Oncogenic NRAS Primes Primary Acute Myeloid Leukemia Cells for Differentiation
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{"title"=>"Oncogenic NRAS primes primary acute myeloid leukemia cells for differentiation", "type"=>"journal", "authors"=>[{"first_name"=>"Cornelia", "last_name"=>"Brendel", "scopus_author_id"=>"6603965680"}, {"first_name"=>"Sabine", "last_name"=>"Teichler", "scopus_author_id"=>"24463947200"}, {"first_name"=>"Axel", "last_name"=>"Millahn", "scopus_author_id"=>"56674743300"}, {"first_name"=>"Thorsten", "last_name"=>"Stiewe", "scopus_author_id"=>"6602734956"}, {"first_name"=>"Michael", "last_name"=>"Krause", "scopus_author_id"=>"56932629700"}, {"first_name"=>"Kathleen", "last_name"=>"Stabla", "scopus_author_id"=>"24462739500"}, {"first_name"=>"Petra", "last_name"=>"Ross", "scopus_author_id"=>"57197393205"}, {"first_name"=>"Minh", "last_name"=>"Huynh", "scopus_author_id"=>"7004928371"}, {"first_name"=>"Thomas", "last_name"=>"Illmer", "scopus_author_id"=>"6701801332"}, {"first_name"=>"Marco", "last_name"=>"Mernberger", "scopus_author_id"=>"35337300100"}, {"first_name"=>"Christina", "last_name"=>"Barckhausen", "scopus_author_id"=>"55653360100"}, {"first_name"=>"Andreas", "last_name"=>"Neubauer", "scopus_author_id"=>"7102006569"}], "year"=>2015, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-84930672014", "sgr"=>"84930672014", "issn"=>"19326203", "doi"=>"10.1371/journal.pone.0123181", "pmid"=>"25901794", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "pui"=>"604612744"}, "id"=>"5d91350d-99d7-37e6-965b-150f266589a3", "abstract"=>"RAS mutations are frequently found among acute myeloid leukemia patients (AML), generating a constitutively active signaling protein changing cellular proliferation, differentiation and apoptosis. We have previously shown that treatment of AML patients with high-dose cytarabine is preferentially beneficial for those harboring oncogenic RAS. On the basis of a murine AML cell culture model, we ascribed this effect to a RAS-driven, p53-dependent induction of differentiation. Hence, in this study we sought to confirm the correlation between RAS status and differentiation of primary blasts obtained from AML patients. The gene expression signature of AML blasts with oncogenic NRAS indeed corresponded to a more mature profile compared to blasts with wildtype RAS, as demonstrated by gene set enrichment analysis (GSEA) and real-time PCR analysis of myeloid ecotropic viral integration site 1 homolog (MEIS1) in a unique cohort of AML patients. In addition, in vitro cell culture experiments with established cell lines and a second set of primary AML cells showed that oncogenic NRAS mutations predisposed cells to cytarabine (AraC) driven differentiation. Taken together, our findings show that AML with inv(16) and NRAS mutation have a differentiation gene signature, supporting the notion that NRAS mutation may predispose leukemic cells to AraC induced differentiation. We therefore suggest that promotion of differentiation pathways by specific genetic alterations could explain the superior treatment outcome after therapy in some AML patient subgroups. Whether a differentiation gene expression status may generally predict for a superior treatment outcome in AML needs to be addressed in future studies.", "link"=>"http://www.mendeley.com/research/oncogenic-nras-primes-primary-acute-myeloid-leukemia-cells-differentiation", "reader_count"=>18, "reader_count_by_academic_status"=>{"Researcher"=>6, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>5, "Student > Master"=>3, "Student > Bachelor"=>2, "Lecturer"=>1}, "reader_count_by_user_role"=>{"Researcher"=>6, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>5, "Student > Master"=>3, "Student > Bachelor"=>2, "Lecturer"=>1}, "reader_count_by_subject_area"=>{"Biochemistry, Genetics and Molecular Biology"=>4, "Medicine