Role of the TNF-α receptor type 1 on prostate carcinogenesis in knockout mice
BACKGROUND TNF‐α is a key cytokine involved in prostate carcinogenesis and is mediated by the TNF‐α receptor type 1 (TNFR‐1). This receptor triggers two opposite pathways: cell death or cell survival and presents a protective or stimulator role in cancer. Thus, the purpose of this study was to evalu...
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creator | Galheigo, Maria Raquel Unterkircher Cruz, Amanda Rodrigues Cabral, Ágata Silva Faria, Paulo Rogério Cordeiro, Renato Simões Silva, Marcelo José Barbosa Tomiosso, Tatiana Carla Gonçalves, Bianca Fachim Pinto-Fochi, Maria Etelvina Taboga, Sebastião Roberto Góes, Rejane Maira Ribeiro, Daniele Lisboa |
description | BACKGROUND
TNF‐α is a key cytokine involved in prostate carcinogenesis and is mediated by the TNF‐α receptor type 1 (TNFR‐1). This receptor triggers two opposite pathways: cell death or cell survival and presents a protective or stimulator role in cancer. Thus, the purpose of this study was to evaluate the role of TNF signaling in chemically induced prostate carcinogenesis in mice.
METHODS
C57bl/6 wild type (WT) and p55 TNFR‐1 knockout mice (KO) were treated with mineral oil (control) or N‐methyl N‐nitrosurea (MNU) in association with testosterone (MNU+T, single injection of 40 mg/kg and weekly injection 2 mg/kg, respectively) over the course of 6 months. After this induction period, prostate samples were processed for histological and biochemical analysis.
RESULTS
MNU+T treatment led to the development of prostate intraepithelial neoplasia (PIN) and adenocarcinoma (PCa) in both WT and KO animals; however, the incidence of PCa was lower in KO group than in WT. Cell proliferation analysis showed that PCNA levels were significantly lower in the KO group, even after carcinogenesis induction. Furthermore, the prostate of KO animals had lower levels of p65 and p‐mTOR after treatment with MNU+T than WT. There was also a decrease in prostate androgen receptor levels after induction of carcinogenesis in both KO and WT mice. Regarding the extracellular matrix in the prostate, KO mice had higher levels of fibronectin and lower levels of matrix metalloproteinase 2 (MMP2) after carcinogenesis. Finally, there was a similar increase in apoptosis in both groups after carcinogenesis, indicating that the TNAFr1 pathway in prostate carcinogenesis presented proliferative, and not apoptotic, stimuli.
CONCLUSIONS
TNF‐α, through its receptor TNFR‐1, promoted cell proliferation and cell survival in prostate by activation of the AKT/mTOR and NFKB pathway, which stimulated prostate carcinogenesis in chemically induced mice. Prostate 76: 917–926, 2016. © 2016 Wiley Periodicals, Inc. |
doi_str_mv | 10.1002/pros.23181 |
format | Article |
fullrecord | <record><control><sourceid>istex_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1002_pros_23181</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ark_67375_WNG_P09K9M2F_M</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3671-90f853f3b654629f88e5b7439884dc17570832861b208fc05e816e456dcebbd63</originalsourceid><addsrcrecordid>eNp9kM1OwzAQhC0EoqVw4QGQz0gpazuxnSOqaEH0T6WIo5W4GwhtkyhOBX0sXoRnIiW0R04rjb6ZHQ0hlwy6DIDfFGXuulwwzY5Im0GoPAA_OCZt4Ao8nwnVImfOvQPUOPBT0qp1ppXUbTKe5SukeUKrN6Tzcd_7_qIlWiyqvKTVtkDKaJ7R3YsqqpDaqLRplr9ihi51NM3oMsvtMt9UdJ1aPCcnSbRyePF3O-S5fzfv3XvDyeChdzv0rJCKeSEkOhCJiGXgSx4mWmMQK1-EWvsLy1SgQAuuJYs56MRCgJpJ9AO5sBjHCyk65LrJtXUxV2JiijJdR-XWMDC7UcyusfkdpYavGrjYxGtcHND9CjXAGuAjXeH2nygznU2e9qFe40ldhZ8HT1QujVRCBeZlPDBTCB_DEe-bkfgBgQd7Mg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Role of the TNF-α receptor type 1 on prostate carcinogenesis in knockout mice</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Galheigo, Maria Raquel Unterkircher ; Cruz, Amanda Rodrigues ; Cabral, Ágata Silva ; Faria, Paulo Rogério ; Cordeiro, Renato Simões ; Silva, Marcelo José Barbosa ; Tomiosso, Tatiana Carla ; Gonçalves, Bianca Fachim ; Pinto-Fochi, Maria Etelvina ; Taboga, Sebastião Roberto ; Góes, Rejane Maira ; Ribeiro, Daniele Lisboa</creator><creatorcontrib>Galheigo, Maria Raquel Unterkircher ; Cruz, Amanda Rodrigues ; Cabral, Ágata Silva ; Faria, Paulo Rogério ; Cordeiro, Renato Simões ; Silva, Marcelo José Barbosa ; Tomiosso, Tatiana Carla ; Gonçalves, Bianca Fachim ; Pinto-Fochi, Maria Etelvina ; Taboga, Sebastião Roberto ; Góes, Rejane Maira ; Ribeiro, Daniele Lisboa</creatorcontrib><description>BACKGROUND
