Phosphatase PPM1A is a novel prognostic marker in pancreatic ductal adenocarcinoma
Pancreatic ductal adenocarcinoma (PDAC) harbors complex molecular alterations and remains a lethal disease. Aberrant TGF-β/Smads signaling is a well-known mechanism involved in the progression of PDACs. However, loss of Smad4 expression is reported in only ~ 50% of PDACs and is generally associated...
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| Veröffentlicht in: | Human pathology 2016-09, Vol.55, p.151-158 |
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| creator | Fan, Jie, MD Yang, Michelle X., MD, PhD Ouyang, Qi, MD Fu, Deliang, MD Xu, Zude, MD Liu, Xiuping, MD Mno-Kenudson, Mari, MD Geng, Jiang, MD Tang, Feng, MD, PhD |
| description | Pancreatic ductal adenocarcinoma (PDAC) harbors complex molecular alterations and remains a lethal disease. Aberrant TGF-β/Smads signaling is a well-known mechanism involved in the progression of PDACs. However, loss of Smad4 expression is reported in only ~ 50% of PDACs and is generally associated with worse prognosis. Investigating additional prognostic markers is warranted. PPM1A is a phosphatase that dephosphorylates TGF-β activated Smad2/3 and inactivates the TGF-β signaling. Little is known about the clinical significance of PPM1A in PDACs and its functional relationship with Smad4. In this study, PPM1A and Smad4 immunohistochemistry (IHC) was assessed in 180 R0 resected human PDACs. PPM1A was lost in 41.7% cases, while Smad4 was lost in 45.7% cases. The median survival rate with negative and positive PPM1A was 10.9 and 16.8 months, respectively. Loss of PPM1A was significantly associated with larger tumor size and higher stage and was an independent predictor of unfavorable outcomes. Intriguingly, the overall survival of this cohort was divided into three groups based on the expression pattern of PPM1A and Smad4, with the Smad4 +/PPM1A + pattern associated with favorable survival, the Smad4 +/PPM1A- or Smad4 −/PPM1A- pattern associated with unfavorable, and the PPM1A +/Smad4- pattern fell between these two groups. In 82 cases with negative Smad4, PPM1A or P-Smad2/3 expression was retained. Using SMAD4 -deficient human PDAC cell line, BxPC3, we further demonstrated that TGF-β1 treatment induced PPM1A and P-Smad2/3 expression in this cell line. PPM1A and Smad4 IHC in surgical specimens may provide more accurate prognostic stratification for patients with PDAC. |
| doi_str_mv | 10.1016/j.humpath.2016.05.002 |
| format | Article |
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Aberrant TGF-β/Smads signaling is a well-known mechanism involved in the progression of PDACs. However, loss of Smad4 expression is reported in only ~ 50% of PDACs and is generally associated with worse prognosis. Investigating additional prognostic markers is warranted. PPM1A is a phosphatase that dephosphorylates TGF-β activated Smad2/3 and inactivates the TGF-β signaling. Little is known about the clinical significance of PPM1A in PDACs and its functional relationship with Smad4. In this study, PPM1A and Smad4 immunohistochemistry (IHC) was assessed in 180 R0 resected human PDACs. PPM1A was lost in 41.7% cases, while Smad4 was lost in 45.7% cases. The median survival rate with negative and positive PPM1A was 10.9 and 16.8 months, respectively. Loss of PPM1A was significantly associated with larger tumor size and higher stage and was an independent predictor of unfavorable outcomes. Intriguingly, the overall survival of this cohort was divided into three groups based on the expression pattern of PPM1A and Smad4, with the Smad4 +/PPM1A + pattern associated with favorable survival, the Smad4 +/PPM1A- or Smad4 −/PPM1A- pattern associated with unfavorable, and the PPM1A +/Smad4- pattern fell between these two groups. In 82 cases with negative Smad4, PPM1A or P-Smad2/3 expression was retained. Using SMAD4 -deficient human PDAC cell line, BxPC3, we further demonstrated that TGF-β1 treatment induced PPM1A and P-Smad2/3 expression in this cell line. PPM1A and Smad4 IHC in surgical specimens may provide more accurate prognostic stratification for patients with PDAC.