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Loss of PTEN Expression Is Associated with Poor Prognosis in Patients with Intraductal Papillary Mucinous Neoplasms of the Pancreas
Previously, we reported PIK3CA gene mutations in high-grade intraductal papillary mucinous neoplasms (IPMN). However, the contribution of phosphatidylinositol-3 kinase pathway (PI3K) dysregulation to pancreatic carcinogenesis is not fully understood and its prognostic value unknown. We investigated...
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| Published in: | Clinical cancer research 2013-12, Vol.19 (24), p.6830-6841 |
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| container_title | Clinical cancer research |
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| creator | GARCIA-CARRACEDO, Dario TURK, Andrew T SU, Gloria H FINE, Stuart A AKHAVAN, Nathan TWEEL, Benjamin C PARSONS, Ramon CHABOT, John A ALLENDORF, John D GENKINGER, Jeanine M REMOTTI, Helen E |
| description | Previously, we reported PIK3CA gene mutations in high-grade intraductal papillary mucinous neoplasms (IPMN). However, the contribution of phosphatidylinositol-3 kinase pathway (PI3K) dysregulation to pancreatic carcinogenesis is not fully understood and its prognostic value unknown. We investigated the dysregulation of the PI3K signaling pathway in IPMN and its clinical implication.
Thirty-six IPMN specimens were examined by novel mutant-enriched sequencing methods for hot-spot mutations in the PIK3CA and AKT1 genes. PIK3CA and AKT1 gene amplifications and loss of heterozygosity at the PTEN locus were also evaluated. In addition, the expression levels of PDPK1/PDK1, PTEN, and Ki67 were analyzed by immunohistochemistry.
Three cases carrying the E17K mutation in the AKT1 gene and one case harboring the H1047R mutation in the PIK3CA gene were detected among the 36 cases. PDK1 was significantly overexpressed in the high-grade IPMN versus low-grade IPMN (P = 0.034) and in pancreatic and intestinal-type of IPMN versus gastric-type of IPMN (P = 0.020). Loss of PTEN expression was strongly associated with presence of invasive carcinoma and poor survival in these IPMN patients (P = 0.014).
This is the first report of AKT1 mutations in IPMN. Our data indicate that oncogenic activation of the PI3K pathway can contribute to the progression of IPMN, in particular loss of PTEN expression. This finding suggests the potential employment of PI3K pathway-targeted therapies for IPMN patients. The incorporation of PTEN expression status in making surgical decisions may also benefit IPMN patients and should warrant further investigation. |
| doi_str_mv | 10.1158/1078-0432.CCR-13-0624 |
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Thirty-six IPMN specimens were examined by novel mutant-enriched sequencing methods for hot-spot mutations in the PIK3CA and AKT1 genes. PIK3CA and AKT1 gene amplifications and loss of heterozygosity at the PTEN locus were also evaluated. In addition, the expression levels of PDPK1/PDK1, PTEN, and Ki67 were analyzed by immunohistochemistry.
Three cases carrying the E17K mutation in the AKT1 gene and one case harboring the H1047R mutation in the PIK3CA gene were detected among the 36 cases. PDK1 was significantly overexpressed in the high-grade IPMN versus low-grade IPMN (P = 0.034) and in pancreatic and intestinal-type of IPMN versus gastric-type of IPMN (P = 0.020). Loss of PTEN expression was strongly associated with presence of invasive carcinoma and poor survival in these IPMN patients (P = 0.014).
