Hepatitis A virus cellular receptor 1 / kidney injury molecule-1 is a susceptibility gene for clear cell renal cell carcinoma and hepatitis A virus cellular receptor/kidney injury molecule-1 ectodomain shedding a predictive biomarker of tumour progression
Abstract Aim of the study To correlate hepatitis A virus cellular receptor (HAVCR)/kidney injury molecule-1 (KIM-1) expression in clear cell renal cell carcinoma (ccRCC) tumours with patient outcome and study the consequences of HAVCR/KIM-1 ectodomain shedding. Methods HAVCR/KIM-1 expression in ccRC...
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creator | Cuadros, Thaïs Trilla, Enric Vilà, Maria Rosa de Torres, Inés Vilardell, Jordi Messaoud, Nabil Ben Salcedo, Mayte Sarró, Eduard López-Hellin, Joan Blanco, Albert Mir, Carmen Ramón y Cajal, Santiago Itarte, Emilio Morote, Juan Meseguer, Anna |
description | Abstract Aim of the study To correlate hepatitis A virus cellular receptor (HAVCR)/kidney injury molecule-1 (KIM-1) expression in clear cell renal cell carcinoma (ccRCC) tumours with patient outcome and study the consequences of HAVCR/KIM-1 ectodomain shedding. Methods HAVCR/KIM-1 expression in ccRCC, oncocytomes, papillary carcinomas and unaffected tissue counterparts was evaluated. Minimal change disease and pre-clamping normal and ccRCC tissue biopsies were included. Tissue microarrays from 98 ccRCC tumours were analysed. Tumour registry data and patient outcome were retrospectivelly collected. Deletions in HAVCR/KIM-1 ectodomain and lentiviral infection of 786-O cells with HAVCR/KIM-1 mutated constructs to determine their subcellular distribution and invasive capacity were performed. Results HAVCR/KIM-1 was expressed in ccRCC, papillary tumours and in tubule cells of adjacent and distal unaffected counterparts of ccRCC tumours. The latest was not related to ischemic or tumour-related paracrine effects since pre-clamping normal biopsies were positive for HAVCR/KIM-1 and unaffected counterparts of papillary tumours were negative. HAVCR/KIM-1 analyses in patients and the invasive capacity of HAVCR/KIM-1 shedding mutants in cell lines demonstrated that: (i) relative low HAVCR/KIM-1 membrane levels correlate with activated shedding in ccRCC patients and mutant cell lines; (ii) augmented shedding directly correlates with higher invasiveness and tumour malignancy. Concluding statements Constitutive expression of HAVCR/KIM-1 in kidney might constitute a susceptibility trait for ccRCC tumour development. Enhanced HAVCR/KIM-1 ectodomain shedding promotes invasive phenotype in vitro and more aggressive tumours in vivo. |
doi_str_mv | 10.1016/j.ejca.2012.12.020 |
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Methods HAVCR/KIM-1 expression in ccRCC, oncocytomes, papillary carcinomas and unaffected tissue counterparts was evaluated. Minimal change disease and pre-clamping normal and ccRCC tissue biopsies were included. Tissue microarrays from 98 ccRCC tumours were analysed. Tumour registry data and patient outcome were retrospectivelly collected. Deletions in HAVCR/KIM-1 ectodomain and lentiviral infection of 786-O cells with HAVCR/KIM-1 mutated constructs to determine their subcellular distribution and invasive capacity were performed. Results HAVCR/KIM-1 was expressed in ccRCC, papillary tumours and in tubule cells of adjacent and distal unaffected counterparts of ccRCC tumours. The latest was not related to ischemic or tumour-related paracrine effects since pre-clamping normal biopsies were positive for HAVCR/KIM-1 and unaffected counterparts of papillary tumours were negative. HAVCR/KIM-1 analyses in patients and the invasive capacity of HAVCR/KIM-1 shedding mutants in cell lines demonstrated that: (i) relative low HAVCR/KIM-1 membrane levels correlate with activated shedding in ccRCC patients and mutant cell lines; (ii) augmented shedding directly correlates with higher invasiveness and tumour malignancy. Concluding statements Constitutive expression of HAVCR/KIM-1 in kidney might constitute a susceptibility trait for ccRCC tumour development. Enhanced HAVCR/KIM-1 ectodomain shedding promotes invasive phenotype in vitro and more aggressive tumours in vivo.