</description><identifier>ISSN: 0046-8177</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1016/j.humpath.2016.05.002</identifier><identifier>PMID: 27195906</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cancer therapies ; Carcinoma, Pancreatic Ductal - enzymology ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - pathology ; Carcinoma, Pancreatic Ductal - surgery ; Cell Line ; Cloning ; Confidence intervals ; Female ; Genomes ; Hospitals ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Male ; Medical prognosis ; Metastasis ; Middle Aged ; Mortality ; Multivariate analysis ; Neoplasm Staging ; Pancreatic ductal adenocarcinoma ; Pancreatic Neoplasms - enzymology ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Pancreatic Neoplasms - surgery ; Pathology ; Phosphatase ; Polymerase chain reaction ; PPM1A ; Prognosis, marker ; Prostate cancer ; Protein Phosphatase 2C - metabolism ; Proteins ; Retrospective Studies ; RNA Interference ; Signal Transduction - drug effects ; Smad2 Protein - metabolism ; Smad3 Protein - metabolism ; Smad4 ; Smad4 Protein - genetics ; Smad4 Protein - metabolism ; Studies ; TGF-β ; Time Factors ; Transfection ; Transforming Growth Factor beta1 - metabolism ; Transforming Growth Factor beta1 - pharmacology ; Tumor Burden ; Tumor Suppressor Proteins - metabolism</subject><ispartof>Human pathology, 2016-09, Vol.55, p.151-158</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Sep 01, 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-ef1cc89139d2206f6820c3ca7e5324855b87d3324066fe65ca2ac5cc2ce4fc533</citedby><cites>FETCH-LOGICAL-c448t-ef1cc89139d2206f6820c3ca7e5324855b87d3324066fe65ca2ac5cc2ce4fc533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0046817716300764$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27195906$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fan, Jie, MD</creatorcontrib><creatorcontrib>Yang, Michelle X., MD, PhD</creatorcontrib><creatorcontrib>Ouyang, Qi, MD</creatorcontrib><creatorcontrib>Fu, Deliang, MD</creatorcontrib><creatorcontrib>Xu, Zude, MD</creatorcontrib><creatorcontrib>Liu, Xiuping, MD</creatorcontrib><creatorcontrib>Mno-Kenudson, Mari, MD</creatorcontrib><creatorcontrib>Geng, Jiang, MD</creatorcontrib><creatorcontrib>Tang, Feng, MD, PhD</creatorcontrib><title>Phosphatase PPM1A is a novel prognostic marker in pancreatic ductal adenocarcinoma</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>Pancreatic ductal adenocarcinoma (PDAC) harbors complex molecular alterations and remains a lethal disease. Aberrant TGF-β/Smads signaling is a well-known mechanism involved in the progression of PDACs. However, loss of Smad4 expression is reported in only ~ 50% of PDACs and is generally associated with worse prognosis. Investigating additional prognostic markers is warranted. PPM1A is a phosphatase that dephosphorylates TGF-β activated Smad2/3 and inactivates the TGF-β signaling. Little is known about the clinical significance of PPM1A in PDACs and its functional relationship with Smad4. In this study, PPM1A and Smad4 immunohistochemistry (IHC) was assessed in 180 R0 resected human PDACs. PPM1A was lost in 41.7% cases, while Smad4 was lost in 45.7% cases. The median survival rate with negative and positive PPM1A was 10.9 and 16.8 months, respectively. Loss of PPM1A was significantly associated with larger tumor size and higher stage and was an independent predictor of unfavorable outcomes. Intriguingly, the overall survival of this cohort was divided into three groups based on the expression pattern of PPM1A and Smad4, with the Smad4 +/PPM1A + pattern associated with favorable survival, the Smad4 +/PPM1A- or Smad4 −/PPM1A- pattern associated with unfavorable, and the PPM1A +/Smad4- pattern fell between these two groups. In 82 cases with negative Smad4, PPM1A or P-Smad2/3 expression was retained. Using SMAD4 -deficient human PDAC cell line, BxPC3, we further demonstrated that TGF-β1 treatment induced PPM1A and P-Smad2/3 expression in this cell line. PPM1A and Smad4 IHC in surgical specimens may provide more accurate prognostic stratification for patients with PDAC.