TNF‐α is a key cytokine involved in prostate carcinogenesis and is mediated by the TNF‐α receptor type 1 (TNFR‐1). This receptor triggers two opposite pathways: cell death or cell survival and presents a protective or stimulator role in cancer. Thus, the purpose of this study was to evaluate the role of TNF signaling in chemically induced prostate carcinogenesis in mice.
METHODS
C57bl/6 wild type (WT) and p55 TNFR‐1 knockout mice (KO) were treated with mineral oil (control) or N‐methyl N‐nitrosurea (MNU) in association with testosterone (MNU+T, single injection of 40 mg/kg and weekly injection 2 mg/kg, respectively) over the course of 6 months. After this induction period, prostate samples were processed for histological and biochemical analysis.
RESULTS
MNU+T treatment led to the development of prostate intraepithelial neoplasia (PIN) and adenocarcinoma (PCa) in both WT and KO animals; however, the incidence of PCa was lower in KO group than in WT. Cell proliferation analysis showed that PCNA levels were significantly lower in the KO group, even after carcinogenesis induction. Furthermore, the prostate of KO animals had lower levels of p65 and p‐mTOR after treatment with MNU+T than WT. There was also a decrease in prostate androgen receptor levels after induction of carcinogenesis in both KO and WT mice. Regarding the extracellular matrix in the prostate, KO mice had higher levels of fibronectin and lower levels of matrix metalloproteinase 2 (MMP2) after carcinogenesis. Finally, there was a similar increase in apoptosis in both groups after carcinogenesis, indicating that the TNAFr1 pathway in prostate carcinogenesis presented proliferative, and not apoptotic, stimuli.
CONCLUSIONS
TNF‐α, through its receptor TNFR‐1, promoted cell proliferation and cell survival in prostate by activation of the AKT/mTOR and NFKB pathway, which stimulated prostate carcinogenesis in chemically induced mice. Prostate 76: 917–926, 2016. © 2016 Wiley Periodicals, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.23181</identifier><identifier>PMID: 27018768</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma - pathology ; AKT/mTOR ; Animals ; Apoptosis ; carcinogenesis ; Carcinogenesis - pathology ; Cell Proliferation ; Cell Survival ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B - metabolism ; Proliferating Cell Nuclear Antigen - analysis ; prostate ; Prostatic Intraepithelial Neoplasia - pathology ; Prostatic Neoplasms - chemistry ; Prostatic Neoplasms - pathology ; Proto-Oncogene Proteins c-akt - metabolism ; Receptors, Androgen - analysis ; Receptors, Tumor Necrosis Factor, Type I - deficiency ; Receptors, Tumor Necrosis Factor, Type I - genetics ; Receptors, Tumor Necrosis Factor, Type I - physiology ; TNF-α ; TNFR-1 ; TOR Serine-Threonine Kinases - analysis ; TOR Serine-Threonine Kinases - metabolism ; Transcription Factor RelA - analysis ; Tumor Necrosis Factor-alpha - physiology</subject><ispartof>The Prostate, 2016-07, Vol.76 (10), p.917-926</ispartof><rights>2016 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3671-90f853f3b654629f88e5b7439884dc17570832861b208fc05e816e456dcebbd63</citedby><cites>FETCH-LOGICAL-c3671-90f853f3b654629f88e5b7439884dc17570832861b208fc05e816e456dcebbd63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpros.23181$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpros.23181$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27018768$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galheigo, Maria