This is the first report of AKT1 mutations in IPMN. Our data indicate that oncogenic activation of the PI3K pathway can contribute to the progression of IPMN, in particular loss of PTEN expression. This finding suggests the potential employment of PI3K pathway-targeted therapies for IPMN patients. The incorporation of PTEN expression status in making surgical decisions may also benefit IPMN patients and should warrant further investigation.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-13-0624</identifier><identifier>PMID: 24132918</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Antineoplastic agents ; Biological and medical sciences ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - pathology ; Carcinoma, Papillary - genetics ; Carcinoma, Papillary - pathology ; Class I Phosphatidylinositol 3-Kinases ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Mutation ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Pharmacology. Drug treatments ; Phosphatidylinositol 3-Kinases - biosynthesis ; Prognosis ; PTEN Phosphohydrolase - biosynthesis ; PTEN Phosphohydrolase - genetics ; Signal Transduction - genetics ; Tumors</subject><ispartof>Clinical cancer research, 2013-12, Vol.19 (24), p.6830-6841</ispartof><rights>2015 INIST-CNRS</rights><rights>2013 AACR.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-508bf16872d095dff2885327a58af6171003927d62a3ebf619ed8ae7d59ddcb93</citedby><cites>FETCH-LOGICAL-c441t-508bf16872d095dff2885327a58af6171003927d62a3ebf619ed8ae7d59ddcb93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,783,787,888,27936,27937</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28044866$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24132918$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GARCIA-CARRACEDO, Dario</creatorcontrib><creatorcontrib>TURK, Andrew T</creatorcontrib><creatorcontrib>SU, Gloria H</creatorcontrib><creatorcontrib>FINE, Stuart A</creatorcontrib><creatorcontrib>AKHAVAN, Nathan</creatorcontrib><creatorcontrib>TWEEL, Benjamin C</creatorcontrib><creatorcontrib>PARSONS, Ramon</creatorcontrib><creatorcontrib>CHABOT, John A</creatorcontrib><creatorcontrib>ALLENDORF, John D</creatorcontrib><creatorcontrib>GENKINGER, Jeanine M</creatorcontrib><creatorcontrib>REMOTTI, Helen E</creatorcontrib><title>Loss of PTEN Expression Is Associated with Poor Prognosis in Patients with Intraductal Papillary Mucinous Neoplasms of the Pancreas</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Previously, we reported PIK3CA gene mutations in high-grade intraductal papillary mucinous neoplasms (IPMN). However, the contribution of phosphatidylinositol-3 kinase pathway (PI3K) dysregulation to pancreatic carcinogenesis is not fully understood and its prognostic value unknown. We investigated the dysregulation of the PI3K signaling pathway in IPMN and its clinical implication.
Thirty-six IPMN specimens were examined by novel mutant-enriched sequencing methods for hot-spot mutations in the PIK3CA and AKT1 genes. PIK3CA and AKT1 gene amplifications and loss of heterozygosity at the PTEN locus were also evaluated. In addition, the expression levels of PDPK1/PDK1, PTEN, and Ki67 were analyzed by immunohistochemistry.
Three cases carrying the E17K mutation in the AKT1 gene and one case harboring the H1047R mutation in the PIK3CA gene were detected among the 36 cases. PDK1 was significantly overexpressed in the high-grade IPMN versus low-grade IPMN (P = 0.034) and in pancreatic and intestinal-type of IPMN versus gastric-type of IPMN (P = 0.020). Loss of PTEN expression was strongly associated with presence of invasive carcinoma and poor survival in these IPMN patients (P = 0.014).
This is the first report of AKT1 mutations in IPMN. Our data indicate that oncogenic activation of the PI3K pathway can contribute to the progression of IPMN, in particular loss of PTEN expression. This finding suggests the potential employment of PI3K pathway-targeted therapies for IPMN patients. The incorporation of PTEN expression status in making surgical decisions may also benefit IPMN patients and should warrant further investigation.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Carcinoma, Papillary - genetics</subject><subject>Carcinoma, Papillary - pathology</subject><subject>Class I Phosphatidylinositol 3-Kinases</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Mutation</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphatidylinositol 3-Kinases - biosynthesis</subject><subject>Prognosis</subject><subject>PTEN Phosphohydrolase - biosynthesis</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>Signal Transduction - genetics</subject><subject>Tumors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNpVUU1v1DAQtRCIlsJPAPnCMcXjj8S5IFWrLay0tCtUzpbXdrpG2TjyZKGc-eM4bFvoySO_jxm9R8hbYOcASn8A1uiKScHPF4uvFYiK1Vw-I6egVFMJXqvnZX7gnJBXiN8ZAwlMviQnXILgLehT8nudEGnq6OZmeUWXd2MOiDENdIX0AjG5aKfg6c847egmpUw3Od0OCSPSONCNnWIYJjziq2HK1h_cZPuCjLHvbf5FvxxcHNIB6VVIY29x_3fdtAuFM7gcLL4mLzrbY3hz_56Rb5fLm8Xnan39abW4WFdOSpgqxfS2g1o33LNW-a7jWivBG6u07WpogDHR8sbX3IqwLT9t8NqGxqvWe7dtxRn5ePQdD9t98C7M9_ZmzHFfDjXJRvMUGeLO3KYfRrSgGK-LgToauFxSy6F71AIzcytmTtzMiZvSigFh5laK7t3_ix9VDzUUwvt7gkVn-y6XZCL-42kmpa5r8Qcvq5iT</recordid><startdate>20131215</startdate><enddate>20131215</enddate><creator>GARCIA-CARRACEDO, Dario</creator><creator>TURK, Andrew