Ampulla of Vater Carcinoma: Sequencing Analysis Identifies TP53 Status as a Novel Independent Prognostic Factor and Potentially Actionable ERBB, PI3K, and WNT Pathways Gene Mutations
OBJECTIVE:To identify molecular prognostic factors and potentially actionable mutations in ampulla of Vater cancer (AVC). BACKGROUND:The largely variable outcomes of AVCs make clinical decisions difficult regarding the need of postsurgical therapy, which is based on morphological and immunohistochem...
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| Veröffentlicht in: | Annals of surgery 2018-01, Vol.267 (1), p.149-156 |
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| creator | Mafficini, Andrea Amato, Eliana Cataldo, Ivana Rusev, Borislav C Bertoncello, Luca Corbo, Vincenzo Simbolo, Michele Luchini, Claudio Fassan, Matteo Cantù, Cinzia Salvia, Roberto Marchegiani, Giovanni Tortora, Giampaolo Lawlor, Rita T Bassi, Claudio Scarpa, Aldo |
| description | OBJECTIVE:To identify molecular prognostic factors and potentially actionable mutations in ampulla of Vater cancer (AVC).
BACKGROUND:The largely variable outcomes of AVCs make clinical decisions difficult regarding the need of postsurgical therapy, which is based on morphological and immunohistochemical classification that do not adequately consider the varying degrees of heterogeneity present in many AVCs. No approved targeted therapies for AVC exist, but some show promising results requiring better molecular characterization to identify potential responders.
METHODS:We assessed 80 AVCs for the prognostic value of mutations of kirsten rat sarcoma (KRAS), neuroblastoma RAS (NRAS), B rapidly accelerated fibrosarcoma (BRAF), TP53, and 4 membrane erythroblastosis oncogene B (ERBB) receptor tyrosine kinases (EGFR-ERBB1, HER2-ERBB2, HER3-ERBB3, HER4-ERBB4) amenable to pharmacological inhibition. Moreover, we evaluated mutations in 16 key components of rat sarcoma (RAS), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), protein 53 (P53), transforming growth factor beta (TGF-β), and wingless/integrated (WNT) pathways, recently associated to AVC by whole-exome sequencing.
RESULTS:TP53 and KRAS were mutated in 41% and 35% of cases, respectively, and emerged as independent prognostic factors together with tumor stage and regardless of the histotype (TP53P = 0.0006; KRASP = 0.0018; stage IIBP = 0.0117; stage III–IVP = 0.0020). ERBB, WNT and PI3K pathway genes were mutated in 37.5% of cases.
CONCLUSIONS:KRAS and TP53 mutations are negative predictors of survival in AVCs, regardless of histotype. Potentially actionable mutations in ERBB, WNT, and PI3K signaling pathway genes are present in 37.5% of all cases. These might be amenable to target therapy using available drugs like Everolimus in PI3K-mutated cases or compounds under active screening against ERBB and WNT signaling. |
| doi_str_mv | 10.1097/SLA.0000000000001999 |
| format | Article |
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BACKGROUND:The largely variable outcomes of AVCs make clinical decisions difficult regarding the need of postsurgical therapy, which is based on morphological and immunohistochemical classification that do not adequately consider the varying degrees of heterogeneity present in many AVCs. No approved targeted therapies for AVC exist, but some show promising results requiring better molecular characterization to identify potential responders.
METHODS:We assessed 80 AVCs for the prognostic value of mutations of kirsten rat sarcoma (KRAS), neuroblastoma RAS (NRAS), B rapidly accelerated fibrosarcoma (BRAF), TP53, and 4 membrane erythroblastosis oncogene B (ERBB) receptor tyrosine kinases (EGFR-ERBB1, HER2-ERBB2, HER3-ERBB3, HER4-ERBB4) amenable to pharmacological inhibition. Moreover, we evaluated mutations in 16 key components of rat sarcoma (RAS), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), protein 53 (P53), transforming growth factor beta (TGF-β), and wingless/integrated (WNT) pathways, recently associated to AVC by whole-exome sequencing.
RESULTS:TP53 and KRAS were mutated in 41% and 35% of cases, respectively, and emerged as independent prognostic factors together with tumor stage and regardless of the histotype (TP53P = 0.0006; KRASP = 0.0018; stage IIBP = 0.0117; stage III–IVP = 0.0020). ERBB, WNT and PI3K pathway genes were mutated in 37.5% of cases.
