ArticleMolecular therapy : the journal of the American Society of Gene Therapy2009
Self-inactivating retroviral vector-mediated gene transfer induces oncogene activation and immortalization of primary murine bone marrow cells.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- CAR-T cell therapy in breast cancer management: expanding horizon and overcoming challenges beyond hematologic cancers.Molecular biology reports · 2026Review
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Review
- Advances in HIV Gene Therapy.International journal of molecular sciences · 2024Review
- Improved functionality and potency of next generation BinMLV viral vectors toward safer gene therapy.Molecular therapy. Methods & clinical development · 2021Article
- Improvement of mRNA Delivery Efficiency to a T Cell Line by Modulating PEG-Lipid Content and Phospholipid Components of Lipid Nanoparticles.Pharmaceutics · 2021Article
- Review
- The Impact of the Cellular Origin in Acute Myeloid Leukemia: Learning From Mouse Models.HemaSphere · 2019Review
- Engineering Approaches in Human Gamma Delta T Cells for Cancer Immunotherapy.Frontiers in immunology · 2018Review
- Article
- Insulated Foamy Viral Vectors.Human gene therapy · 2016Article
- Effects of transforming growth factor-β1 on the proliferation and invasion of the HTR-8/SVneo cell line.Oncology letters · 2014Article
- Transcriptional targeting of DCs with lentiviral vectors induces antigen-specific tolerance in a mouse model of multiple sclerosis.Gene therapy · 2013Article
- Deletion of the LTR enhancer/promoter has no impact on the integration profile of MLV vectors in human hematopoietic progenitors.PloS one · 2013Article
- Stably integrated and expressed retroviral sequences can influence nuclear location and chromatin condensation of the integration locus.Chromosoma · 2012Article
- Evaluation of residual promoter activity in γ-retroviral self-inactivating (SIN) vectors.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Contributions of gene marking to cell and gene therapies.Human gene therapy · 2011Review
- Reconstitutable charged polymeric (PLGA)(2)-b-PEI micelles for gene therapeutics delivery.Biomaterials · 2011Article
- Article
- Gene therapy of chronic granulomatous disease: the engraftment dilemma.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Insertional mutagenesis leading to insurgence of leukemia has been shown as a consequence of retroviral (RV)-mediated gene transfer in animal models and in clinical trials of gene therapy for X-linked severe combined immunodeficiency. Aberrant expression of oncogenes neighboring the gamma-RV vector insertion site via induction by the enhancer element of the viral long terminal repeats (LTRs) is thought to have played a role in leukemogenesis. Consequently, RV vectors devoid of LTR enhancer elements could prove as safer tools for gene transfer. To test this hypothesis, we evaluated the immortalization ability of two RV vectors: one carrying the full-length Moloney leukemia virus (MLV) LTR and one with the same LTR in which the enhancer element was deleted [MLV self-inactivating (SIN)]. Unexpectedly, transduction with MLV SIN resulted in an only slightly and not significant decreased immortalization frequency of primary bone marrow (BM) cultures (about 37%) compared to transduction with MLV (about 48%). Similar to MLV, immortalization by MLV SIN is likely caused by insertional activation of oncogenes including Evi1, Mds1, Mef2c, and Hoxa7. Our results indicate that the MLV SIN, devoid of the LTR enhancer element, was still able to immortalize BM cells by activating nearby gene expression, indicating the need of an accurate selection of the internal promoter to obtain safer SIN RV vectors.
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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.