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Decreased E-cadherin expression correlates with higher stage of Wilms' tumors
The aim of this study was to examine the association between E-cadherin expression and markers of Wilms' tumor aggression, including metastasis and recurrence. Forty Wilms' tumor samples from the National Wilms' Tumor Study Group underwent immunohistochemical staining for E-cadherin....
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| Published in: | Journal of pediatric surgery 2005-02, Vol.40 (2), p.341-348 |
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| container_end_page | 348 |
| container_issue | 2 |
| container_start_page | 341 |
| container_title | Journal of pediatric surgery |
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| creator | Safford, Shawn D. Freemerman, Alex J. Langdon, Scott Bentley, Rex Goyeau, Dominique Grundy, Paul E. Skinner, Michael A. |
| description | The aim of this study was to examine the association between E-cadherin expression and markers of Wilms' tumor aggression, including metastasis and recurrence.
Forty Wilms' tumor samples from the National Wilms' Tumor Study Group underwent immunohistochemical staining for E-cadherin. Tumor stage at diagnosis, recurrence, and loss of heterozygosity at 16q status was known for each of the tumor samples. E-Cadherin cell staining was defined as high (>33%) or low ( |
| doi_str_mv | 10.1016/j.jpedsurg.2004.10.030 |
| format | article |
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Forty Wilms' tumor samples from the National Wilms' Tumor Study Group underwent immunohistochemical staining for E-cadherin. Tumor stage at diagnosis, recurrence, and loss of heterozygosity at 16q status was known for each of the tumor samples. E-Cadherin cell staining was defined as high (>33%) or low (<33%), and values were assigned by a pathologist blinded to the tumor characteristics. Five stage IV tumors were ineligible for assay because of lack of a tubular component. To identify a mechanism of downregulation, we screened tumor DNA for genetic mutations in exons 1-16 using a combination of WAVE and sequence analysis. To assess the functional significance of the identified mutations, the authors compared amino acid homology across multiple species. Finally, they performed reverse transcriptase–polymerase chain reaction for those tumors with intronic single nucleotide polymorphisms (SNPs) to evaluate for mRNA splice variants.
Wilms' tumors presenting with metastatic (stage IV) disease demonstrated decreased levels of E-cadherin expression compared with localized tumors (stage I) (Fisher's Exact test,
P < .01). In a search for the mechanism of the downregulation of E-cadherin, we identified 5 different mutations in 7 high stage tumors (7/15) and 1 mutation in a low stage tumor (1/20). The mutations occurred in amino acids that were conserved across multiple species. Additionally, 11 of 15 high stage tumors contained an intronic SNP located within 6 bp of the 5′ intronic splice junction immediately downstream of exon 1. However, examination of 5 of these tumors using reverse transcriptase–polymerase chain reaction showed that this intronic SNP does not appear to disrupt the assembly of full-length E-cadherin transcripts. Lastly, no correlation was identified between E-cadherin expression and recurrence of disease.
In this study, the authors have found an association between decreased E-cadherin expression and metastatic Wilms' tumor. Mutations identified may help identify a mechanism for downregulation. The functional significance of these mutations is supported by the conserved nature of the amino acids across multiple species. The authors believe these findings support the involvement of E-cadherin in the evolution of Wilms' tumor.</description><identifier>ISSN: 0022-3468</identifier><identifier>EISSN: 1531-5037</identifier><identifier>DOI: 10.1016/j.jpedsurg.2004.10.030</identifier><identifier>PMID: 15750927</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Cadherins - analysis ; Cadherins - biosynthesis ; Cadherins - genetics ; Cell Adhesion ; Child ; Chromatography, High Pressure Liquid - methods ; Chromosomes, Human, Pair 16 ; DNA Mutational Analysis ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Humans ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Loss of Heterozygosity ; Neoplasm Metastasis - genetics ; Neoplasm Recurrence, Local - genetics ; Neoplasm Staging ; Polymorphism, Single Nucleotide ; RNA, Messenger - analysis ; Wilms Tumor - genetics ; Wilms Tumor - metabolism ; Wilms Tumor - pathology</subject><ispartof>Journal of pediatric surgery, 2005-02, Vol.40 (2), p.341-348</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c366t-4cfdbfef653b8b7f2c1b853643cb35d9629faeead7f0fadc0baaad6a25bc01753</citedby><cites>FETCH-LOGICAL-c366t-4cfdbfef653b8b7f2c1b853643cb35d9629faeead7f0fadc0baaad6a25bc01753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15750927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Safford, Shawn D.</creatorcontrib><creatorcontrib>Freemerman, Alex J.</creatorcontrib><creatorcontrib>Langdon, Scott</creatorcontrib><creatorcontrib>Bentley, Rex</creatorcontrib><creatorcontrib>Goyeau, Dominique</creatorcontrib><creatorcontrib>Grundy, Paul E.</creatorcontrib><creatorcontrib>Skinner, Michael A.</creatorcontrib><title>Decreased E-cadherin expression correlates with higher stage of Wilms' tumors</title><title>Journal of pediatric surgery</title><addtitle>J Pediatr Surg</addtitle><description>The aim of this study was to examine the association between E-cadherin expression and markers of Wilms' tumor aggression, including metastasis and recurrence.
