دورية أكاديمية
أعرض في EDS

An insertional mutagenesis screen identifies genes that cooperate with Mll-AF9 in a murine leukemogenesis model.

التفاصيل البيبلوغرافية
العنوان: An insertional mutagenesis screen identifies genes that cooperate with Mll-AF9 in a murine leukemogenesis model.
المؤلفون: Bergerson RJ; Department of Genetics, Cell Biology and Development, Masonic Cancer Center, University of Minnesota Twin Cities, Minneapolis, MN 55455, USA., Collier LS, Sarver AL, Been RA, Lugthart S, Diers MD, Zuber J, Rappaport AR, Nixon MJ, Silverstein KA, Fan D, Lamblin AF, Wolff L, Kersey JH, Delwel R, Lowe SW, O'Sullivan MG, Kogan SC, Adams DJ, Largaespada DA
المصدر: Blood [Blood] 2012 May 10; Vol. 119 (19), pp. 4512-23. Date of Electronic Publication: 2012 Mar 16.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 7603509 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1528-0020 (Electronic) Linking ISSN: 00064971 NLM ISO Abbreviation: Blood Subsets: MEDLINE
أسماء مطبوعة: Publication: 2021- : [New York] : Elsevier
Original Publication: New York, Grune & Stratton [etc.]
مواضيع طبية MeSH: Mutagenesis, Insertional*/physiology, Cell Transformation, Neoplastic/*genetics , Gene Regulatory Networks/*genetics , Leukemia/*genetics , Myeloid-Lymphoid Leukemia Protein/*physiology , Oncogene Proteins, Fusion/*physiology, Animals ; Animals, Newborn ; Cells, Cultured ; DNA Mutational Analysis/methods ; Disease Models, Animal ; HEK293 Cells ; Humans ; Leukemia/pathology ; Mice ; Mice, Inbred C57BL ; Myeloid-Lymphoid Leukemia Protein/genetics ; Oncogene Proteins, Fusion/genetics ; U937 Cells
مستخلص: Patients with a t(9;11) translocation (MLL-AF9) develop acute myeloid leukemia (AML), and while in mice the expression of this fusion oncogene also results in the development of myeloid leukemia, it is with long latency. To identify mutations that cooperate with Mll-AF9, we infected neonatal wild-type (WT) or Mll-AF9 mice with a murine leukemia virus (MuLV). MuLV-infected Mll-AF9 mice succumbed to disease significantly faster than controls presenting predominantly with myeloid leukemia while infected WT animals developed predominantly lymphoid leukemia. We identified 88 candidate cancer genes near common sites of proviral insertion. Analysis of transcript levels revealed significantly elevated expression of Mn1, and a trend toward increased expression of Bcl11a and Fosb in Mll-AF9 murine leukemia samples with proviral insertions proximal to these genes. Accordingly, FOSB and BCL11A were also overexpressed in human AML harboring MLL gene translocations. FOSB was revealed to be essential for growth in mouse and human myeloid leukemia cells using shRNA lentiviral vectors in vitro. Importantly, MN1 cooperated with Mll-AF9 in leukemogenesis in an in vivo BM viral transduction and transplantation assay. Together, our data identified genes that define transcription factor networks and important genetic pathways acting during progression of leukemia induced by MLL fusion oncogenes.
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معلومات مُعتمدة: U01 CA084221 United States CA NCI NIH HHS; United States HHMI Howard Hughes Medical Institute; T32 CA009138 United States CA NCI NIH HHS; CA009138 United States CA NCI NIH HHS; F32 CA106192 United States CA NCI NIH HHS; K01 CA122183 United States CA NCI NIH HHS; United Kingdom WT_ Wellcome Trust; 13031 United Kingdom CRUK_ Cancer Research UK; U01 CA84221 United States CA NCI NIH HHS
المشرفين على المادة: 0 (MLL-AF9 fusion protein, human)
0 (Oncogene Proteins, Fusion)
149025-06-9 (Myeloid-Lymphoid Leukemia Protein)
تواريخ الأحداث: Date Created: 20120320 Date Completed: 20120716 Latest Revision: 20240629
رمز التحديث: 20240629
مُعرف محوري في PubMed: PMC3362364
DOI: 10.1182/blood-2010-04-281428
PMID: 22427200
قاعدة البيانات: MEDLINE
الوصف
تدمد:1528-0020
DOI:10.1182/blood-2010-04-281428