CONCLUSIONS:KRAS and TP53 mutations are negative predictors of survival in AVCs, regardless of histotype. Potentially actionable mutations in ERBB, WNT, and PI3K signaling pathway genes are present in 37.5% of all cases. These might be amenable to target therapy using available drugs like Everolimus in PI3K-mutated cases or compounds under active screening against ERBB and WNT signaling.</description><identifier>ISSN: 0003-4932</identifier><identifier>EISSN: 1528-1140</identifier><identifier>DOI: 10.1097/SLA.0000000000001999</identifier><identifier>PMID: 27611608</identifier><language>eng</language><publisher>United States: Copyright Wolters Kluwer Health, Inc. All rights reserved</publisher><subject>Ampulla of Vater ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Common Bile Duct Neoplasms - diagnosis ; Common Bile Duct Neoplasms - genetics ; Common Bile Duct Neoplasms - metabolism ; DNA Mutational Analysis ; DNA, Neoplasm - genetics ; Female ; Humans ; Male ; Middle Aged ; Mutation ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Prognosis ; Receptor, ErbB-3 - genetics ; Receptor, ErbB-3 - metabolism ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Wnt Signaling Pathway - genetics</subject><ispartof>Annals of surgery, 2018-01, Vol.267 (1), p.149-156</ispartof><rights>Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2869-6a1aa2dae3f9c32746aa89ae6bb430e2f9e8d16653532ff4abaea33a4e0d9d33</citedby><cites>FETCH-LOGICAL-c2869-6a1aa2dae3f9c32746aa89ae6bb430e2f9e8d16653532ff4abaea33a4e0d9d33</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/27611608$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mafficini, Andrea</creatorcontrib><creatorcontrib>Amato, Eliana</creatorcontrib><creatorcontrib>Cataldo, Ivana</creatorcontrib><creatorcontrib>Rusev, Borislav C</creatorcontrib><creatorcontrib>Bertoncello, Luca</creatorcontrib><creatorcontrib>Corbo, Vincenzo</creatorcontrib><creatorcontrib>Simbolo, Michele</creatorcontrib><creatorcontrib>Luchini, Claudio</creatorcontrib><creatorcontrib>Fassan, Matteo</creatorcontrib><creatorcontrib>Cantù, Cinzia</creatorcontrib><creatorcontrib>Salvia, Roberto</creatorcontrib><creatorcontrib>Marchegiani, Giovanni</creatorcontrib><creatorcontrib>Tortora, Giampaolo</creatorcontrib><creatorcontrib>Lawlor, Rita T</creatorcontrib><creatorcontrib>Bassi, Claudio</creatorcontrib><creatorcontrib>Scarpa, Aldo</creatorcontrib><title>Ampulla of Vater Carcinoma: Sequencing Analysis Identifies TP53 Status as a Novel Independent Prognostic Factor and Potentially Actionable ERBB, PI3K, and WNT Pathways Gene Mutations</title><title>Annals of surgery</title><addtitle>Ann Surg</addtitle><description>OBJECTIVE:To identify molecular prognostic factors and potentially actionable mutations in ampulla of Vater cancer (AVC).
BACKGROUND:The largely variable outcomes of AVCs make clinical decisions difficult regarding the need of postsurgical therapy, which is based on morphological and immunohistochemical classification that do not adequately consider the varying degrees of heterogeneity present in many AVCs. No approved targeted therapies for AVC exist, but some show promising results requiring better molecular characterization to identify potential responders.
METHODS:We assessed 80 AVCs for the prognostic value of mutations of kirsten rat sarcoma (KRAS), neuroblastoma RAS (NRAS), B rapidly accelerated fibrosarcoma (BRAF), TP53, and 4 membrane erythroblastosis oncogene B (ERBB) receptor tyrosine kinases (EGFR-ERBB1, HER2-ERBB2, HER3-ERBB3, HER4-ERBB4) amenable to pharmacological inhibition. Moreover, we evaluated mutations in 16 key components of rat sarcoma (RAS), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), protein 53 (P53), transforming growth factor beta (TGF-β), and wingless/integrated (WNT) pathways, recently associated to AVC by whole-exome sequencing.
RESULTS:TP53 and KRAS were mutated in 41% and 35% of cases, respectively, and emerged as independent prognostic factors together with tumor stage and regardless of the histotype (TP53P = 0.0006; KRASP = 0.0018; stage IIBP = 0.0117; stage III–IVP = 0.0020). ERBB, WNT and PI3K pathway genes were mutated in 37.5% of cases.
