AustralieFrV1, PascalFrancis, Corpus, bibRecord, 006707

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 : 006707 ( PascalFrancis/Corpus ); précédent : 006706; suivant : 006708

Mutation of the transforming growth factor-β type II receptor gene in right-sided colorectal cancer : Relationship to clinicopathological features and genetic alterations

Auteurs : B. J. Iacopetta ; J. Welch ; R. Soong ; A. K. House ; X.-P. Zhou ; R. Hamelin

Source :

Journal of pathology [ 0022-3417 ] ; 1998.

RBID : Pascal:98-0229469

Descripteurs français

Pascal (Inist)
- Carcinome, Côlon droit, Réaction chaîne polymérase, Polymorphisme conformation simple brin, Mutation, Facteur croissance transformant, Facteur croissance transformant β, Récepteur biologique, Protooncogène, Gène onc cellulaire, Gène suppresseur tumeur, Gène TP53, Réplication, Erreur, Carcinogenèse, Homme, Gène K-ras, Gène APC.

English descriptors

KwdEn :
- Biological receptor, C-Onc gene, Carcinogenesis, Carcinoma, Error, Human, Mutation, Polymerase chain reaction, Protooncogene, Replication, Right colon, Single strand conformation polymorphism, TP53 Gene, Transforming growth factor, Transforming growth factor β, Tumor suppressor gene.

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 (361210) of right-sided tumours and in 86 per cent (32137) 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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 IACOPETTA (B. J.)`
A11	`02`	`1`		`@1 WELCH (J.)`
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A11	`05`	`1`		`@1 ZHOU (X.-P.)`
A11	`06`	`1`		`@1 HAMELIN (R.)`
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A64		`1`		`@0 Journal of pathology`
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C01	`01`		`ENG`	@0 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 (361210) of right-sided tumours and in 86 per cent (32137) 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.
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C03	`05`	`X`	`SPA`	`@0 Mutación @5 06`
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Format Inist (serveur)

NO :	PASCAL 98-0229469 INIST
ET :	Mutation of the transforming growth factor-β type II receptor gene in right-sided colorectal cancer : Relationship to clinicopathological features and genetic alterations
AU :	IACOPETTA (B. J.); WELCH (J.); SOONG (R.); HOUSE (A. K.); ZHOU (X.-P.); HAMELIN (R.)
AF :	Department of Surgery, University of Western Australia/Nedlands 6907/Australie (1 aut., 2 aut., 3 aut., 4 aut.); U434, CEPH, 27 rue Juliette Dodu/75010 Paris/France (5 aut., 6 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of pathology; ISSN 0022-3417; Coden JPTLAS; Royaume-Uni; Da. 1998; Vol. 184; No. 4; Pp. 390-395; Bibl. 39 ref.
LA :	Anglais
EA :	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 (361210) of right-sided tumours and in 86 per cent (32137) 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.
CC :	002B13B01
FD :	Carcinome; Côlon droit; Réaction chaîne polymérase; Polymorphisme conformation simple brin; Mutation; Facteur croissance transformant; Facteur croissance transformant β; Récepteur biologique; Protooncogène; Gène onc cellulaire; Gène suppresseur tumeur; Gène TP53; Réplication; Erreur; Carcinogenèse; Homme; Gène K-ras; Gène APC
FG :	Tumeur maligne; Appareil digestif pathologie; Intestin pathologie; Côlon pathologie; Biologie moléculaire; Facteur croissance; Polypeptide; Cytokine
ED :	Carcinoma; Right colon; Polymerase chain reaction; Single strand conformation polymorphism; Mutation; Transforming growth factor; Transforming growth factor β; Biological receptor; Protooncogene; C-Onc gene; Tumor suppressor gene; TP53 Gene; Replication; Error; Carcinogenesis; Human
EG :	Malignant tumor; Digestive diseases; Intestinal disease; Colonic disease; Molecular biology; Growth factor; Polypeptide; Cytokine
GD :	Abweichung
SD :	Carcinoma; Colón derecho; Reacción cadena polimerasa; Polimorfismo conformación cadena única; Mutación; Factor crecimiento transformante; Factor crecimiento transformante β; Receptor biológico; Protooncogen; Gen onc celular; Gen supresor tumor; Gen TP53; Replicación; Error; Carcinogénesis; Hombre
LO :	INIST-988A.354000079331390050
ID :	98-0229469