T</creator><creator>SU, Gloria H</creator><creator>FINE, Stuart A</creator><creator>AKHAVAN, Nathan</creator><creator>TWEEL, Benjamin C</creator><creator>PARSONS, Ramon</creator><creator>CHABOT, John A</creator><creator>ALLENDORF, John D</creator><creator>GENKINGER, Jeanine M</creator><creator>REMOTTI, Helen E</creator><general>American Association for Cancer Research</general><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>5PM</scope></search><sort><creationdate>20131215</creationdate><title>Loss of PTEN Expression Is Associated with Poor Prognosis in Patients with Intraductal Papillary Mucinous Neoplasms of the Pancreas</title><author>GARCIA-CARRACEDO, Dario ; TURK, Andrew T ; SU, Gloria H ; FINE, Stuart A ; AKHAVAN, Nathan ; TWEEL, Benjamin C ; PARSONS, Ramon ; CHABOT, John A ; ALLENDORF, John D ; GENKINGER, Jeanine M ; REMOTTI, Helen E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-508bf16872d095dff2885327a58af6171003927d62a3ebf619ed8ae7d59ddcb93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Carcinoma, Papillary - genetics</topic><topic>Carcinoma, Papillary - pathology</topic><topic>Class I Phosphatidylinositol 3-Kinases</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Mutation</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphatidylinositol 3-Kinases - biosynthesis</topic><topic>Prognosis</topic><topic>PTEN Phosphohydrolase - biosynthesis</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>Signal Transduction - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GARCIA-CARRACEDO, Dario</creatorcontrib><creatorcontrib>TURK, Andrew T</creatorcontrib><creatorcontrib>SU, Gloria H</creatorcontrib><creatorcontrib>FINE, Stuart A</creatorcontrib><creatorcontrib>AKHAVAN, Nathan</creatorcontrib><creatorcontrib>TWEEL, Benjamin C</creatorcontrib><creatorcontrib>PARSONS, Ramon</creatorcontrib><creatorcontrib>CHABOT, John A</creatorcontrib><creatorcontrib>ALLENDORF, John D</creatorcontrib><creatorcontrib>GENKINGER, Jeanine M</creatorcontrib><creatorcontrib>REMOTTI, Helen E</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GARCIA-CARRACEDO, Dario</au><au>TURK, Andrew T</au><au>SU, Gloria H</au><au>FINE, Stuart A</au><au>AKHAVAN, Nathan</au><au>TWEEL, Benjamin C</au><au>PARSONS, Ramon</au><au>CHABOT, John A</au><au>ALLENDORF, John D</au><au>GENKINGER, Jeanine M</au><au>REMOTTI, Helen E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of PTEN Expression Is Associated with Poor Prognosis in Patients with Intraductal Papillary Mucinous Neoplasms of the Pancreas</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2013-12-15</date><risdate>2013</risdate><volume>19</volume><issue>24</issue><spage>6830</spage><epage>6841</epage><pages>6830-6841</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Previously, we reported PIK3CA gene mutations in high-grade intraductal papillary mucinous neoplasms (IPMN). However, the contribution of phosphatidylinositol-3 kinase pathway (PI3K) dysregulation to pancreatic carcinogenesis is not fully understood and its prognostic value unknown. We investigated the dysregulation of the PI3K signaling pathway in IPMN and its clinical implication.
Thirty-six IPMN specimens were examined by novel mutant-enriched sequencing methods for hot-spot mutations in the PIK3CA and AKT1 genes. PIK3CA and AKT1 gene amplifications and loss of heterozygosity at the PTEN locus were also evaluated. In addition, the expression levels of PDPK1/PDK1, PTEN, and Ki67 were analyzed by immunohistochemistry.
Three cases carrying the E17K mutation in the AKT1 gene and one case harboring the H1047R mutation in the PIK3CA gene were detected among the 36 cases. PDK1 was significantly overexpressed in the high-grade IPMN versus low-grade IPMN (P = 0.034) and in pancreatic and intestinal-type of IPMN versus gastric-type of IPMN (P = 0.020). Loss of PTEN expression was strongly associated with presence of invasive carcinoma and poor survival in these IPMN patients (P = 0.014).
This is the first report of AKT1 mutations in IPMN. Our data indicate that oncogenic activation of the PI3K pathway can contribute to the progression of IPMN, in particular loss of PTEN expression. This finding suggests the potential employment of PI3K pathway-targeted therapies for IPMN patients. The incorporation of PTEN expression status in making surgical decisions may also benefit IPMN patients and should warrant further investigation.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>24132918</pmid><doi>10.1158/1078-0432.CCR-13-0624</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Antineoplastic agents Biological and medical sciences Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Carcinoma, Papillary - genetics Carcinoma, Papillary - pathology Class I Phosphatidylinositol 3-Kinases Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Humans Immunohistochemistry Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Mutation Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Pharmacology. Drug treatments Phosphatidylinositol 3-Kinases - biosynthesis Prognosis PTEN Phosphohydrolase - biosynthesis PTEN Phosphohydrolase - genetics Signal Transduction - genetics Tumors |
| title | Loss of PTEN Expression Is Associated with Poor Prognosis in Patients with Intraductal Papillary Mucinous Neoplasms of the Pancreas |
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