ArticleThe British journal of cancer. Supplement1996
The interaction of buthionine sulphoximide (BSO) and the topoisomerase I inhibitor CPT-11.
Article in The British journal of cancer. Supplement, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Phytochemicals in Chemoprevention: A Cost-Effective Complementary Approach.Journal of Cancer · 2021Review
- Alkenyl group is responsible for the disruption of microtubule network formation in human colon cancer cell line HT-29 cells.Carcinogenesis · 2008Article
- Differential effect of nitrogen species on changes in mitochondrial membrane permeability due to mitomycin c in lung epithelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
- Hammerhead ribozyme against gamma-glutamylcysteine synthetase attenuates resistance to ionizing radiation and cisplatin in human T98G glioblastoma cells.Japanese journal of cancer research : Gann · 2002Article
- Glutathione depletion induced by c-Myc downregulation triggers apoptosis on treatment with alkylating agents.Neoplasia (New York, N.Y.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Buthionine sulphoximide (BSO)-induced depletion of glutathione (GSH) was found to be associated with an increased sensitivity to CPT-11 (topoisomerase I-reactive agent) in V79 hamster lung fibroblast cells. When V79 cells were exposed to 2.5 mM BSO for 28 h beginning 4 h prior to a 24 h coincubation with CPT-11, cytotoxicity was increased compared with CPT-11 alone. It was determined that BSO resulted in a G1 cell cycle arrest and a decrease in the percentage of cells in S-phase. Since CPT-11 is known to be S-phase-specific, this BSO-induced cell cycle redistribution did not appear to account for the chemosensitisation of CPT-11. Additionally, BSO did not alter intracellular accumulation of CPT-11, conversion of CPT-11 to its active metabolite SN-38, or efflux of either CPT-11 or SN-38 from the cell. Finally, BSO resulted in a slight reduction, rather than an increase, in the number of stabilised DNA-topoisomerase I complexes induced by CPT-11. Therefore, these results suggest that BSO-induced sensitisation of V79 cells to the cytotoxic effects of CPT-11 occurs by a mechanism independent of the stabilisation of DNA-topoisomerase I complexes.
Indexed as
Identifiers
8763860PMC2150031W1896083778What 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.