Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas
Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/β-catenin signalling. Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours. Sixty adenomas from six FAP patients with...
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| Veröffentlicht in: | The Journal of pathology 2010-05, Vol.221 (1), p.57-67 |
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| creator | Obrador-Hevia, Antònia Chin, Suet-Feung González, Sara Rees, Jonathan Vilardell, Felip Greenson, Joel K Cordero, David Moreno, Víctor Caldas, Carlos Capellá, Gabriel |
| description | Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/β-catenin signalling. Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours. Sixty adenomas from six FAP patients with known pathogenic APC mutations were included. Somatic APC and KRAS mutations, β-catenin immunostaining, and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analysed. Array-comparative genomic hybridization (aCGH) was also assessed in 26 FAP adenomas and 24 paired adenoma-carcinoma samples. A somatic APC alteration was present in 15 adenomas (LOH in 11 and four point mutations). KRAS mutations were detected in 10% of the cases. APC mRNA was overexpressed in adenomas. MYC and AXIN2 were also overexpressed, with significant intra-case heterogeneity. Increased cytoplasmic and/or nuclear β-catenin staining was seen in 94% and 80% of the adenomas. β-Catenin nuclear staining was strongly associated with MYC levels (p value 0.03) but not with KRAS mutations. Copy number aberrations were rare. However, the recurrent chromosome changes observed more frequently contained Wnt pathway genes (p value 0.012). Based on β-catenin staining and Wnt pathway target genes alterations the Wnt pathway appears to be constitutively activated in all APC-FAP tumours, with alterations occurring both upstream and downstream of APC. Wnt aberrations are present at both the DNA and the RNA level. Somatic profiling of APC-FAP tumours provides new insights into the role of APC in tumourigenesis. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| doi_str_mv | 10.1002/path.2685 |
| format | Article |
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Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours. Sixty adenomas from six FAP patients with known pathogenic APC mutations were included. Somatic APC and KRAS mutations, β-catenin immunostaining, and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analysed. Array-comparative genomic hybridization (aCGH) was also assessed in 26 FAP adenomas and 24 paired adenoma-carcinoma samples. A somatic APC alteration was present in 15 adenomas (LOH in 11 and four point mutations). KRAS mutations were detected in 10% of the cases. APC mRNA was overexpressed in adenomas. MYC and AXIN2 were also overexpressed, with significant intra-case heterogeneity. Increased cytoplasmic and/or nuclear β-catenin staining was seen in 94% and 80% of the adenomas. β-Catenin nuclear staining was strongly associated with MYC levels (p value 0.03) but not with KRAS mutations. Copy number aberrations were rare. However, the recurrent chromosome changes observed more frequently contained Wnt pathway genes (p value 0.012). Based on β-catenin staining and Wnt pathway target genes alterations the Wnt pathway appears to be constitutively activated in all APC-FAP tumours, with alterations occurring both upstream and downstream of APC. Wnt aberrations are present at both the DNA and the RNA level. Somatic profiling of APC-FAP tumours provides new insights into the role of APC in tumourigenesis. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><identifier>ISSN: 0022-3417</identifier><identifier>EISSN: 1096-9896</identifier><identifier>DOI: 10.1002/path.2685</identifier><identifier>PMID: 20196079</identifier><identifier>CODEN: JPTLAS</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Adenoma ; Adenomatous Polyposis Coli - genetics ; Adenomatous Polyposis Coli - metabolism ; Adenomatous Polyposis Coli Protein - biosynthesis ; Adenomatous Polyposis Coli Protein - genetics ; Adult ; APC ; beta Catenin - metabolism ; Biological and medical sciences ; catenin ; Cell Nucleus - metabolism ; Chromosomes ; colorectal cancer ; Comparative Genomic Hybridization ; copy number ; DNA ; Familial adenomatous polyposis ; Female ; Frizzled-related protein 1 ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Genes, APC ; Genetic Predisposition to Disease ; genomic profiling ; genomics ; Germ-Line Mutation ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; K-Ras protein ; Loss of Heterozygosity ; Male ; Medical sciences ; mRNA ; Myc protein ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Point mutation ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins p21(ras) ; ras Proteins - genetics ; ras Proteins - physiology ; Signal transduction ; Signal Transduction - physiology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumorigenesis ; Tumors ; Wnt protein ; Wnt Proteins - physiology ; Wnt signalling ; Young Adult</subject><ispartof>The Journal of pathology, 2010-05, Vol.221 (1), p.57-67</ispartof><rights>Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright (c) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4835-cbc18935ed027f5848d22b8d1fbb82e0354b4675743ec7b3b9324856a897c5743</citedby><cites>FETCH-LOGICAL-c4835-cbc18935ed027f5848d22b8d1fbb82e0354b4675743ec7b3b9324856a897c5743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpath.2685$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpath.2685$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22758548$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20196079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Obrador-Hevia, Antònia</creatorcontrib><creatorcontrib>Chin, Suet-Feung</creatorcontrib><creatorcontrib>González, Sara</creatorcontrib><creatorcontrib>Rees, Jonathan</creatorcontrib><creatorcontrib>Vilardell, Felip</creatorcontrib><creatorcontrib>Greenson, Joel K</creatorcontrib><creatorcontrib>Cordero, David</creatorcontrib><creatorcontrib>Moreno, Víctor</creatorcontrib><creatorcontrib>Caldas, Carlos</creatorcontrib><creatorcontrib>Capellá, Gabriel</creatorcontrib><title>Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas</title><title>The Journal of pathology</title><addtitle>J. Pathol</addtitle><description>Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/β-catenin signalling. Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours. Sixty adenomas from six FAP patients with known pathogenic APC mutations were included. Somatic APC and KRAS mutations, β-catenin immunostaining, and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analysed. Array-comparative genomic hybridization (aCGH) was also assessed in 26 FAP adenomas and 24 paired adenoma-carcinoma samples. A somatic APC alteration was present in 15 adenomas (LOH in 11 and four point mutations). KRAS mutations were detected in 10% of the cases. APC mRNA was overexpressed in adenomas. MYC and AXIN2 were also overexpressed, with significant intra-case heterogeneity. Increased cytoplasmic and/or nuclear β-catenin staining was seen in 94% and 80% of the adenomas. β-Catenin nuclear staining was strongly associated with MYC levels (p value 0.03) but not with KRAS mutations. Copy number aberrations were rare. However, the recurrent chromosome changes observed more frequently contained Wnt pathway genes (p value 0.012). Based on β-catenin staining and Wnt pathway target genes alterations the Wnt pathway appears to be constitutively activated in all APC-FAP tumours, with alterations occurring both upstream and downstream of APC. Wnt aberrations are present at both the DNA and the RNA level. Somatic profiling of APC-FAP tumours provides new insights into the role of APC in tumourigenesis. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><subject>Adenoma</subject><subject>Adenomatous Polyposis Coli - genetics</subject><subject>Adenomatous Polyposis Coli - metabolism</subject><subject>Adenomatous Polyposis Coli Protein - biosynthesis</subject><subject>Adenomatous Polyposis Coli Protein - genetics</subject><subject>Adult</subject><subject>APC</subject><subject>beta Catenin - metabolism</subject><subject>Biological and medical sciences</subject><subject>catenin</subject><subject>Cell Nucleus - metabolism</subject><subject>Chromosomes</subject><subject>colorectal cancer</subject><subject>Comparative Genomic Hybridization</subject><subject>copy number</subject><subject>DNA</subject><subject>Familial adenomatous polyposis</subject><subject>Female</subject><subject>Frizzled-related protein 1</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, APC</subject><subject>Genetic Predisposition to Disease</subject><subject>genomic profiling</subject><subject>genomics</subject><subject>Germ-Line Mutation</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>K-Ras protein</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>mRNA</subject><subject>Myc protein</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Point mutation</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins p21(ras)</subject><subject>ras Proteins - genetics</subject><subject>ras Proteins - physiology</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Wnt protein</subject><subject>Wnt Proteins - physiology</subject><subject>Wnt signalling</subject><subject>Young Adult</subject><issn>0022-3417</issn><issn>1096-9896</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0E1rFDEYB_Agil1XD34BzUXEw7R5mbwdp6ttxWIXt6UXIWQymTU6m6zJrNpvb5ZZ60mEQCD5PS_8AXiO0TFGiJxszfjlmHDJHoAZRopXSir-EMzKH6lojcUReJLzV4SQUow9BkcEYcWRUDPw-SrYuHbBW_jhU7OCPsMQRxicdTmbdAf7mOBtGGH262CGwYc1NHb0P8zoY4A-wGa5qEzO0Xozug6eNUtoOhfixuSn4FFvhuyeHe45uDl7d724qC6vzt8vmsvK1pKyyrYWS0WZ6xARPZO17AhpZYf7tpXEIcrqtuaCiZo6K1raKkpqybiRStj96xy8nvpuU_y-c3nUG5-tGwYTXNxlrZDAnCL6fykoxbIcXOSbSdoUc06u19vkNyURjZHep673qet96sW-OHTdtRvX3cs_MRfw6gBMtmbokwnW57-OCCZZyWIOTib30w_u7t8T9bK5vjiMrqYKn0f3677CpG-aCyqYvv14rk9PV0jh5UK_Lf7l5HsTtVmnssXNquxJEZaEYyLpb9ZUr2I</recordid><startdate>201005</startdate><enddate>201005</enddate><creator>Obrador-Hevia, Antònia</creator><creator>Chin, Suet-Feung</creator><creator>González, Sara</creator><creator>Rees, Jonathan</creator><creator>Vilardell, Felip</creator><creator>Greenson, Joel