</description><subject>Aged</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cancer therapies</subject><subject>Carcinoma, Pancreatic Ductal - enzymology</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Carcinoma, Pancreatic Ductal - surgery</subject><subject>Cell Line</subject><subject>Cloning</subject><subject>Confidence intervals</subject><subject>Female</subject><subject>Genomes</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Mortality</subject><subject>Multivariate analysis</subject><subject>Neoplasm Staging</subject><subject>Pancreatic ductal adenocarcinoma</subject><subject>Pancreatic Neoplasms - enzymology</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pancreatic Neoplasms - surgery</subject><subject>Pathology</subject><subject>Phosphatase</subject><subject>Polymerase chain reaction</subject><subject>PPM1A</subject><subject>Prognosis, marker</subject><subject>Prostate cancer</subject><subject>Protein Phosphatase 2C - metabolism</subject><subject>Proteins</subject><subject>Retrospective Studies</subject><subject>RNA Interference</subject><subject>Signal Transduction - drug effects</subject><subject>Smad2 Protein - metabolism</subject><subject>Smad3 Protein - metabolism</subject><subject>Smad4</subject><subject>Smad4 Protein - genetics</subject><subject>Smad4 Protein - metabolism</subject><subject>Studies</subject><subject>TGF-β</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Tumor Burden</subject><subject>Tumor Suppressor Proteins - metabolism</subject><issn>0046-8177</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVtv1DAQhS0EokvhJ4Ai8cJLwtiJHecFVFXcpCJWXJ4tdzJhvc3awU4q9d_jaBeQ-sKTL_rmzJwzjD3nUHHg6vW-2i2Hyc67SuRnBbICEA_YhstalLruxEO2AWhUqXnbnrEnKe0BOJeNfMzORMs72YHasK_bXUjTzs42UbHdfuYXhUuFLXy4pbGYYvjpQ5odFgcbbygWzheT9RjJrp_9grMdC9uTD2gjOh8O9il7NNgx0bPTec5-vH_3_fJjefXlw6fLi6sSm0bPJQ0cUXe87nohQA1KC8AabUvZQaOlvNZtX-crKDWQkmiFRYkokJoBZV2fs1dH3Tzlr4XSbA4uIY2j9RSWZLjmoJXSGjL68h66D0v0ebqVEqIVTdtmSh4pjCGlSIOZosu-7wwHs4Zu9uYUullDNyBNDj3XvTipL9cH6v9W_Uk5A2-PAOU4bh1Fk9CRR-pdJJxNH9x_W7y5p4Cj8w7teEN3lP65MUkYMN_Wza-L56oGaFVT_waTZql1</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Fan, Jie, MD</creator><creator>Yang, Michelle X., MD, PhD</creator><creator>Ouyang, Qi, MD</creator><creator>Fu, Deliang, MD</creator><creator>Xu, Zude, MD</creator><creator>Liu, Xiuping, MD</creator><creator>Mno-Kenudson, Mari, MD</creator><creator>Geng, Jiang, MD</creator><creator>Tang, Feng, MD, PhD</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>20160901</creationdate><title>Phosphatase PPM1A is a novel prognostic marker in pancreatic ductal adenocarcinoma</title><author>Fan, Jie, MD ; Yang, Michelle X., MD, PhD ; Ouyang, Qi, MD ; Fu, Deliang, MD ; Xu, Zude, MD ; Liu, Xiuping, MD ; Mno-Kenudson, Mari, MD ; Geng, Jiang, MD ; Tang, Feng, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-ef1cc89139d2206f6820c3ca7e5324855b87d3324066fe65ca2ac5cc2ce4fc533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cancer therapies</topic><topic>Carcinoma, Pancreatic Ductal - enzymology</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Carcinoma, Pancreatic Ductal - surgery</topic><topic>Cell Line</topic><topic>Cloning</topic><topic>Confidence intervals</topic><topic>Female</topic><topic>Genomes</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Mortality</topic><topic>Multivariate analysis</topic><topic>Neoplasm Staging</topic><topic>Pancreatic ductal adenocarcinoma</topic><topic>Pancreatic Neoplasms - enzymology</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pancreatic Neoplasms - surgery</topic><topic>Pathology</topic><topic>Phosphatase</topic><topic>Polymerase chain reaction</topic><topic>PPM1A</topic><topic>Prognosis, marker</topic><topic>Prostate cancer</topic><topic>Protein Phosphatase 2C - metabolism</topic><topic>Proteins</topic><topic>Retrospective Studies</topic><topic>RNA Interference</topic><topic>Signal Transduction - drug effects</topic><topic>Smad2 Protein - metabolism</topic><topic>Smad3 Protein - metabolism</topic><topic>Smad4</topic><topic>Smad4 Protein - genetics</topic><topic>Smad4 Protein - metabolism</topic><topic>Studies</topic><topic>TGF-β</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Tumor Burden</topic><topic>Tumor