and Dentistry"=>3, "Agricultural and Biological Sciences"=>9, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Chemistry"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Chemistry"=>{"Chemistry"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>9}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>4}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"United States"=>1, "Germany"=>1}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/2035779"], "description"=>"<p>(A) Left panel: Example of gating for lymphocytes (LC) and AML blasts (BL) according to SSC/CD45 signals after live gating. wt<i>RAS</i> panels: CD11c expression of wt<i>RAS</i> AML blasts (left) and LC (right) in untreated samples (solid grey curve) or samples treated with 100 nM AraC (black line). mt<i>RAS</i> panels: CD11c expression of mt<i>NRAS</i>12/13 blasts (left) and LC (right) treated as indicated above. (B) Summary of the <i>in vitro</i> responses to AraC treatment in terms of differentiation of 22 primary AML blasts with or without <i>NRAS</i> mutation. <i>Samples with differentiation</i> describes the portion of samples with differentiation response (diff. ↑) to AraC in relation to all samples in the wt<i>RAS</i> or mt<i>NRAS</i> cohort, respectively. Fisher`s exact test: p = 0.02. (C) Summary of the <i>in vitro</i> responses to AraC treatment in terms of differentiation of 22 primary AML blasts with or without FLT3-ITD. Fisher`s exact test: p = 0.19.</p>", "links"=>[], "tags"=>["Differentiation RAS mutations", "myeloid leukemia patients", "NRAS mutation", "Acute Myeloid Leukemia Cells", "meis", "integration site 1 homolog", "Oncogenic NRAS Primes", "pcr", "AML patients", "cell culture experiments", "gsea", "oncogenic NRAS mutations", "murine AML cell culture model", "differentiation gene expression status", "gene expression signature", "AML patient subgroups", "differentiation gene signature", "treatment Outcome"], "article_id"=>1391397, "categories"=>["Biological Sciences"], "users"=>["Cornelia Brendel", "Sabine Teichler", "Axel Millahn", "Thorsten Stiewe", "Michael Krause", "Kathleen Stabla", "Petra Ross", "Minh Huynh", "Thomas Illmer", "Marco Mernberger", "Christina Barckhausen", "Andreas Neubauer"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0123181.g003", "stats"=>{"downloads"=>0, "page_views"=>17, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AraC_induces_differentiation_predominantly_in_primary_AML_blasts_with_oncogenic_NRAS_/1391397", "title"=>"AraC induces differentiation predominantly in primary AML blasts with oncogenic <i>NRAS</i>.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-04-22 03:51:05"}
  • {"files"=>["https://ndownloader.figshare.com/files/2035780"], "description"=>"<p>GSEA: gene set enrichment analysis</p><p>AML patient cohorts used in this study.</p>", "links"=>[], "tags"=>["Differentiation RAS mutations", "myeloid leukemia patients", "NRAS mutation", "Acute Myeloid Leukemia Cells", "meis", "integration site 1 homolog", "Oncogenic NRAS Primes", "pcr", "AML patients", "cell culture experiments", "gsea", "oncogenic NRAS mutations", "murine AML cell culture model", "differentiation gene expression status", "gene expression signature", "AML patient subgroups", "differentiation gene signature", "treatment Outcome"], "article_id"=>1391398, "categories"=>["Biological Sciences"], "users"=>["Cornelia Brendel", "Sabine Teichler", "Axel Millahn", "Thorsten Stiewe", "Michael Krause", "Kathleen Stabla", "Petra Ross", "Minh Huynh", "Thomas Illmer", "Marco Mernberger", "Christina Barckhausen", "Andreas Neubauer"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0123181.t001", "stats"=>{"downloads"=>2, "page_views"=>29, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AML_patient_cohorts_used_in_this_study_/1391398", "title"=>"AML patient cohorts used in this study.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2015-04-22 03:51:05"}
