ArticleLeukemia2003
Flavopiridol downregulates the expression of both the inducible NO synthase and p27(kip1) in malignant cells from B-cell chronic lymphocytic leukemia.
Article in Leukemia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Exploiting the neoantigen landscape for immunotherapy of pancreatic ductal adenocarcinoma.Scientific reports · 2016Article
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- T cells from indolent CLL patients prevent apoptosis of leukemic B cells in vitro and have altered gene expression profile.Cancer immunology, immunotherapy : CII · 2013Article
- Cell death signaling and anticancer therapy.Frontiers in oncology · 2011Article
- Potential of plant-derived natural products in the treatment of leukemia and lymphoma.Current drug targets · 2010Review
- Noxa upregulation is associated with apoptosis of chronic lymphocytic leukemia cells induced by hyperforin but not flavopiridol.Leukemia · 2009Article
- Article
- Hyperforin inhibits MMP-9 secretion by B-CLL cells and microtubule formation by endothelial cells.Leukemia · 2006Article
- Pro-apoptotic properties of hyperforin in leukemic cells from patients with B-cell chronic lymphocytic leukemia.Leukemia · 2006Article
- Is targeted chemotherapy an alternative to immunotherapy in chronic lymphocytic leukemia?Cancer immunology, immunotherapy : CII · 2006Review
- Article
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5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Flavopiridol, an inhibitor of cyclin-dependent kinases and other protein kinases, induces in vitro apoptosis of malignant cells from B-cell chronic lymphocytic leukemia (B-CLL). Previously, we reported that nitric oxide (NO), produced by an inducible NO synthase (iNOS), spontaneously expressed by the B-CLL cells, contributed to their deficiency in apoptosis. In the present work, we show that ex vivo treatment of leukemic cells from B-CLL patients with flavopiridol results in the inhibition of iNOS expression, as determined by immunofluorescence and Western blotting, and in a marked inhibition of NO production measured in situ with a specific fluorescent probe (DAF-2 DA). These effects are accompanied by membrane, mitochondrial and nuclear events of apoptosis. Flavopiridol exposure also results in the stimulation of caspase 3 activity and in caspase-dependent cleavage of p27(kip1), a negative regulator of the cell cycle, which is overexpressed in B-CLL. Thus, flavopiridol is capable of downregulating both iNOS and p27(kip1) expression in B-CLL cells. Furthermore, flavopiridol-promoted apoptosis is partly reverted by an NO donor, suggesting that inhibition of the NO pathway could participate in the apoptotic effects of flavopiridol on the leukemic cells.
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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.