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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1997-3-20
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pubmed:abstractText |
Cholecystokinin (CCK) acting via CCK(A) receptors and gastrin acting via CCK(B) receptors exert trophic effects on a variety of nontransformed tissues. However, their role as hormonal regulators of pancreatic cancer is controversial. The aim of this study was to determine the effects of activation of CCK(A) and CCK(B) receptors on the growth of human pancreatic cancer cells in vitro.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0016-5085
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
112
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
952-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9041258-Cell Division,
pubmed-meshheading:9041258-DNA,
pubmed-meshheading:9041258-Dose-Response Relationship, Drug,
pubmed-meshheading:9041258-Humans,
pubmed-meshheading:9041258-Pancreatic Neoplasms,
pubmed-meshheading:9041258-Receptors, Cholecystokinin,
pubmed-meshheading:9041258-Sincalide,
pubmed-meshheading:9041258-Tumor Cells, Cultured
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pubmed:year |
1997
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pubmed:articleTitle |
Transfected cholecystokinin receptors mediate growth inhibitory effects on human pancreatic cancer cell lines.
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pubmed:affiliation |
Department of Physiology, University of Michigan, Ann Arbor, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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