  • {"files"=>["https://ndownloader.figshare.com/files/2035778"], "description"=>"<p>(A) May-Grünwald-Giemsa staining of HL-60 and U937 (wt<i>RAS</i>) cells 48h after AraC treatment at indicated doses. (B) <i>CD14</i> expression in HL-60 and U937 cells 48 h after AraC-treatment at indicated doses as determined by quantitative real-time PCR. <i>GAPDH</i> was used for normalization. The graph shows the median with 95% confidence interval. Results were normalized to the respective control of each cell line. **: p = 0.002 (Student’s t-test).</p>", "links"=>[], "tags"=>["Differentiation RAS mutations", "myeloid leukemia patients", "NRAS mutation", "Acute Myeloid Leukemia Cells", "meis", "integration site 1 homolog", "Oncogenic NRAS Primes", "pcr", "AML patients", "cell culture experiments", "gsea", "oncogenic NRAS mutations", "murine AML cell culture model", "differentiation gene expression status", "gene expression signature", "AML patient subgroups", "differentiation gene signature", "treatment Outcome"], "article_id"=>1391396, "categories"=>["Biological Sciences"], "users"=>["Cornelia Brendel", "Sabine Teichler", "Axel Millahn", "Thorsten Stiewe", "Michael Krause", "Kathleen Stabla", "Petra Ross", "Minh Huynh", "Thomas Illmer", "Marco Mernberger", "Christina Barckhausen", "Andreas Neubauer"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0123181.g002", "stats"=>{"downloads"=>0, "page_views"=>30, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AraC_induces_differentiation_in_the_mt_NRAS_harboring_AML_cell_line_HL_60_/1391396", "title"=>"AraC induces differentiation in the mt<i>NRAS</i> harboring AML cell line HL-60.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-04-22 03:51:05"}
  • {"files"=>["https://ndownloader.figshare.com/files/2035783", "https://ndownloader.figshare.com/files/2035784", "https://ndownloader.figshare.com/files/2035785", "https://ndownloader.figshare.com/files/2035786", "https://ndownloader.figshare.com/files/2035787", "https://ndownloader.figshare.com/files/2035788", "https://ndownloader.figshare.com/files/2035789", "https://ndownloader.figshare.com/files/2035790"], "description"=>"<div><p><i>RAS</i> mutations are frequently found among acute myeloid leukemia patients (AML), generating a constitutively active signaling protein changing cellular proliferation, differentiation and apoptosis. We have previously shown that treatment of AML patients with high-dose cytarabine is preferentially beneficial for those harboring oncogenic RAS. On the basis of a murine AML cell culture model, we ascribed this effect to a RAS-driven, p53-dependent induction of differentiation. Hence, in this study we sought to confirm the correlation between <i>RAS</i> status and differentiation of primary blasts obtained from AML patients. The gene expression signature of AML blasts with oncogenic <i>NRAS</i> indeed corresponded to a more mature profile compared to blasts with wildtype <i>RAS</i>, as demonstrated by gene set enrichment analysis (GSEA) and real-time PCR analysis of myeloid ecotropic viral integration site 1 homolog (<i>MEIS1</i>) in a unique cohort of AML patients. In addition, <i>in vitro</i> cell culture experiments with established cell lines and a second set of primary AML cells showed that oncogenic <i>NRAS</i> mutations predisposed cells to cytarabine (AraC) driven differentiation. Taken together, our findings show that AML with inv(16) and <i>NRAS</i> mutation have a differentiation gene signature, supporting the notion that <i>NRAS</i> mutation may predispose leukemic cells to AraC induced differentiation. We therefore suggest that promotion of differentiation pathways by specific genetic alterations could explain the superior treatment outcome after therapy in some AML patient subgroups. Whether a differentiation gene expression status may generally predict for a superior treatment outcome in AML needs to be addressed in future studies.