ArticleHaematologica2010
Genetic modification of primary chronic lymphocytic leukemia cells with a lentivirus expressing CD38.
Article in Haematologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 10 citations in OpenAlex.
- Kinase Inhibition in Relapsed/Refractory Leukemia and Lymphoma Settings: Recent Prospects into Clinical Investigations.Pharmaceutics · 2021Review
- Ectonucleotidases in Blood Malignancies: A Tale of Surface Markers and Therapeutic Targets.Frontiers in immunology · 2019Review
- Calcium-RasGRP2-Rap1 signaling mediates CD38-induced migration of chronic lymphocytic leukemia cells.Blood advances · 2018Article
- The enzymatic activities of CD38 enhance CLL growth and trafficking: implications for therapeutic targeting.Leukemia · 2015Article
- Phorbol myristate acetate, but not CD40L, induces the differentiation of CLL B cells into Ab-secreting cells.Immunology and cell biology · 2014Article
- The pathogenic relevance of the prognostic markers CD38 and CD49d in chronic lymphocytic leukemia.Annals of hematology · 2014Review
- Reactive oxygen species and mitochondrial sensitivity to oxidative stress determine induction of cancer cell death by p21.The Journal of biological chemistry · 2012Article
- CD38 increases CXCL12-mediated signals and homing of chronic lymphocytic leukemia cells.Leukemia · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies of the role of individual genes in chronic lymphocytic leukemia (CLL) have been hampered by the inability to consistently transfect primary tumor cells. Here, we describe a highly efficient method of genetically modifying primary CLL cells using a VSVG pseudotyped lentiviral vector. We transduced CD38 negative CLL cells with a lentiviral vector encoding CD38 which caused increased surface CD38 expression in all the samples tested (n=17) with no evidence of plasmacytoid differentiation. The mean percentage of positive cells expressing CD38 was 87%+/-8.5% and the mean cell viability 74%+/-17%. This high level of transduction of all the CLL cell samples tested demonstrates the utility of this technique which should prove applicable for the introduction and analysis of other genes in these non-dividing cells.
Indexed as
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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.