal hematopoiesis–associated cardiovascular risk

    Zhi Yu / Trevor P. Fidler / Yunfeng Ruan / Caitlyn Vlasschaert / Tetsushi Nakao / Md Mesbah Uddin / Taralynn Mack / Abhishek Niroula / J. Brett Heimlich / Seyedeh M. Zekavat / Christopher J. Gibson / Gabriel K. Griffin / Yuxuan Wang / Gina M. Peloso / Nancy Heard-Costa / Daniel Levy / Ramachandran S. Vasan / François Aguet / Kristin G. Ardlie /
    Kent D. Taylor / Stephen S. Rich / Jerome I. Rotter / Peter Libby / Siddhartha Jaiswal / Benjamin L. Ebert / Alexander G. Bick / Alan R. Tall / Pradeep Natarajan

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Band 18

    Abstract: Clonal hematopoiesis of indeterminate potential (CHIP) is associated with an increased risk of cardiovascular diseases (CVDs), putatively via inflammasome activation. We pursued an inflammatory gene modifier scan for CHIP-associated CVD risk among 424, ... ...

    Abstract Clonal hematopoiesis of indeterminate potential (CHIP) is associated with an increased risk of cardiovascular diseases (CVDs), putatively via inflammasome activation. We pursued an inflammatory gene modifier scan for CHIP-associated CVD risk among 424,651 UK Biobank participants. We identified CHIP using whole-exome sequencing data of blood DNA and modeled as a composite, considering all driver genes together, as well as separately for common drivers (DNMT3A, TET2, ASXL1, and JAK2). We developed predicted gene expression scores for 26 inflammasome-related genes and assessed how they modify CHIP-associated CVD risk. We identified IL1RAP as a potential key molecule for CHIP-associated CVD risk across genes and increased AIM2 gene expression leading to heightened JAK2- and ASXL1-associated CVD risk. We show that CRISPR-induced Asxl1-mutated murine macrophages had a particularly heightened inflammatory response to AIM2 agonism, associated with an increased DNA damage response, as well as increased IL-10 secretion, mirroring a CVD-protective effect of IL10 expression in ASXL1 CHIP. Our study supports the role of inflammasomes in CHIP-associated CVD and provides evidence to support gene-specific strategies to address CHIP-associated CVD risk.
    Schlagwörter Cardiology ; Genetics ; Medicine ; R
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2023-09-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: CXCR4 Signaling Has a CXCL12-Independent Essential Role in Murine MLL-AF9-Driven Acute Myeloid Leukemia

    Ramprasad Ramakrishnan / Pablo Peña-Martínez / Puneet Agarwal / Maria Rodriguez-Zabala / Marion Chapellier / Carl Högberg / Mia Eriksson / David Yudovich / Mansi Shah / Mats Ehinger / Björn Nilsson / Jonas Larsson / Anna Hagström-Andersson / Benjamin L. Ebert / Ravi Bhatia / Marcus Järås

    Cell Reports, Vol 31, Iss 8, Pp - (2020)

    2020  

    Abstract: Summary: Acute myeloid leukemia (AML) is defined by an accumulation of immature myeloid blasts in the bone marrow. To identify key dependencies of AML stem cells in vivo, here we use a CRISPR-Cas9 screen targeting cell surface genes in a syngeneic MLL- ... ...

    Abstract Summary: Acute myeloid leukemia (AML) is defined by an accumulation of immature myeloid blasts in the bone marrow. To identify key dependencies of AML stem cells in vivo, here we use a CRISPR-Cas9 screen targeting cell surface genes in a syngeneic MLL-AF9 AML mouse model and show that CXCR4 is a top cell surface regulator of AML cell growth and survival. Deletion of Cxcr4 in AML cells eradicates leukemia cells in vivo without impairing their homing to the bone marrow. In contrast, the CXCR4 ligand CXCL12 is dispensable for leukemia development in recipient mice. Moreover, expression of mutated Cxcr4 variants reveals that CXCR4 signaling is essential for leukemia cells. Notably, loss of CXCR4 signaling in leukemia cells leads to oxidative stress and differentiation in vivo. Taken together, our results identify CXCR4 signaling as essential for AML stem cells by protecting them from differentiation independent of CXCL12 stimulation.
    Schlagwörter acute myeloid leukemia ; CRISPR ; screen ; CXCR4 ; CXCL12 ; oxidative stress ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2020-05-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray syndrome

