Characterization of gastrin-releasing peptide receptors aberrantly expressed by non-antral gastric adenocarcinomas
Identifieur interne : 003956 ( Main/Exploration ); précédent : 003955; suivant : 003957Characterization of gastrin-releasing peptide receptors aberrantly expressed by non-antral gastric adenocarcinomas
Auteurs : Robert E. Carroll [États-Unis] ; Rosemary Carroll [États-Unis] ; Richard V. Benya [États-Unis]Source :
- Peptides [ 0196-9781 ] ; 1999.
English descriptors
- KwdEn :
- Teeft :
- Abacus concepts, Aberrant expression, Activation causes, Adenocarcinoma, Agonist, Antagonist methyl ester, Autocrine growth factor, Basal phosphate levels, Benya, Bind agonist, Biopsy, Bombesin, Cancer cell lines, Cancer lett, Cdna, Cflp, Cflp analysis, Chicago veterans administration, Colon, Consecutive patients, Constitutive activation, Constitutively, Double biopsies, Elsevier science, Epithelial, Extracellular loop, Gastric, Gastric adenocarcinoma, Gastric adenocarcinomas, Gastric antrum, Gastric cancer, Gastric cancers, Human colon cancers, Human colon epithelial cell line, Human pancreatic cancer cells, Lane marker, Logrank analysis, Methyl ester, Missense mutations, Mucosal, Mucosal epithelial cells, Mucosal epithelium, Mutant, Mutant receptors, Mutation, Nonsaturable binding, Normal expression, Nude mice, Patient outcome, Patient prognosis, Patient survival, Peptide, Peptide hormone receptors, Peptide receptor, Peptide receptors, Primer, Proceeding orad, Reaction mixture, Reaction products, Receptor, Receptor expression, Scatchard analysis, Separate clones, Stomach pancreas, Total phosphates, Transiently transfected cells, Tumor cell growth, Tumor growth, Unlabeled primer, Wild type, Wild type receptor.
Abstract
Abstract: 1Epithelial cells lining the GI tract except in the gastric antrum do not normally express gastrin-releasing peptide receptors (GRP-R). Because GRP-R activation causes the proliferation of many GI cancer cell lines, aberrant expression has been presumed to negatively influence patient survival. We therefore determined the incidence and quality of GRP-R aberrantly expressed by non-antral gastric adenocarcinomas, and evaluated the impact of receptor expression on patient survival. We studied RNA isolated from 20 consecutive non-antral gastric adenocarcinomas, and determined that 8 (40%) aberrantly expressed GRP-R. Of these, 6 (75%) were found to be mutated. Pharmacologically, the effect of these mutations ranged from rendering the GRP-R non-functional to constitutively active. Contrary to expectations, however, survival of patients whose tumor expressed functional GRP-R (18.5 ± 9.8 months) was not statistically different from those that did not (8.3 ± 1.8 months; p = 0.24). Thus our data indicate that mutated isoforms of GRP-R are commonly expressed by non-antral gastric adenocarcinomas. However, expression of functional GRP-R does not alter patient survival, suggesting that this receptor may not be clinically important to the growth of gastric cancers.