</description><identifier>ISSN: 0959-8049</identifier><identifier>EISSN: 1879-0852</identifier><identifier>DOI: 10.1016/j.ejca.2012.12.020</identifier><identifier>PMID: 23352434</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Binding Sites - genetics ; Biological and medical sciences ; Biomarker ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Blotting, Western ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - pathology ; Cell Line, Tumor ; Clear cell renal cell carcinoma (ccRCC) ; Disease Progression ; Female ; Genetic Predisposition to Disease - genetics ; HEK293 Cells ; Hematology, Oncology and Palliative Medicine ; Hepatitis A virus ; Hepatitis A Virus Cellular Receptor 1 ; hHAVcr-1 ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Kidney - metabolism ; Kidney - pathology ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Kidney tumours ; KIM-1 ; Male ; Medical sciences ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; Microscopy, Fluorescence ; Middle Aged ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Multivariate Analysis ; Mutation ; Pharmacology. Drug treatments ; Prognosis ; Receptors, Virus - genetics ; Receptors, Virus - metabolism ; Retrospective Studies ; Tumors ; Tumour progression</subject><ispartof>European journal of cancer (1990), 2013-05, Vol.49 (8), p.2034-2047</ispartof><rights>Elsevier Ltd</rights><rights>2013 Elsevier Ltd</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-697d9db2a1ac307b33edd4b2af2b8e37a769c5fde5009108094d2fd2a990a4293</citedby><cites>FETCH-LOGICAL-c507t-697d9db2a1ac307b33edd4b2af2b8e37a769c5fde5009108094d2fd2a990a4293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0959804912010295$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27285876$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23352434$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cuadros, Thaïs</creatorcontrib><creatorcontrib>Trilla, Enric</creatorcontrib><creatorcontrib>Vilà, Maria Rosa</creatorcontrib><creatorcontrib>de Torres, Inés</creatorcontrib><creatorcontrib>Vilardell, Jordi</creatorcontrib><creatorcontrib>Messaoud, Nabil Ben</creatorcontrib><creatorcontrib>Salcedo, Mayte</creatorcontrib><creatorcontrib>Sarró, Eduard</creatorcontrib><creatorcontrib>López-Hellin, Joan</creatorcontrib><creatorcontrib>Blanco, Albert</creatorcontrib><creatorcontrib>Mir, Carmen</creatorcontrib><creatorcontrib>Ramón y Cajal, Santiago</creatorcontrib><creatorcontrib>Itarte, Emilio</creatorcontrib><creatorcontrib>Morote, Juan</creatorcontrib><creatorcontrib>Meseguer, Anna</creatorcontrib><title>Hepatitis A virus cellular receptor 1 / kidney injury molecule-1 is a susceptibility gene for clear cell renal cell carcinoma and hepatitis A virus cellular receptor/kidney injury molecule-1 ectodomain shedding a predictive biomarker of tumour progression</title><title>European journal of cancer (1990)</title><addtitle>Eur J Cancer</addtitle><description>Abstract Aim of the study To correlate hepatitis A virus cellular receptor (HAVCR)/kidney injury molecule-1 (KIM-1) expression in clear cell renal cell carcinoma (ccRCC) tumours with patient outcome and study the consequences of HAVCR/KIM-1 ectodomain shedding. Methods HAVCR/KIM-1 expression in ccRCC, oncocytomes, papillary carcinomas and unaffected tissue counterparts was evaluated. Minimal change disease and pre-clamping normal and ccRCC tissue biopsies were included. Tissue microarrays from 98 ccRCC tumours were analysed. Tumour registry data and patient outcome were retrospectivelly collected. Deletions in HAVCR/KIM-1 ectodomain and lentiviral infection of 786-O cells with HAVCR/KIM-1 mutated constructs to determine their subcellular distribution and invasive capacity were performed. Results HAVCR/KIM-1 was expressed in ccRCC, papillary tumours and in tubule cells of adjacent and distal unaffected counterparts of ccRCC tumours. The latest was not related to ischemic or tumour-related paracrine effects since pre-clamping normal biopsies were positive for HAVCR/KIM-1 and unaffected counterparts of papillary tumours were negative. HAVCR/KIM-1 analyses in patients and the invasive capacity of HAVCR/KIM-1 shedding mutants in cell lines demonstrated that: (i) relative low HAVCR/KIM-1 membrane levels correlate with activated shedding in ccRCC patients and mutant cell lines; (ii) augmented shedding directly correlates with higher invasiveness and tumour malignancy. Concluding statements Constitutive expression of HAVCR/KIM-1 in kidney might constitute a susceptibility trait for ccRCC tumour development. Enhanced HAVCR/KIM-1 ectodomain shedding promotes invasive phenotype in vitro and more aggressive tumours in vivo.