</p></div>", "links"=>[], "tags"=>["Differentiation RAS mutations", "myeloid leukemia patients", "NRAS mutation", "Acute Myeloid Leukemia Cells", "meis", "integration site 1 homolog", "Oncogenic NRAS Primes", "pcr", "AML patients", "cell culture experiments", "gsea", "oncogenic NRAS mutations", "murine AML cell culture model", "differentiation gene expression status", "gene expression signature", "AML patient subgroups", "differentiation gene signature", "treatment Outcome"], "article_id"=>1391401, "categories"=>["Biological Sciences"], "users"=>["Cornelia Brendel", "Sabine Teichler", "Axel Millahn", "Thorsten Stiewe", "Michael Krause", "Kathleen Stabla", "Petra Ross", "Minh Huynh", "Thomas Illmer", "Marco Mernberger", "Christina Barckhausen", "Andreas Neubauer"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0123181.s001", "https://dx.doi.org/10.1371/journal.pone.0123181.s002", "https://dx.doi.org/10.1371/journal.pone.0123181.s003", "https://dx.doi.org/10.1371/journal.pone.0123181.s004", "https://dx.doi.org/10.1371/journal.pone.0123181.s005", "https://dx.doi.org/10.1371/journal.pone.0123181.s006", "https://dx.doi.org/10.1371/journal.pone.0123181.s007", "https://dx.doi.org/10.1371/journal.pone.0123181.s008"], "stats"=>{"downloads"=>9, "page_views"=>13, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Oncogenic_NRAS_Primes_Primary_Acute_Myeloid_Leukemia_Cells_for_Differentiation/1391401", "title"=>"Oncogenic <i>NRAS</i> Primes Primary Acute Myeloid Leukemia Cells for Differentiation", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2015-04-22 03:51:05"}
  • {"files"=>["https://ndownloader.figshare.com/files/2035776"], "description"=>"<p>(A-E) Enrichment plots as obtained by GSEA software for the gene sets CROONQUIST_NRAS_SIGNALING_UP, positive control; IVANOVA HEMATO-POIESIS_MATURE_CELL; JAATINEN_HEMATOPOIETIC_STEM _CELL _UP; BENPORATH_MYC_TARGETS_WITH_EBOX; IVANOVA_HEMATOPOIESIS_INTER-MEDIATE_PROGENITOR. Primary AML blasts harboring wt<i>NRAS</i> were compared with mt<i>NRAS</i> (12/13 or 61) blasts. (F) Relative expression of <i>MEIS1</i> in primary AML blasts carrying wt<i>RAS</i> or mt<i>NRAS</i> as examined by real-time PCR. The graph shows the median with 95% confidence interval. Results were normalized to <i>MEIS1</i> expression of mt<i>NRAS</i> blasts. <i>GAPDH</i> expression served as internal control. *: p = 0.025 (Mann Whitney test).</p>", "links"=>[], "tags"=>["Differentiation RAS mutations", "myeloid leukemia patients", "NRAS mutation", "Acute Myeloid Leukemia Cells", "meis", "integration site 1 homolog", "Oncogenic NRAS Primes", "pcr", "AML patients", "cell culture experiments", "gsea", "oncogenic NRAS mutations", "murine AML cell culture model", "differentiation gene expression status", "gene expression signature", "AML patient subgroups", "differentiation gene signature", "treatment Outcome"], "article_id"=>1391394, "categories"=>["Biological Sciences"], "users"=>["Cornelia Brendel", "Sabine Teichler", "Axel Millahn", "Thorsten Stiewe", "Michael Krause", "Kathleen Stabla", "Petra Ross", "Minh Huynh", "Thomas Illmer", "Marco Mernberger", "Christina Barckhausen", "Andreas Neubauer"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0123181.g001", "stats"=>{"downloads"=>0, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Impact_of_NRAS_status_on_the_transcriptome_of_primary_AML_blasts_/1391394", "title"=>"Impact of <i>NRAS</i> status on the transcriptome of primary AML blasts.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-04-22 03:51:05"}

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Relative Metric

{"start_date"=>"2015-01-01T00:00:00Z", "end_date"=>"2015-12-31T00:00:00Z", "subject_areas"=>[]}
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