Url:
DOI: 10.1016/S0196-9781(98)00164-8
Affiliations:
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Carroll</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Illinois at Chicago; and Chicago Veterans Administration Medical Center (West Side Division), Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation></author><author><name sortKey="Carroll, Rosemary" sort="Carroll, Rosemary" uniqKey="Carroll R" first="Rosemary" last="Carroll">Rosemary Carroll</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Illinois at Chicago; and Chicago Veterans Administration Medical Center (West Side Division), Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation></author><author><name sortKey="Benya, Richard V" sort="Benya, Richard V" uniqKey="Benya R" first="Richard V." last="Benya">Richard V. Benya</name><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Illinois at Chicago; and Chicago Veterans Administration Medical Center (West Side Division), Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Peptides</title><title level="j" type="abbrev">PEP</title><idno type="ISSN">0196-9781</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999">1999</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="229">229</biblScope><biblScope unit="page" to="237">237</biblScope></imprint><idno type="ISSN">0196-9781</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0196-9781</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Gastrin-releasing peptide</term><term>Non-antral gastric adenocarcinomas</term><term>Patient survival</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Abacus concepts</term><term>Aberrant expression</term><term>Activation causes</term><term>Adenocarcinoma</term><term>Agonist</term><term>Antagonist methyl ester</term><term>Autocrine growth factor</term><term>Basal phosphate levels</term><term>Benya</term><term>Bind agonist</term><term>Biopsy</term><term>Bombesin</term><term>Cancer cell lines</term><term>Cancer lett</term><term>Cdna</term><term>Cflp</term><term>Cflp analysis</term><term>Chicago veterans administration</term><term>Colon</term><term>Consecutive patients</term><term>Constitutive activation</term><term>Constitutively</term><term>Double biopsies</term><term>Elsevier science</term><term>Epithelial</term><term>Extracellular loop</term><term>Gastric</term><term>Gastric adenocarcinoma</term><term>Gastric adenocarcinomas</term><term>Gastric antrum</term><term>Gastric cancer</term><term>Gastric cancers</term><term>Human colon cancers</term><term>Human colon epithelial cell line</term><term>Human pancreatic cancer cells</term><term>Lane marker</term><term>Logrank analysis</term><term>Methyl ester</term><term>Missense mutations</term><term>Mucosal</term><term>Mucosal epithelial cells</term><term>Mucosal epithelium</term><term>Mutant</term><term>Mutant receptors</term><term>Mutation</term><term>Nonsaturable binding</term><term>Normal expression</term><term>Nude mice</term><term>Patient outcome</term><term>Patient prognosis</term><term>Patient survival</term><term>Peptide</term><term>Peptide hormone receptors</term><term>Peptide receptor</term><term>Peptide receptors</term><term>Primer</term><term>Proceeding orad</term><term>Reaction mixture</term><term>Reaction products</term><term>Receptor</term><term>Receptor expression</term><term>Scatchard analysis</term><term>Separate clones</term><term>Stomach pancreas</term><term>Total phosphates</term><term>Transiently transfected cells</term><term>Tumor cell growth</term><term>Tumor growth</term><term>Unlabeled primer</term><term>Wild type</term><term>Wild type receptor</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: 1Epithelial cells lining the GI tract except in the gastric antrum do not normally express gastrin-releasing peptide receptors (GRP-R). Because GRP-R activation causes the proliferation of many GI cancer cell lines, aberrant expression has been presumed to negatively influence patient survival. We therefore determined the incidence and quality of GRP-R aberrantly expressed by non-antral gastric adenocarcinomas, and evaluated the impact of receptor expression on patient survival. We studied RNA isolated from 20 consecutive non-antral gastric adenocarcinomas, and determined that 8 (40%) aberrantly expressed GRP-R. Of these, 6 (75%) were found to be mutated. Pharmacologically, the effect of these mutations ranged from rendering the GRP-R non-functional to constitutively active. Contrary to expectations, however, survival of patients whose tumor expressed functional GRP-R (18.5 ± 9.8 months) was not statistically different from those that did not (8.3 ± 1.8 months; p = 0.24). Thus our data indicate that mutated isoforms of GRP-R are commonly expressed by non-antral gastric adenocarcinomas. However, expression of functional GRP-R does not alter patient survival, suggesting that this receptor may not be clinically important to the growth of gastric cancers.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Carroll, Robert E" sort="Carroll, Robert E" uniqKey="Carroll R" first="Robert E." last="Carroll">Robert E. Carroll</name></noRegion><name sortKey="Benya, Richard V" sort="Benya, Richard V" uniqKey="Benya R" first="Richard V." last="Benya">Richard V. Benya</name><name sortKey="Benya, Richard V" sort="Benya, Richard V" uniqKey="Benya R" first="Richard V." last="Benya">Richard V. Benya</name><name sortKey="Carroll, Rosemary" sort="Carroll, Rosemary" uniqKey="Carroll R" first="Rosemary" last="Carroll">Rosemary Carroll</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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