    Katherine A Donovan / Jian An / Radosław P Nowak / Jingting C Yuan / Emma C Fink / Bethany C Berry / Benjamin L Ebert / Eric S Fischer

    eLife, Vol

    2018  Band 7

    Abstract: In historical attempts to treat morning sickness, use of the drug thalidomide led to the birth of thousands of children with severe birth defects. Despite their teratogenicity, thalidomide and related IMiD drugs are now a mainstay of cancer treatment; ... ...

    Abstract In historical attempts to treat morning sickness, use of the drug thalidomide led to the birth of thousands of children with severe birth defects. Despite their teratogenicity, thalidomide and related IMiD drugs are now a mainstay of cancer treatment; however, the molecular basis underlying the pleiotropic biology and characteristic birth defects remains unknown. Here we show that IMiDs disrupt a broad transcriptional network through induced degradation of several C2H2 zinc finger transcription factors, including SALL4, a member of the spalt-like family of developmental transcription factors. Strikingly, heterozygous loss of function mutations in SALL4 result in a human developmental condition that phenocopies thalidomide-induced birth defects such as absence of thumbs, phocomelia, defects in ear and eye development, and congenital heart disease. We find that thalidomide induces degradation of SALL4 exclusively in humans, primates, and rabbits, but not in rodents or fish, providing a mechanistic link for the species-specific pathogenesis of thalidomide syndrome.
    Schlagwörter chemical biology ; teratogenicity ; ubiquitin ; transcription factors ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2018-08-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Degradation of GSPT1 causes TP53-independent cell death in leukemia while sparing normal hematopoietic stem cells

    Rob S. Sellar / Adam S. Sperling / Mikołaj Słabicki / Jessica A. Gasser / Marie E. McConkey / Katherine A. Donovan / Nada Mageed / Dylan N. Adams / Charles Zou / Peter G. Miller / Ravi K. Dutta / Steffen Boettcher / Amy E. Lin / Brittany Sandoval / Vanessa A. Quevedo Barrios / Veronica Kovalcik / Jonas Koeppel / Elizabeth K. Henderson / Emma C. Fink /
    Lu Yang / Anthony Chan / Sheela Pangeni Pokharel / Erik J. Bergstrom / Rajan Burt / Namrata D. Udeshi / Steven A. Carr / Eric S. Fischer / Chun-Wei Chen / Benjamin L. Ebert

    The Journal of Clinical Investigation, Vol 132, Iss

    2022  Band 16

    Abstract: Targeted protein degradation is a rapidly advancing and expanding therapeutic approach. Drugs that degrade GSPT1 via the CRL4CRBN ubiquitin ligase are a new class of cancer therapy in active clinical development with evidence of activity against acute ... ...

    Abstract Targeted protein degradation is a rapidly advancing and expanding therapeutic approach. Drugs that degrade GSPT1 via the CRL4CRBN ubiquitin ligase are a new class of cancer therapy in active clinical development with evidence of activity against acute myeloid leukemia in early-phase trials. However, other than activation of the integrated stress response, the downstream effects of GSPT1 degradation leading to cell death are largely undefined, and no murine models are available to study these agents. We identified the domains of GSPT1 essential for cell survival and show that GSPT1 degradation leads to impaired translation termination, activation of the integrated stress response pathway, and TP53-independent cell death. CRISPR/Cas9 screens implicated decreased translation initiation as protective following GSPT1 degradation, suggesting that cells with higher levels of translation are more susceptible to the effects of GSPT1 degradation. We defined 2 Crbn amino acids that prevent Gspt1 degradation in mice, generated a knockin mouse with alteration of these residues, and demonstrated the efficacy of GSPT1-degrading drugs in vivo with relative sparing of numbers and function of long-term hematopoietic stem cells. Our results provide a mechanistic basis for the use of GSPT1 degraders for the treatment of cancer, including TP53-mutant acute myeloid leukemia.
    Schlagwörter Hematology ; Therapeutics ; Medicine ; R
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2022-08-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Allosteric inhibition of PPM1D serine/threonine phosphatase via an altered conformational state