K</creator><creator>Cordero, David</creator><creator>Moreno, Víctor</creator><creator>Caldas, Carlos</creator><creator>Capellá, Gabriel</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</general><scope>FBQ</scope><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>201005</creationdate><title>Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas</title><author>Obrador-Hevia, Antònia ; Chin, Suet-Feung ; González, Sara ; Rees, Jonathan ; Vilardell, Felip ; Greenson, Joel K ; Cordero, David ; Moreno, Víctor ; Caldas, Carlos ; Capellá, Gabriel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4835-cbc18935ed027f5848d22b8d1fbb82e0354b4675743ec7b3b9324856a897c5743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adenoma</topic><topic>Adenomatous Polyposis Coli - genetics</topic><topic>Adenomatous Polyposis Coli - metabolism</topic><topic>Adenomatous Polyposis Coli Protein - biosynthesis</topic><topic>Adenomatous Polyposis Coli Protein - genetics</topic><topic>Adult</topic><topic>APC</topic><topic>beta Catenin - metabolism</topic><topic>Biological and medical sciences</topic><topic>catenin</topic><topic>Cell Nucleus - metabolism</topic><topic>Chromosomes</topic><topic>colorectal cancer</topic><topic>Comparative Genomic Hybridization</topic><topic>copy number</topic><topic>DNA</topic><topic>Familial adenomatous polyposis</topic><topic>Female</topic><topic>Frizzled-related protein 1</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, APC</topic><topic>Genetic Predisposition to Disease</topic><topic>genomic profiling</topic><topic>genomics</topic><topic>Germ-Line Mutation</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>K-Ras protein</topic><topic>Loss of Heterozygosity</topic><topic>Male</topic><topic>Medical sciences</topic><topic>mRNA</topic><topic>Myc protein</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Point mutation</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>ras Proteins - genetics</topic><topic>ras Proteins - physiology</topic><topic>Signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>Stomach. Duodenum. Small intestine. Colon. 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Pathol</addtitle><date>2010-05</date><risdate>2010</risdate><volume>221</volume><issue>1</issue><spage>57</spage><epage>67</epage><pages>57-67</pages><issn>0022-3417</issn><eissn>1096-9896</eissn><coden>JPTLAS</coden><abstract>Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/β-catenin signalling. Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours. Sixty adenomas from six FAP patients with known pathogenic APC mutations were included. Somatic APC and KRAS mutations, β-catenin immunostaining, and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analysed. Array-comparative genomic hybridization (aCGH) was also assessed in 26 FAP adenomas and 24 paired adenoma-carcinoma samples. A somatic APC alteration was present in 15 adenomas (LOH in 11 and four point mutations). KRAS mutations were detected in 10% of the cases. APC mRNA was overexpressed in adenomas. MYC and AXIN2 were also overexpressed, with significant intra-case heterogeneity. Increased cytoplasmic and/or nuclear β-catenin staining was seen in 94% and 80% of the adenomas. β-Catenin nuclear staining was strongly associated with MYC levels (p value 0.03) but not with KRAS mutations. Copy number aberrations were rare. However, the recurrent chromosome changes observed more frequently contained Wnt pathway genes (p value 0.012). Based on β-catenin staining and Wnt pathway target genes alterations the Wnt pathway appears to be constitutively activated in all APC-FAP tumours, with alterations occurring both upstream and downstream of APC. Wnt aberrations are present at both the DNA and the RNA level. Somatic profiling of APC-FAP tumours provides new insights into the role of APC in tumourigenesis. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>20196079</pmid><doi>10.1002/path.2685</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of pathology, 2010-05, Vol.221 (1), p.57-67 |
| issn | 0022-3417 1096-9896 |
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| subjects | Adenoma Adenomatous Polyposis Coli - genetics Adenomatous Polyposis Coli - metabolism Adenomatous Polyposis Coli Protein - biosynthesis Adenomatous Polyposis Coli Protein - genetics Adult APC beta Catenin - metabolism Biological and medical sciences catenin Cell Nucleus - metabolism Chromosomes colorectal cancer Comparative Genomic Hybridization copy number DNA Familial adenomatous polyposis Female Frizzled-related protein 1 Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Genes, APC Genetic Predisposition to Disease genomic profiling genomics Germ-Line Mutation Humans Investigative techniques, diagnostic techniques (general aspects) K-Ras protein Loss of Heterozygosity Male Medical sciences mRNA Myc protein Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Point mutation Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins p21(ras) ras Proteins - genetics ras Proteins - physiology Signal transduction Signal Transduction - physiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumorigenesis Tumors Wnt protein Wnt Proteins - physiology Wnt signalling Young Adult |
| title | Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas |
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