ArticleBlood2008
Quantitative expression profiling guided by common retroviral insertion sites reveals novel and cell type specific cancer genes in leukemia.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Loss of microglial EED impairs synapse density, learning, and memory.Molecular psychiatry · 2022Article
- Conditionally immortalised leukaemia initiating cells co-expressing Hoxa9/Meis1 demonstrate microenvironmental adaptation properties ex vivo while maintaining myelomonocytic memory.Scientific reports · 2021Article
- Review
- Propagation of trimethylated H3K27 regulated by polycomb protein EED is required for embryogenesis, hematopoietic maintenance, and tumor suppression.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Outlier analysis of functional genomic profiles enriches for oncology targets and enables precision medicine.BMC genomics · 2016Article
- Loss of aryl hydrocarbon receptor promotes gene changes associated with premature hematopoietic stem cell exhaustion and development of a myeloproliferative disorder in aging mice.Stem cells and development · 2014Article
- Cancer gene discovery: exploiting insertional mutagenesis.Molecular cancer research : MCR · 2013Review
- Ectopic expression of Zmiz1 induces cutaneous squamous cell malignancies in a mouse model of cancer.The Journal of investigative dermatology · 2013Article
- Article
- Polycomb-group proteins in hematopoietic stem cell regulation and hematopoietic neoplasms.Leukemia · 2013Review
- EED mutants impair polycomb repressive complex 2 in myelodysplastic syndrome and related neoplasms.Leukemia · 2012Article
- A key role for EZH2 and associated genes in mouse and human adult T-cell acute leukemia.Genes & development · 2012Article
- Computational identification of insertional mutagenesis targets for cancer gene discovery.Nucleic acids research · 2011Article
- Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer.Cell stem cell · 2010Review
- Article
- Activation of alternative Jdp2 promoters and functional protein isoforms in T-cell lymphomas by retroviral insertion mutagenesis.Nucleic acids research · 2009Article
- High-throughput insertional mutagenesis screens in mice to identify oncogenic networks.Nature reviews. Cancer · 2009Review
- Murine leukemias with retroviral insertions at Lmo2 are predictive of the leukemias induced in SCID-X1 patients following retroviral gene therapy.PLoS genetics · 2009Article
- Integration site preference of xenotropic murine leukemia virus-related virus, a new human retrovirus associated with prostate cancer.Journal of virology · 2008Article
- Polycomb group genes: keeping stem cell activity in balance.PLoS biology · 2008Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Proviral insertional mutagenesis is a powerful tool for the discovery of cancer-associated genes. The ability of integrated proviruses to affect gene expression over long distances combined with the lack of methods to determine the expression levels of large numbers of genes in a systematic and truly quantitative manner have limited the identification of cancer genes by proviral insertional mutagenesis. Here, we have characterized a new model of proviral insertional mutagenesis-induced lymphoid tumors derived from Eed Polycomb group gene mutant mice and quantitatively determined the expression levels of all genes within 100 kb of 20 different retroviral common insertion sites (CISs) identified in these tumors. Using high-throughput quantitative reverse transcription-polymerase chain reaction (Q-RT-PCR), we document an average of 13 CIS-associated genes deregulated per tumor, half of which are leukemia subtype-specific, while the others are coordinately deregulated in the majority of tumors analyzed. Interestingly, we find that genes located distantly from common proviral integration sites are as frequently deregulated as proximal genes, with multiple genes affected per integration. Our studies reveal an unsuspected conservation in the group of genes deregulated among phenotypically similar subtypes of lymphoid leukemias, and suggest that identification of common molecular determinants of this disease is within reach.
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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.