Suppressor Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fan, Jie, MD</creatorcontrib><creatorcontrib>Yang, Michelle X., MD, PhD</creatorcontrib><creatorcontrib>Ouyang, Qi, MD</creatorcontrib><creatorcontrib>Fu, Deliang, MD</creatorcontrib><creatorcontrib>Xu, Zude, MD</creatorcontrib><creatorcontrib>Liu, Xiuping, MD</creatorcontrib><creatorcontrib>Mno-Kenudson, Mari, MD</creatorcontrib><creatorcontrib>Geng, Jiang, MD</creatorcontrib><creatorcontrib>Tang, Feng, MD, PhD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fan, Jie, MD</au><au>Yang, Michelle X., MD, PhD</au><au>Ouyang, Qi, MD</au><au>Fu, Deliang, MD</au><au>Xu, Zude, MD</au><au>Liu, Xiuping, MD</au><au>Mno-Kenudson, Mari, MD</au><au>Geng, Jiang, MD</au><au>Tang, Feng, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Phosphatase PPM1A is a novel prognostic marker in pancreatic ductal adenocarcinoma</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>55</volume><spage>151</spage><epage>158</epage><pages>151-158</pages><issn>0046-8177</issn><eissn>1532-8392</eissn><abstract>Pancreatic ductal adenocarcinoma (PDAC) harbors complex molecular alterations and remains a lethal disease. Aberrant TGF-β/Smads signaling is a well-known mechanism involved in the progression of PDACs. However, loss of Smad4 expression is reported in only ~ 50% of PDACs and is generally associated with worse prognosis. Investigating additional prognostic markers is warranted. PPM1A is a phosphatase that dephosphorylates TGF-β activated Smad2/3 and inactivates the TGF-β signaling. Little is known about the clinical significance of PPM1A in PDACs and its functional relationship with Smad4. In this study, PPM1A and Smad4 immunohistochemistry (IHC) was assessed in 180 R0 resected human PDACs. PPM1A was lost in 41.7% cases, while Smad4 was lost in 45.7% cases. The median survival rate with negative and positive PPM1A was 10.9 and 16.8 months, respectively. Loss of PPM1A was significantly associated with larger tumor size and higher stage and was an independent predictor of unfavorable outcomes. Intriguingly, the overall survival of this cohort was divided into three groups based on the expression pattern of PPM1A and Smad4, with the Smad4 +/PPM1A + pattern associated with favorable survival, the Smad4 +/PPM1A- or Smad4 −/PPM1A- pattern associated with unfavorable, and the PPM1A +/Smad4- pattern fell between these two groups. In 82 cases with negative Smad4, PPM1A or P-Smad2/3 expression was retained. Using SMAD4 -deficient human PDAC cell line, BxPC3, we further demonstrated that TGF-β1 treatment induced PPM1A and P-Smad2/3 expression in this cell line. PPM1A and Smad4 IHC in surgical specimens may provide more accurate prognostic stratification for patients with PDAC.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27195906</pmid><doi>10.1016/j.humpath.2016.05.002</doi><tpages>8</tpages></addata></record> |
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| subjects | Aged Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cancer therapies Carcinoma, Pancreatic Ductal - enzymology Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Carcinoma, Pancreatic Ductal - surgery Cell Line Cloning Confidence intervals Female Genomes Hospitals Humans Immunohistochemistry Kaplan-Meier Estimate Male Medical prognosis Metastasis Middle Aged Mortality Multivariate analysis Neoplasm Staging Pancreatic ductal adenocarcinoma Pancreatic Neoplasms - enzymology Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Pancreatic Neoplasms - surgery Pathology Phosphatase Polymerase chain reaction PPM1A Prognosis, marker Prostate cancer Protein Phosphatase 2C - metabolism Proteins Retrospective Studies RNA Interference Signal Transduction - drug effects Smad2 Protein - metabolism Smad3 Protein - metabolism Smad4 Smad4 Protein - genetics Smad4 Protein - metabolism Studies TGF-β Time Factors Transfection Transforming Growth Factor beta1 - metabolism Transforming Growth Factor beta1 - pharmacology Tumor Burden Tumor Suppressor Proteins - metabolism |
| title | Phosphatase PPM1A is a novel prognostic marker in pancreatic ductal adenocarcinoma |
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