ArticleBlood2012
An insertional mutagenesis screen identifies genes that cooperate with Mll-AF9 in a murine leukemogenesis model.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines.Annals of hematology · 2023Article
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
- Genome-Wide Association Study of Susceptibility Loci for TCF3-PBX1 Acute Lymphoblastic Leukemia in Children.Journal of the National Cancer Institute · 2021Article
- In vivo functional screening for systems-level integrative cancer genomics.Nature reviews. Cancer · 2020Review
- Role of Meningioma 1 for maintaining the transformed state in MLL-rearranged acute myeloid leukemia: potential for therapeutic intervention?Haematologica · 2020Article
- Meningioma 1 is indispensable for mixed lineage leukemia-rearranged acute myeloid leukemia.Haematologica · 2020Article
- BCL11A: a potential diagnostic biomarker and therapeutic target in human diseases.Bioscience reports · 2019Review
- Ex Vivo Transposon-Mediated Genetic Screens for Cancer Gene Discovery.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Identification of the Gene Expression Rules That Define the Subtypes in Glioma.Journal of clinical medicine · 2018Article
- Childhood Leukemia and Primary Prevention.Current problems in pediatric and adolescent health care · 2016Article
- Constitutive IRF8 expression inhibits AML by activation of repressed immune response signaling.Leukemia · 2015Article
- Article
- In focus: MLL-rearranged leukemia.Leukemia · 2013Review
- MLL-AF9-mediated immortalization of human hematopoietic cells along different lineages changes during ontogeny.Leukemia · 2013Article
- Evaluating risks of insertional mutagenesis by DNA transposons in gene therapy.Translational research : the journal of laboratory and clinical medicine · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 8 institutions in 3 countries.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.