Mutation of the transforming growth factor‐β type II receptor gene in right‐sided colorectal cancer: relationship to clinicopathological features and genetic alterations
Identifieur interne : 00C978 ( Main/Exploration ); précédent : 00C977; suivant : 00C979Mutation of the transforming growth factor‐β type II receptor gene in right‐sided colorectal cancer: relationship to clinicopathological features and genetic alterations
Auteurs : Barry J. Iacopetta [Australie] ; John Welch [Australie] ; Richie Soong [Australie] ; Anthony K. House [Australie] ; Xiao-Ping Zhou [France] ; Richard Hamelin [France]Source :
- The Journal of Pathology [ 0022-3417 ] ; 1998-04.
Descripteurs français
- Pascal (Inist)
- Carcinogenèse, Carcinome, Côlon droit, Erreur, Facteur croissance transformant, Facteur croissance transformant β, Gène APC, Gène K-ras, Gène TP53, Gène onc cellulaire, Gène suppresseur tumeur, Homme, Mutation, Polymorphisme conformation simple brin, Protooncogène, Réaction chaîne polymérase, Récepteur biologique, Réplication.
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Alternative pathway, Biological receptor, C-Onc gene, Carcinogenesis, Carcinoma, Clinicopathological, Clinicopathological features, Coding region, Colon, Colon cancer, Colorectal, Colorectal cancer, Colorectal carcinomas, Colorectal tumourigenesis, Colorectal tumours, Deletion, Error, Frameshift, Frameshift mutations, Gene mutation, Gene mutations, Genetic alterations, Genomic instability, Growth factor, Human, Inverse correlation, John wiley sons, Large series, Microsatellite, Microsatellite instability, Mutant, Mutant tumours, Mutation, Nature genet, Patient survival, Phenotype, Polymerase chain reaction, Protein overexpression, Protooncogene, Proximal colon, Receptor, Receptor gene, Replication, Right colon, Single strand conformation polymorphism, Sporadic colorectal cancers, TP53 Gene, Transforming growth factor, Transforming growth factor β, Tumor suppressor gene, Tumour, Tumour samples, Western australia.
- Teeft :
- Alternative pathway, Carcinoma, Clinicopathological, Clinicopathological features, Coding region, Colon, Colon cancer, Colorectal, Colorectal cancer, Colorectal carcinomas, Colorectal tumourigenesis, Colorectal tumours, Deletion, Frameshift, Frameshift mutations, Gene mutation, Gene mutations, Genetic alterations, Genomic instability, Growth factor, Inverse correlation, John wiley sons, Large series, Microsatellite, Microsatellite instability, Mutant, Mutant tumours, Mutation, Nature genet, Patient survival, Phenotype, Protein overexpression, Proximal colon, Receptor, Receptor gene, Sporadic colorectal cancers, Tumour, Tumour samples, Western australia.
Abstract
The presence of inactivating mutations in the transforming growth factor‐β (TGF‐β) type II receptor (RII) gene in colon cancer suggests that it may behave like a tumour suppressor gene. RII is mutated in the majority of colon tumours exhibiting widespread microsatellite instability, a characteristic generally referred to as the replication error phenotype (RER+). We investigated the association between RII mutations and various clinicopathological variables and genetic alterations in a large series of sporadic adenocarcinomas arising in the proximal colon. RII mutations were found in 17 per cent (36/210) of right‐sided tumours and in 86 per cent (32/37) of those displaying RER+. They were associated with the absence of lymph node invasion (P=0·04), poor histological differentiation (P=0·006), and with a trend for improved patient survival. Tumours with an RII mutation also showed non‐significant trends for a lower incidence of p53 protein overexpression and of p53, K‐ras, and APC gene mutation compared with tumours with normal RII. These results indicate that right‐sided colorectal tumours containing RII mutations resemble those with the RER+ phenotype in terms of their clinicopathological features and genetic alterations. © 1998 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/(SICI)1096-9896(199804)184:4<390::AID-PATH1230>3.0.CO;2-Q
Affiliations:
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<term>Carcinoma</term>
<term>Clinicopathological</term>
<term>Clinicopathological features</term>
<term>Coding region</term>
<term>Colon</term>
<term>Colon cancer</term>
<term>Colorectal</term>
<term>Colorectal cancer</term>
<term>Colorectal carcinomas</term>
<term>Colorectal tumourigenesis</term>
<term>Colorectal tumours</term>
<term>Deletion</term>
<term>Error</term>
<term>Frameshift</term>
<term>Frameshift mutations</term>
<term>Gene mutation</term>
<term>Gene mutations</term>
<term>Genetic alterations</term>
<term>Genomic instability</term>
<term>Growth factor</term>
<term>Human</term>
<term>Inverse correlation</term>
<term>John wiley sons</term>
<term>Large series</term>
<term>Microsatellite</term>
<term>Microsatellite instability</term>
<term>Mutant</term>
<term>Mutant tumours</term>
<term>Mutation</term>
<term>Nature genet</term>
<term>Patient survival</term>
<term>Phenotype</term>
<term>Polymerase chain reaction</term>
<term>Protein overexpression</term>
<term>Protooncogene</term>
<term>Proximal colon</term>
<term>Receptor</term>
<term>Receptor gene</term>
<term>Replication</term>
<term>Right colon</term>
<term>Single strand conformation polymorphism</term>
<term>Sporadic colorectal cancers</term>
<term>TP53 Gene</term>
<term>Transforming growth factor</term>
<term>Transforming growth factor β</term>
<term>Tumor suppressor gene</term>
<term>Tumour</term>
<term>Tumour samples</term>
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<term>Carcinome</term>
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<term>Erreur</term>
<term>Facteur croissance transformant</term>
<term>Facteur croissance transformant β</term>
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<term>Gène TP53</term>
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<term>Gène suppresseur tumeur</term>
<term>Homme</term>
<term>Mutation</term>
<term>Polymorphisme conformation simple brin</term>
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<term>Réaction chaîne polymérase</term>
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<front><div type="abstract" xml:lang="en">The presence of inactivating mutations in the transforming growth factor‐β (TGF‐β) type II receptor (RII) gene in colon cancer suggests that it may behave like a tumour suppressor gene. RII is mutated in the majority of colon tumours exhibiting widespread microsatellite instability, a characteristic generally referred to as the replication error phenotype (RER+). We investigated the association between RII mutations and various clinicopathological variables and genetic alterations in a large series of sporadic adenocarcinomas arising in the proximal colon. RII mutations were found in 17 per cent (36/210) of right‐sided tumours and in 86 per cent (32/37) of those displaying RER+. They were associated with the absence of lymph node invasion (P=0·04), poor histological differentiation (P=0·006), and with a trend for improved patient survival. Tumours with an RII mutation also showed non‐significant trends for a lower incidence of p53 protein overexpression and of p53, K‐ras, and APC gene mutation compared with tumours with normal RII. These results indicate that right‐sided colorectal tumours containing RII mutations resemble those with the RER+ phenotype in terms of their clinicopathological features and genetic alterations. © 1998 John Wiley & Sons, Ltd.</div>
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