Forty Wilms' tumor samples from the National Wilms' Tumor Study Group underwent immunohistochemical staining for E-cadherin. Tumor stage at diagnosis, recurrence, and loss of heterozygosity at 16q status was known for each of the tumor samples. E-Cadherin cell staining was defined as high (>33%) or low (<33%), and values were assigned by a pathologist blinded to the tumor characteristics. Five stage IV tumors were ineligible for assay because of lack of a tubular component. To identify a mechanism of downregulation, we screened tumor DNA for genetic mutations in exons 1-16 using a combination of WAVE and sequence analysis. To assess the functional significance of the identified mutations, the authors compared amino acid homology across multiple species. Finally, they performed reverse transcriptase–polymerase chain reaction for those tumors with intronic single nucleotide polymorphisms (SNPs) to evaluate for mRNA splice variants.
Wilms' tumors presenting with metastatic (stage IV) disease demonstrated decreased levels of E-cadherin expression compared with localized tumors (stage I) (Fisher's Exact test,
P < .01). In a search for the mechanism of the downregulation of E-cadherin, we identified 5 different mutations in 7 high stage tumors (7/15) and 1 mutation in a low stage tumor (1/20). The mutations occurred in amino acids that were conserved across multiple species. Additionally, 11 of 15 high stage tumors contained an intronic SNP located within 6 bp of the 5′ intronic splice junction immediately downstream of exon 1. However, examination of 5 of these tumors using reverse transcriptase–polymerase chain reaction showed that this intronic SNP does not appear to disrupt the assembly of full-length E-cadherin transcripts. Lastly, no correlation was identified between E-cadherin expression and recurrence of disease.
In this study, the authors have found an association between decreased E-cadherin expression and metastatic Wilms' tumor. Mutations identified may help identify a mechanism for downregulation. The functional significance of these mutations is supported by the conserved nature of the amino acids across multiple species. The authors believe these findings support the involvement of E-cadherin in the evolution of Wilms' tumor.</description><subject>Cadherins - analysis</subject><subject>Cadherins - biosynthesis</subject><subject>Cadherins - genetics</subject><subject>Cell Adhesion</subject><subject>Child</subject><subject>Chromatography, High Pressure Liquid - methods</subject><subject>Chromosomes, Human, Pair 16</subject><subject>DNA Mutational Analysis</subject><subject>Down-Regulation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Loss of Heterozygosity</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Neoplasm Staging</subject><subject>Polymorphism, Single Nucleotide</subject><subject>RNA, Messenger - analysis</subject><subject>Wilms Tumor - genetics</subject><subject>Wilms Tumor - metabolism</subject><subject>Wilms Tumor - pathology</subject><issn>0022-3468</issn><issn>1531-5037</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkMFu2zAMhoWiRZOmfYVAp_Vkl7IsObmtSLt1QIteNuwoyBKVKLDjTLS39e3nIBl67InAj-8nwY-xuYBcgNB323y7R09DWucFQDmGOUg4Y1OhpMgUyOqcTQGKIpOlXkzYFdEWYIxBXLKJUJWCZVFN2csDuoSW0PPHzFm_wRR3HP_uExLFbsddlxI2tkfif2K_4Zu4HhlOvV0j7wL_GZuWbnk_tF2ia3YRbEN4c5oz9uPL4_fVU_b8-vXb6v45c1LrPitd8HXAoJWsF3UVCifqhZK6lK6Wyi91sQwW0foqQLDeQW2t9doWqnYgKiVn7NNx7z51vwak3rSRHDaN3WE3kNFVuVhqWY2gPoIudUQJg9mn2Nr0ZgSYg0izNf9FmoPIQz6KHIvz04WhbtG_107mRuDzEcDxz98RkyEXcefQx4SuN76LH934B77bigM</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>Safford, Shawn D.</creator><creator>Freemerman, Alex J.</creator><creator>Langdon, Scott</creator><creator>Bentley, Rex</creator><creator>Goyeau, Dominique</creator><creator>Grundy, Paul E.</creator><creator>Skinner, Michael A.</creator><general>Elsevier Inc</general><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></search><sort><creationdate>20050201</creationdate><title>Decreased E-cadherin expression correlates with higher stage of Wilms' tumors</title><author>Safford, Shawn D. ; Freemerman, Alex J. ; Langdon, Scott ; Bentley, Rex ; Goyeau, Dominique ; Grundy, Paul E. ; Skinner, Michael A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c366t-4cfdbfef653b8b7f2c1b853643cb35d9629faeead7f0fadc0baaad6a25bc01753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Cadherins - analysis</topic><topic>Cadherins - biosynthesis</topic><topic>Cadherins - genetics</topic><topic>Cell Adhesion</topic><topic>Child</topic><topic>Chromatography, High Pressure Liquid - methods</topic><topic>Chromosomes, Human, Pair 16</topic><topic>DNA Mutational Analysis</topic><topic>Down-Regulation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>Loss of Heterozygosity</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Neoplasm Recurrence, Local - genetics</topic><topic>Neoplasm Staging</topic><topic>Polymorphism, Single Nucleotide</topic><topic>RNA, Messenger - analysis</topic><topic>Wilms Tumor - genetics</topic><topic>Wilms Tumor - metabolism</topic><topic>Wilms Tumor - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Safford, Shawn D.