Linked Life Data

8422427

Source:http://linkedlifedata.com/resource/pubmed/id/8422427

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-2-25
pubmed:abstractText
Several possible mechanisms of the synergistic interactions of IL-1 alpha and VP-16 against A375-C6 human melanoma cells were investigated. Studies indicate that IL-1 alpha did not increase topoisomerase II-dependent VP-16-mediated DNA damage, nor did IL-1 alpha inhibit the repair of VP-16-induced DNA damage in these cells. Furthermore, IL-1 alpha by itself or in combination with VP-16 did not cause significant fragmentation of cellular DNA into oligomers, indicating programmed cell death (apoptosis) was not involved in the mechanism of synergy. In contrast, an IL-1-specific receptor antagonist significantly decreased IL-1 alpha toxicity toward the melanoma cells and nearly eliminated the synergistic interactions of IL-1 alpha with VP-16. These results strongly indicate that synergism of IL-1 alpha with VP-16 was dependent upon an IL-1-receptor-mediated processes. DNA-strand breakage was unlikely to be a primary intracellular target for IL-1 alpha cytotoxicity and synergism with VP-16.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
1180
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
231-5
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Synergistic interactions of etoposide and interleukin-1 alpha are not due to DNA damage in human melanoma cells.
pubmed:affiliation
Biochemical and Molecular Pharmacology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
pubmed:publicationType
Journal Article