Links to Exploration step

Pascal:98-0229469

Le document en format XML

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<term>Mutation</term>
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<term>Facteur croissance transformant</term>
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<term>Gène onc cellulaire</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 (361210) of right-sided tumours and in 86 per cent (32137) 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.</div>
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<fA11 i1="02" i2="1"><s1>WELCH (J.)</s1>
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<fA11 i1="03" i2="1"><s1>SOONG (R.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>HOUSE (A. K.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>ZHOU (X.-P.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>HAMELIN (R.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Surgery, University of Western Australia</s1>
<s2>Nedlands 6907</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>U434, CEPH, 27 rue Juliette Dodu</s1>
<s2>75010 Paris</s2>
<s3>FRA</s3>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>390-395</s1>
</fA20>
<fA21><s1>1998</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>988A</s2>
<s5>354000079331390050</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 1998 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>39 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>98-0229469</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i2="1"><s0>Journal of pathology</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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 (361210) of right-sided tumours and in 86 per cent (32137) 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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B13B01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Carcinome</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Carcinoma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Carcinoma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Côlon droit</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Right colon</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Colón derecho</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Réaction chaîne polymérase</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Polymerase chain reaction</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Reacción cadena polimerasa</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Polymorphisme conformation simple brin</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Single strand conformation polymorphism</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Polimorfismo conformación cadena única</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Mutation</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Mutation</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Mutación</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Facteur croissance transformant</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Transforming growth factor</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Factor crecimiento transformante</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Facteur croissance transformant β</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Transforming growth factor β</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Factor crecimiento transformante β</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Récepteur biologique</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Biological receptor</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Receptor biológico</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Protooncogène</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Protooncogene</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Protooncogen</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Gène onc cellulaire</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>C-Onc gene</s0>
<s5>11</s5>
<s6>«C»-Onc gene</s6>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Gen onc celular</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Gène suppresseur tumeur</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Tumor suppressor gene</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Gen supresor tumor</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Gène TP53</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>TP53 Gene</s0>
<s5>13</s5>
<s6>«TP53» Gene</s6>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Gen TP53</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Réplication</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Replication</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Replicación</s0>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Erreur</s0>
<s5>15</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Error</s0>
<s5>15</s5>
</fC03>
<fC03 i1="14" i2="X" l="GER"><s0>Abweichung</s0>
<s5>15</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Error</s0>
<s5>15</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Carcinogenèse</s0>
<s5>17</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>Carcinogenesis</s0>
<s5>17</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>Carcinogénesis</s0>
<s5>17</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE"><s0>Gène K-ras</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE"><s0>Gène APC</s0>
<s4>INC</s4>
<s5>87</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Tumeur maligne</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Malignant tumor</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Tumor maligno</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Appareil digestif pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Digestive diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Aparato digestivo patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Intestin pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Intestinal disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Intestino patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Côlon pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Colonic disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Colón patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Biologie moléculaire</s0>
<s5>45</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Molecular biology</s0>
<s5>45</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Biología molecular</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Facteur croissance</s0>
<s5>53</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Growth factor</s0>
<s5>53</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Factor crecimiento</s0>
<s5>53</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Polypeptide</s0>
<s5>54</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Polypeptide</s0>
<s5>54</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Polipéptido</s0>
<s5>54</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>55</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>55</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>55</s5>
</fC07>
<fN21><s1>153</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 98-0229469 INIST</NO>
<ET>Mutation of the transforming growth factor-β type II receptor gene in right-sided colorectal cancer : Relationship to clinicopathological features and genetic alterations</ET>
<AU>IACOPETTA (B. J.); WELCH (J.); SOONG (R.); HOUSE (A. K.); ZHOU (X.-P.); HAMELIN (R.)</AU>
<AF>Department of Surgery, University of Western Australia/Nedlands 6907/Australie (1 aut., 2 aut., 3 aut., 4 aut.); U434, CEPH, 27 rue Juliette Dodu/75010 Paris/France (5 aut., 6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of pathology; ISSN 0022-3417; Coden JPTLAS; Royaume-Uni; Da. 1998; Vol. 184; No. 4; Pp. 390-395; Bibl. 39 ref.</SO>
<LA>Anglais</LA>
<EA>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 (361210) of right-sided tumours and in 86 per cent (32137) 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.</EA>
<CC>002B13B01</CC>
<FD>Carcinome; Côlon droit; Réaction chaîne polymérase; Polymorphisme conformation simple brin; Mutation; Facteur croissance transformant; Facteur croissance transformant β; Récepteur biologique; Protooncogène; Gène onc cellulaire; Gène suppresseur tumeur; Gène TP53; Réplication; Erreur; Carcinogenèse; Homme; Gène K-ras; Gène APC</FD>
<FG>Tumeur maligne; Appareil digestif pathologie; Intestin pathologie; Côlon pathologie; Biologie moléculaire; Facteur croissance; Polypeptide; Cytokine</FG>
<ED>Carcinoma; Right colon; Polymerase chain reaction; Single strand conformation polymorphism; Mutation; Transforming growth factor; Transforming growth factor β; Biological receptor; Protooncogene; C-Onc gene; Tumor suppressor gene; TP53 Gene; Replication; Error; Carcinogenesis; Human</ED>
<EG>Malignant tumor; Digestive diseases; Intestinal disease; Colonic disease; Molecular biology; Growth factor; Polypeptide; Cytokine</EG>
<GD>Abweichung</GD>
<SD>Carcinoma; Colón derecho; Reacción cadena polimerasa; Polimorfismo conformación cadena única; Mutación; Factor crecimiento transformante; Factor crecimiento transformante β; Receptor biológico; Protooncogen; Gen onc celular; Gen supresor tumor; Gen TP53; Replicación; Error; Carcinogénesis; Hombre</SD>
<LO>INIST-988A.354000079331390050</LO>
<ID>98-0229469</ID>
</server>
</inist>
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Mutation of the transforming growth factor-β type II receptor gene in right-sided colorectal cancer : Relationship to clinicopathological features and genetic alterations

Mutation of the transforming growth factor-β type II receptor gene in right-sided colorectal cancer : Relationship to clinicopathological features and genetic alterations

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