    Peter G. Miller / Murugappan Sathappa / Jamie A. Moroco / Wei Jiang / Yue Qian / Sumaiya Iqbal / Qi Guo / Andrew O. Giacomelli / Subrata Shaw / Camille Vernier / Besnik Bajrami / Xiaoping Yang / Cerise Raffier / Adam S. Sperling / Christopher J. Gibson / Josephine Kahn / Cyrus Jin / Matthew Ranaghan / Alisha Caliman /
    Merissa Brousseau / Eric S. Fischer / Robert Lintner / Federica Piccioni / Arthur J. Campbell / David E. Root / Colin W. Garvie / Benjamin L. Ebert

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Band 16

    Abstract: In this work, the authors report a sophisticated combination of genetic, biophysical, and biochemical analyses to identifies the cycling conformational states of PPM1D. The findings reveal how an allosteric inhibitor locks the protein into a ... ...

    Abstract In this work, the authors report a sophisticated combination of genetic, biophysical, and biochemical analyses to identifies the cycling conformational states of PPM1D. The findings reveal how an allosteric inhibitor locks the protein into a conformationally inactive state, and explain the distribution of PPM1D activating mutations in cancer.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2022-06-01T00:00:00Z
    Verlag Nature Portfolio
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    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Cohesin mutations alter DNA damage repair and chromatin structure and create therapeutic vulnerabilities in MDS/AML

    Zuzana Tothova / Anne-Laure Valton / Rebecca A. Gorelov / Mounica Vallurupalli / John M. Krill-Burger / Amie Holmes / Catherine C. Landers / J. Erika Haydu / Edyta Malolepsza / Christina Hartigan / Melanie Donahue / Katerina D. Popova / Sebastian Koochaki / Sergey V. Venev / Jeanne Rivera / Edwin Chen / Kasper Lage / Monica Schenone / Alan D. D’Andrea /
    Steven A. Carr / Elizabeth A. Morgan / Job Dekker / Benjamin L. Ebert

    JCI Insight, Vol 6, Iss

    2021  Band 3

    Abstract: The cohesin complex plays an essential role in chromosome maintenance and transcriptional regulation. Recurrent somatic mutations in the cohesin complex are frequent genetic drivers in cancer, including myelodysplastic syndromes (MDS) and acute myeloid ... ...

    Abstract The cohesin complex plays an essential role in chromosome maintenance and transcriptional regulation. Recurrent somatic mutations in the cohesin complex are frequent genetic drivers in cancer, including myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Here, using genetic dependency screens of stromal antigen 2–mutant (STAG2-mutant) AML, we identified DNA damage repair and replication as genetic dependencies in cohesin-mutant cells. We demonstrated increased levels of DNA damage and sensitivity of cohesin-mutant cells to poly(ADP-ribose) polymerase (PARP) inhibition. We developed a mouse model of MDS in which Stag2 mutations arose as clonal secondary lesions in the background of clonal hematopoiesis driven by tet methylcytosine dioxygenase 2 (Tet2) mutations and demonstrated selective depletion of cohesin-mutant cells with PARP inhibition in vivo. Finally, we demonstrated a shift from STAG2- to STAG1-containing cohesin complexes in cohesin-mutant cells, which was associated with longer DNA loop extrusion, more intermixing of chromatin compartments, and increased interaction with PARP and replication protein A complex. Our findings inform the biology and therapeutic opportunities for cohesin-mutant malignancies.
    Schlagwörter Hematology ; Oncology ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2021-02-01T00:00:00Z
    Verlag American Society for Clinical investigation
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    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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