CONCLUSIONS:KRAS and TP53 mutations are negative predictors of survival in AVCs, regardless of histotype. Potentially actionable mutations in ERBB, WNT, and PI3K signaling pathway genes are present in 37.5% of all cases. These might be amenable to target therapy using available drugs like Everolimus in PI3K-mutated cases or compounds under active screening against ERBB and WNT signaling.</description><subject>Ampulla of Vater</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Common Bile Duct Neoplasms - diagnosis</subject><subject>Common Bile Duct Neoplasms - genetics</subject><subject>Common Bile Duct Neoplasms - metabolism</subject><subject>DNA Mutational Analysis</subject><subject>DNA, Neoplasm - genetics</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Prognosis</subject><subject>Receptor, ErbB-3 - genetics</subject><subject>Receptor, ErbB-3 - metabolism</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Wnt Signaling Pathway - genetics</subject><issn>0003-4932</issn><issn>1528-1140</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kduO0zAQhiMEYsvCGyA0l1xsljjOydxlqz1UlCWiFVxGk2SyDTh213ao-mL7fLh0QYgLLEvWWN_8I80XBK9ZdM4ikb9bLcvz6K_DhBBPghlL4yJkLImeBjP_y8NE8PgkeGHtN88kRZQ_D07iPGMsi4pZ8FCO20lKBN3DF3RkYI6mHZQe8T2s6H4i5as7KBXKvR0sLDpSbugHsrCuUg4rh26ygP7Crf5BEhaqoy2pAweV0XdKWze0cIWt0wZQdVBpdwhBKfdQtm7QChtJcPn54uIMqgX_cPYL-3q7hgrdZod7C9ekCD5OfprH7cvgWY_S0qvH9zRYX12u5zfh8tP1Yl4uwzYuMhFmyBDjDon3ouVxnmSIhUDKmibhEcW9oKJjWZbylMd9n2CDhJxjQlEnOs5Pg7fH2K3RfhXW1eNgW_L7UqQnW7MiFXkcFUns0eSItkZba6ivt2YY0exrFtUHYbUXVv8rzLe9eZwwNSN1f5p-G_JAcQR2Wno99rucdmTqDaF0m_9n_wSoW6OS</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Mafficini, Andrea</creator><creator>Amato, Eliana</creator><creator>Cataldo, Ivana</creator><creator>Rusev, Borislav C</creator><creator>Bertoncello, Luca</creator><creator>Corbo, Vincenzo</creator><creator>Simbolo, Michele</creator><creator>Luchini, Claudio</creator><creator>Fassan, Matteo</creator><creator>Cantù, Cinzia</creator><creator>Salvia, Roberto</creator><creator>Marchegiani, Giovanni</creator><creator>Tortora, Giampaolo</creator><creator>Lawlor, Rita T</creator><creator>Bassi, Claudio</creator><creator>Scarpa, Aldo</creator><general>Copyright Wolters Kluwer Health, Inc. All rights reserved</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>201801</creationdate><title>Ampulla of Vater Carcinoma: Sequencing Analysis Identifies TP53 Status as a Novel Independent Prognostic Factor and Potentially Actionable ERBB, PI3K, and WNT Pathways Gene Mutations</title><author>Mafficini, Andrea ; Amato, Eliana ; Cataldo, Ivana ; Rusev, Borislav C ; Bertoncello, Luca ; Corbo, Vincenzo ; Simbolo, Michele ; Luchini, Claudio ; Fassan, Matteo ; Cantù, Cinzia ; Salvia, Roberto ; Marchegiani, Giovanni ; Tortora, Giampaolo ; Lawlor, Rita T ; Bassi, Claudio ; Scarpa, Aldo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2869-6a1aa2dae3f9c32746aa89ae6bb430e2f9e8d16653532ff4abaea33a4e0d9d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Ampulla of Vater</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Common Bile Duct Neoplasms - diagnosis</topic><topic>Common Bile Duct Neoplasms - genetics</topic><topic>Common Bile Duct Neoplasms - metabolism</topic><topic>DNA Mutational Analysis</topic><topic>DNA, Neoplasm - genetics</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Prognosis</topic><topic>Receptor, ErbB-3 - genetics</topic><topic>Receptor, ErbB-3 - metabolism</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Wnt Signaling Pathway - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mafficini, Andrea</creatorcontrib><creatorcontrib>Amato, Eliana</creatorcontrib><creatorcontrib>Cataldo, Ivana</creatorcontrib><creatorcontrib>Rusev, Borislav C</creatorcontrib><creatorcontrib>Bertoncello, Luca</creatorcontrib><creatorcontrib>Corbo, Vincenzo</creatorcontrib><creatorcontrib>Simbolo, Michele</creatorcontrib><creatorcontrib>Luchini, Claudio</creatorcontrib><creatorcontrib>Fassan, Matteo</creatorcontrib><creatorcontrib>Cantù, Cinzia</creatorcontrib><creatorcontrib>Salvia, Roberto</creatorcontrib><creatorcontrib>Marchegiani, Giovanni</creatorcontrib><creatorcontrib>Tortora, Giampaolo</creatorcontrib><creatorcontrib>Lawlor, Rita