Roles of nitric oxide in tumor growth.
Jenkins, DC
Charles, IG
Thomsen, LL
Moss, DW
Holmes, LS
Baylis, SA
Rhodes, P
Westmore, K
Emson, PC
Moncada, S
- Publication Type:
- Journal Article
- Citation:
- Proc Natl Acad Sci U S A, 1995, 92 (10), pp. 4392 - 4396
- Issue Date:
- 1995-05-09
Closed Access
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![]() | 2009002921OK.pdf | 1.48 MB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Jenkins, DC | en_US |
dc.contributor.author | Charles, IG | en_US |
dc.contributor.author | Thomsen, LL | en_US |
dc.contributor.author | Moss, DW | en_US |
dc.contributor.author | Holmes, LS | en_US |
dc.contributor.author | Baylis, SA | en_US |
dc.contributor.author | Rhodes, P | en_US |
dc.contributor.author | Westmore, K | en_US |
dc.contributor.author | Emson, PC | en_US |
dc.contributor.author | Moncada, S | en_US |
dc.date.issued | 1995-05-09 | en_US |
dc.identifier.citation | Proc Natl Acad Sci U S A, 1995, 92 (10), pp. 4392 - 4396 | en_US |
dc.identifier.issn | 0027-8424 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/13314 | |
dc.description.abstract | A subclone of the human colon adenocarcinoma cell line DLD-1, which grew reproducibly as subcutaneous tumors in nude mice, was isolated. Such cells, when engineered to generate nitric oxide (NO) continuously, grew more slowly in vitro than the wild-type parental cells. This growth retardation was reversed by the addition of N-iminoethyl-L-ornithine. In nude mice, however, the tumors from these cells grew faster than those derived from wild-type cells and were markedly more vascularized, suggesting that NO may act as part of a signaling cascade for neovascularization. Recent observations that the generation of NO in human breast and gynecological cancers correlates positively with tumor grade are consistent with this hypothesis. We suggest that NO may have a dual pro- and antitumor action, depending on the local concentration of the molecule. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Proc Natl Acad Sci U S A | en_US |
dc.relation.isbasedon | 10.1073/pnas.92.10.4392 | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Tumor Cells, Cultured | en_US |
dc.subject.mesh | Macrophages | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Nude | en_US |
dc.subject.mesh | Adenocarcinoma | en_US |
dc.subject.mesh | Colonic Neoplasms | en_US |
dc.subject.mesh | Nitric Oxide | en_US |
dc.subject.mesh | Amino Acid Oxidoreductases | en_US |
dc.subject.mesh | Recombinant Proteins | en_US |
dc.subject.mesh | DNA, Complementary | en_US |
dc.subject.mesh | Oligonucleotide Probes | en_US |
dc.subject.mesh | DNA Primers | en_US |
dc.subject.mesh | Transfection | en_US |
dc.subject.mesh | Polymerase Chain Reaction | en_US |
dc.subject.mesh | Cell Division | en_US |
dc.subject.mesh | Gene Expression | en_US |
dc.subject.mesh | Base Sequence | en_US |
dc.subject.mesh | Kinetics | en_US |
dc.subject.mesh | Time Factors | en_US |
dc.subject.mesh | Molecular Sequence Data | en_US |
dc.subject.mesh | Nitric Oxide Synthase | en_US |
dc.title | Roles of nitric oxide in tumor growth. | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 10 | en_US |
utslib.citation.volume | 92 | en_US |
utslib.location.activity | United States | en_US |
utslib.for | 0601 Biochemistry and Cell Biology | en_US |
dc.location.activity | ISI:A1995QX87600063 | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Strength - ithree - Institute of Infection, Immunity and Innovation | |
utslib.copyright.status | closed_access | |
pubs.issue | 10 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 92 | en_US |
Abstract:
A subclone of the human colon adenocarcinoma cell line DLD-1, which grew reproducibly as subcutaneous tumors in nude mice, was isolated. Such cells, when engineered to generate nitric oxide (NO) continuously, grew more slowly in vitro than the wild-type parental cells. This growth retardation was reversed by the addition of N-iminoethyl-L-ornithine. In nude mice, however, the tumors from these cells grew faster than those derived from wild-type cells and were markedly more vascularized, suggesting that NO may act as part of a signaling cascade for neovascularization. Recent observations that the generation of NO in human breast and gynecological cancers correlates positively with tumor grade are consistent with this hypothesis. We suggest that NO may have a dual pro- and antitumor action, depending on the local concentration of the molecule.
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