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Binding Sites - genetics</subject><subject>Biological and medical sciences</subject><subject>Biomarker</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Blotting, Western</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Clear cell renal cell carcinoma (ccRCC)</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>HEK293 Cells</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Hepatitis A virus</subject><subject>Hepatitis A Virus Cellular Receptor 1</subject><subject>hHAVcr-1</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Kidney tumours</subject><subject>KIM-1</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Microscopy, Fluorescence</subject><subject>Middle Aged</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Multivariate Analysis</subject><subject>Mutation</subject><subject>Pharmacology. Drug treatments</subject><subject>Prognosis</subject><subject>Receptors, Virus - genetics</subject><subject>Receptors, Virus - metabolism</subject><subject>Retrospective Studies</subject><subject>Tumors</subject><subject>Tumour progression</subject><issn>0959-8049</issn><issn>1879-0852</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkl2L1DAUhoso7rj6B7yQ3Ah705l89CMBEZZFXWHBC_U6pMnpbDqddEzagf56PWVGBUFXCLQh7_uck5w3y14yumaUVZtuDZ01a04ZX-OinD7KVkzWKqey5I-zFVWlyiUt1EX2LKWOUlrLgj7NLrgQJS9Escq-38LBjH70iVyTo49TIhb6fupNJBEsHMYhEkY2ZOddgJn40E1xJvuhBzv1kDOCTkPSlBatb3zvx5lsIQBp0Wl7QNBCRFow_enXmmh9GPaGmODI_cMdbP5aHew4OCT5QNI9OOfDFts5RHDejv4IpPF4GncQydCScdoPU8TjYRshJT-E59mT1vQJXpy_l9nX9---3Nzmd58-fLy5vsttSesxr1TtlGu4YcYKWjdCYK0C9y1vJIja1JWyZeugpFQxKqkqHG8dN0pRU3AlLrOrExdrf5sgjXrv03JPE2CYkmYlp6JiVVE-LBVVXciKy_-giqJirJRyofKT1MYhpQitPkSPLzNrRvUSJ93pJU56iZPGhXFC06szf2r24H5ZfuYHBa_PApOs6dtogvXpt67mspR1hbo3Jx3gGx89RJ2sh2BxTDjjUbvB_7uPt3_Ybe-Dx4o7mCF1OFQMF95XJzToz0vwl9wzhFCuSvEDJoMC-A</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Cuadros, Thaïs</creator><creator>Trilla, Enric</creator><creator>Vilà, Maria Rosa</creator><creator>de Torres, Inés</creator><creator>Vilardell, Jordi</creator><creator>Messaoud, Nabil Ben</creator><creator>Salcedo, Mayte</creator><creator>Sarró, Eduard</creator><creator>López-Hellin, Joan</creator><creator>Blanco, Albert</creator><creator>Mir, Carmen</creator><creator>Ramón y Cajal, Santiago</creator><creator>Itarte, Emilio</creator><creator>Morote, Juan</creator><creator>Meseguer, Anna</creator><general>Elsevier Ltd</general><general>Elsevier</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>7X8</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20130501</creationdate><title>Hepatitis A virus cellular receptor 1 / kidney injury molecule-1 is a susceptibility gene for clear cell renal cell carcinoma and hepatitis A virus cellular receptor/kidney injury molecule-1 ectodomain shedding a predictive biomarker of tumour progression</title><author>Cuadros, Thaïs ; Trilla, Enric ; Vilà, Maria Rosa ; de Torres, Inés ; Vilardell, Jordi ; Messaoud, Nabil Ben ; Salcedo, Mayte ; Sarró, Eduard ; López-Hellin, Joan ; Blanco, Albert ; Mir, Carmen ; Ramón y Cajal, Santiago ; Itarte, Emilio ; Morote, Juan ; Meseguer, Anna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-697d9db2a1ac307b33edd4b2af2b8e37a769c5fde5009108094d2fd2a990a4293</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>Binding Sites - genetics</topic><topic>Biological and medical sciences</topic><topic>Biomarker</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Blotting, Western</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Clear cell renal cell carcinoma (ccRCC)</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>HEK293 Cells</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Hepatitis A virus</topic><topic>Hepatitis A Virus Cellular Receptor 1</topic><topic>hHAVcr-1</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>Kidney tumours</topic><topic>KIM-1</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Microscopy, Fluorescence</topic><topic>Middle Aged</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Multivariate Analysis</topic><topic>Mutation</topic><topic>Pharmacology. Drug treatments</topic><topic>Prognosis</topic><topic>Receptors, Virus - genetics</topic><topic>Receptors, Virus - metabolism</topic><topic>Retrospective Studies</topic><topic>Tumors</topic><topic>Tumour progression</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cuadros, Thaïs</creatorcontrib><creatorcontrib>Trilla, Enric</creatorcontrib><creatorcontrib>Vilà, Maria Rosa</creatorcontrib><creatorcontrib>de Torres, Inés</creatorcontrib><creatorcontrib>Vilardell, Jordi</creatorcontrib><creatorcontrib>Messaoud, Nabil Ben</creatorcontrib><creatorcontrib>Salcedo, Mayte</creatorcontrib><creatorcontrib>Sarró, Eduard</creatorcontrib><creatorcontrib>López-Hellin, Joan</creatorcontrib><creatorcontrib>Blanco, Albert</creatorcontrib><creatorcontrib>Mir, Carmen</creatorcontrib><creatorcontrib>Ramón