T</creatorcontrib><creatorcontrib>Bassi, Claudio</creatorcontrib><creatorcontrib>Scarpa, Aldo</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>Annals of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mafficini, Andrea</au><au>Amato, Eliana</au><au>Cataldo, Ivana</au><au>Rusev, Borislav C</au><au>Bertoncello, Luca</au><au>Corbo, Vincenzo</au><au>Simbolo, Michele</au><au>Luchini, Claudio</au><au>Fassan, Matteo</au><au>Cantù, Cinzia</au><au>Salvia, Roberto</au><au>Marchegiani, Giovanni</au><au>Tortora, Giampaolo</au><au>Lawlor, Rita T</au><au>Bassi, Claudio</au><au>Scarpa, Aldo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ampulla of Vater Carcinoma: Sequencing Analysis Identifies TP53 Status as a Novel Independent Prognostic Factor and Potentially Actionable ERBB, PI3K, and WNT Pathways Gene Mutations</atitle><jtitle>Annals of surgery</jtitle><addtitle>Ann Surg</addtitle><date>2018-01</date><risdate>2018</risdate><volume>267</volume><issue>1</issue><spage>149</spage><epage>156</epage><pages>149-156</pages><issn>0003-4932</issn><eissn>1528-1140</eissn><abstract>OBJECTIVE:To identify molecular prognostic factors and potentially actionable mutations in ampulla of Vater cancer (AVC).
BACKGROUND:The largely variable outcomes of AVCs make clinical decisions difficult regarding the need of postsurgical therapy, which is based on morphological and immunohistochemical classification that do not adequately consider the varying degrees of heterogeneity present in many AVCs. No approved targeted therapies for AVC exist, but some show promising results requiring better molecular characterization to identify potential responders.
METHODS:We assessed 80 AVCs for the prognostic value of mutations of kirsten rat sarcoma (KRAS), neuroblastoma RAS (NRAS), B rapidly accelerated fibrosarcoma (BRAF), TP53, and 4 membrane erythroblastosis oncogene B (ERBB) receptor tyrosine kinases (EGFR-ERBB1, HER2-ERBB2, HER3-ERBB3, HER4-ERBB4) amenable to pharmacological inhibition. Moreover, we evaluated mutations in 16 key components of rat sarcoma (RAS), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), protein 53 (P53), transforming growth factor beta (TGF-β), and wingless/integrated (WNT) pathways, recently associated to AVC by whole-exome sequencing.
RESULTS:TP53 and KRAS were mutated in 41% and 35% of cases, respectively, and emerged as independent prognostic factors together with tumor stage and regardless of the histotype (TP53P = 0.0006; KRASP = 0.0018; stage IIBP = 0.0117; stage III–IVP = 0.0020). ERBB, WNT and PI3K pathway genes were mutated in 37.5% of cases.
CONCLUSIONS:KRAS and TP53 mutations are negative predictors of survival in AVCs, regardless of histotype. Potentially actionable mutations in ERBB, WNT, and PI3K signaling pathway genes are present in 37.5% of all cases. These might be amenable to target therapy using available drugs like Everolimus in PI3K-mutated cases or compounds under active screening against ERBB and WNT signaling.</abstract><cop>United States</cop><pub>Copyright Wolters Kluwer Health, Inc. All rights reserved</pub><pmid>27611608</pmid><doi>10.1097/SLA.0000000000001999</doi><tpages>8</tpages></addata></record> |
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| subjects | Ampulla of Vater Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Common Bile Duct Neoplasms - diagnosis Common Bile Duct Neoplasms - genetics Common Bile Duct Neoplasms - metabolism DNA Mutational Analysis DNA, Neoplasm - genetics Female Humans Male Middle Aged Mutation Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Prognosis Receptor, ErbB-3 - genetics Receptor, ErbB-3 - metabolism Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Wnt Signaling Pathway - genetics |
| title | Ampulla of Vater Carcinoma: Sequencing Analysis Identifies TP53 Status as a Novel Independent Prognostic Factor and Potentially Actionable ERBB, PI3K, and WNT Pathways Gene Mutations |
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