</creatorcontrib><creatorcontrib>Freemerman, Alex J.</creatorcontrib><creatorcontrib>Langdon, Scott</creatorcontrib><creatorcontrib>Bentley, Rex</creatorcontrib><creatorcontrib>Goyeau, Dominique</creatorcontrib><creatorcontrib>Grundy, Paul E.</creatorcontrib><creatorcontrib>Skinner, Michael A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of pediatric surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Safford, Shawn D.</au><au>Freemerman, Alex J.</au><au>Langdon, Scott</au><au>Bentley, Rex</au><au>Goyeau, Dominique</au><au>Grundy, Paul E.</au><au>Skinner, Michael A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decreased E-cadherin expression correlates with higher stage of Wilms' tumors</atitle><jtitle>Journal of pediatric surgery</jtitle><addtitle>J Pediatr Surg</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>40</volume><issue>2</issue><spage>341</spage><epage>348</epage><pages>341-348</pages><issn>0022-3468</issn><eissn>1531-5037</eissn><abstract>The aim of this study was to examine the association between E-cadherin expression and markers of Wilms' tumor aggression, including metastasis and recurrence.
Forty Wilms' tumor samples from the National Wilms' Tumor Study Group underwent immunohistochemical staining for E-cadherin. Tumor stage at diagnosis, recurrence, and loss of heterozygosity at 16q status was known for each of the tumor samples. E-Cadherin cell staining was defined as high (>33%) or low (<33%), and values were assigned by a pathologist blinded to the tumor characteristics. Five stage IV tumors were ineligible for assay because of lack of a tubular component. To identify a mechanism of downregulation, we screened tumor DNA for genetic mutations in exons 1-16 using a combination of WAVE and sequence analysis. To assess the functional significance of the identified mutations, the authors compared amino acid homology across multiple species. Finally, they performed reverse transcriptase–polymerase chain reaction for those tumors with intronic single nucleotide polymorphisms (SNPs) to evaluate for mRNA splice variants.
Wilms' tumors presenting with metastatic (stage IV) disease demonstrated decreased levels of E-cadherin expression compared with localized tumors (stage I) (Fisher's Exact test,
P < .01). In a search for the mechanism of the downregulation of E-cadherin, we identified 5 different mutations in 7 high stage tumors (7/15) and 1 mutation in a low stage tumor (1/20). The mutations occurred in amino acids that were conserved across multiple species. Additionally, 11 of 15 high stage tumors contained an intronic SNP located within 6 bp of the 5′ intronic splice junction immediately downstream of exon 1. However, examination of 5 of these tumors using reverse transcriptase–polymerase chain reaction showed that this intronic SNP does not appear to disrupt the assembly of full-length E-cadherin transcripts. Lastly, no correlation was identified between E-cadherin expression and recurrence of disease.
In this study, the authors have found an association between decreased E-cadherin expression and metastatic Wilms' tumor. Mutations identified may help identify a mechanism for downregulation. The functional significance of these mutations is supported by the conserved nature of the amino acids across multiple species. The authors believe these findings support the involvement of E-cadherin in the evolution of Wilms' tumor.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15750927</pmid><doi>10.1016/j.jpedsurg.2004.10.030</doi><tpages>8</tpages></addata></record> |
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| subjects | Cadherins - analysis Cadherins - biosynthesis Cadherins - genetics Cell Adhesion Child Chromatography, High Pressure Liquid - methods Chromosomes, Human, Pair 16 DNA Mutational Analysis Down-Regulation Gene Expression Regulation, Neoplastic Humans Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Loss of Heterozygosity Neoplasm Metastasis - genetics Neoplasm Recurrence, Local - genetics Neoplasm Staging Polymorphism, Single Nucleotide RNA, Messenger - analysis Wilms Tumor - genetics Wilms Tumor - metabolism Wilms Tumor - pathology |
| title | Decreased E-cadherin expression correlates with higher stage of Wilms' tumors |
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