y Cajal, Santiago</creatorcontrib><creatorcontrib>Itarte, Emilio</creatorcontrib><creatorcontrib>Morote, Juan</creatorcontrib><creatorcontrib>Meseguer, Anna</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>MEDLINE - Academic</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>European journal of cancer (1990)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cuadros, Thaïs</au><au>Trilla, Enric</au><au>Vilà, Maria Rosa</au><au>de Torres, Inés</au><au>Vilardell, Jordi</au><au>Messaoud, Nabil Ben</au><au>Salcedo, Mayte</au><au>Sarró, Eduard</au><au>López-Hellin, Joan</au><au>Blanco, Albert</au><au>Mir, Carmen</au><au>Ramón y Cajal, Santiago</au><au>Itarte, Emilio</au><au>Morote, Juan</au><au>Meseguer, Anna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis A virus cellular receptor 1 / kidney injury molecule-1 is a susceptibility gene for clear cell renal cell carcinoma and hepatitis A virus cellular receptor/kidney injury molecule-1 ectodomain shedding a predictive biomarker of tumour progression</atitle><jtitle>European journal of cancer (1990)</jtitle><addtitle>Eur J Cancer</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>49</volume><issue>8</issue><spage>2034</spage><epage>2047</epage><pages>2034-2047</pages><issn>0959-8049</issn><eissn>1879-0852</eissn><abstract>Abstract Aim of the study To correlate hepatitis A virus cellular receptor (HAVCR)/kidney injury molecule-1 (KIM-1) expression in clear cell renal cell carcinoma (ccRCC) tumours with patient outcome and study the consequences of HAVCR/KIM-1 ectodomain shedding. Methods HAVCR/KIM-1 expression in ccRCC, oncocytomes, papillary carcinomas and unaffected tissue counterparts was evaluated. Minimal change disease and pre-clamping normal and ccRCC tissue biopsies were included. Tissue microarrays from 98 ccRCC tumours were analysed. Tumour registry data and patient outcome were retrospectivelly collected. Deletions in HAVCR/KIM-1 ectodomain and lentiviral infection of 786-O cells with HAVCR/KIM-1 mutated constructs to determine their subcellular distribution and invasive capacity were performed. Results HAVCR/KIM-1 was expressed in ccRCC, papillary tumours and in tubule cells of adjacent and distal unaffected counterparts of ccRCC tumours. The latest was not related to ischemic or tumour-related paracrine effects since pre-clamping normal biopsies were positive for HAVCR/KIM-1 and unaffected counterparts of papillary tumours were negative. HAVCR/KIM-1 analyses in patients and the invasive capacity of HAVCR/KIM-1 shedding mutants in cell lines demonstrated that: (i) relative low HAVCR/KIM-1 membrane levels correlate with activated shedding in ccRCC patients and mutant cell lines; (ii) augmented shedding directly correlates with higher invasiveness and tumour malignancy. Concluding statements Constitutive expression of HAVCR/KIM-1 in kidney might constitute a susceptibility trait for ccRCC tumour development. Enhanced HAVCR/KIM-1 ectodomain shedding promotes invasive phenotype in vitro and more aggressive tumours in vivo.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>23352434</pmid><doi>10.1016/j.ejca.2012.12.020</doi><tpages>14</tpages></addata></record> |
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subjects | Adult Aged Aged, 80 and over Binding Sites - genetics Biological and medical sciences Biomarker Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Blotting, Western Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - pathology Cell Line, Tumor Clear cell renal cell carcinoma (ccRCC) Disease Progression Female Genetic Predisposition to Disease - genetics HEK293 Cells Hematology, Oncology and Palliative Medicine Hepatitis A virus Hepatitis A Virus Cellular Receptor 1 hHAVcr-1 Humans Immunohistochemistry Kaplan-Meier Estimate Kidney - metabolism Kidney - pathology Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Kidney tumours KIM-1 Male Medical sciences Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Microscopy, Fluorescence Middle Aged Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Multivariate Analysis Mutation Pharmacology. Drug treatments Prognosis Receptors, Virus - genetics Receptors, Virus - metabolism Retrospective Studies Tumors Tumour progression |
title | Hepatitis A virus cellular receptor 1 / kidney injury molecule-1 is a susceptibility gene for clear cell renal cell carcinoma and hepatitis A virus cellular receptor/kidney injury molecule-1 ectodomain shedding a predictive biomarker of tumour progression |
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