Raquel Unterkircher</creatorcontrib><creatorcontrib>Cruz, Amanda Rodrigues</creatorcontrib><creatorcontrib>Cabral, Ágata Silva</creatorcontrib><creatorcontrib>Faria, Paulo Rogério</creatorcontrib><creatorcontrib>Cordeiro, Renato Simões</creatorcontrib><creatorcontrib>Silva, Marcelo José Barbosa</creatorcontrib><creatorcontrib>Tomiosso, Tatiana Carla</creatorcontrib><creatorcontrib>Gonçalves, Bianca Fachim</creatorcontrib><creatorcontrib>Pinto-Fochi, Maria Etelvina</creatorcontrib><creatorcontrib>Taboga, Sebastião Roberto</creatorcontrib><creatorcontrib>Góes, Rejane Maira</creatorcontrib><creatorcontrib>Ribeiro, Daniele Lisboa</creatorcontrib><title>Role of the TNF-α receptor type 1 on prostate carcinogenesis in knockout mice</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>BACKGROUND
TNF‐α is a key cytokine involved in prostate carcinogenesis and is mediated by the TNF‐α receptor type 1 (TNFR‐1). This receptor triggers two opposite pathways: cell death or cell survival and presents a protective or stimulator role in cancer. Thus, the purpose of this study was to evaluate the role of TNF signaling in chemically induced prostate carcinogenesis in mice.
METHODS
C57bl/6 wild type (WT) and p55 TNFR‐1 knockout mice (KO) were treated with mineral oil (control) or N‐methyl N‐nitrosurea (MNU) in association with testosterone (MNU+T, single injection of 40 mg/kg and weekly injection 2 mg/kg, respectively) over the course of 6 months. After this induction period, prostate samples were processed for histological and biochemical analysis.
RESULTS
MNU+T treatment led to the development of prostate intraepithelial neoplasia (PIN) and adenocarcinoma (PCa) in both WT and KO animals; however, the incidence of PCa was lower in KO group than in WT. Cell proliferation analysis showed that PCNA levels were significantly lower in the KO group, even after carcinogenesis induction. Furthermore, the prostate of KO animals had lower levels of p65 and p‐mTOR after treatment with MNU+T than WT. There was also a decrease in prostate androgen receptor levels after induction of carcinogenesis in both KO and WT mice. Regarding the extracellular matrix in the prostate, KO mice had higher levels of fibronectin and lower levels of matrix metalloproteinase 2 (MMP2) after carcinogenesis. Finally, there was a similar increase in apoptosis in both groups after carcinogenesis, indicating that the TNAFr1 pathway in prostate carcinogenesis presented proliferative, and not apoptotic, stimuli.
CONCLUSIONS
TNF‐α, through its receptor TNFR‐1, promoted cell proliferation and cell survival in prostate by activation of the AKT/mTOR and NFKB pathway, which stimulated prostate carcinogenesis in chemically induced mice. Prostate 76: 917–926, 2016. © 2016 Wiley Periodicals, Inc.</description><subject>Adenocarcinoma - pathology</subject><subject>AKT/mTOR</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>carcinogenesis</subject><subject>Carcinogenesis - pathology</subject><subject>Cell Proliferation</subject><subject>Cell Survival</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>NF-kappa B - metabolism</subject><subject>Proliferating Cell Nuclear Antigen - analysis</subject><subject>prostate</subject><subject>Prostatic Intraepithelial Neoplasia - pathology</subject><subject>Prostatic Neoplasms - chemistry</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptors, Androgen - analysis</subject><subject>Receptors, Tumor Necrosis Factor, Type I - deficiency</subject><subject>Receptors, Tumor Necrosis Factor, Type I - genetics</subject><subject>Receptors, Tumor Necrosis Factor, Type I - physiology</subject><subject>TNF-α</subject><subject>TNFR-1</subject><subject>TOR Serine-Threonine Kinases - analysis</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Transcription Factor RelA - analysis</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1OwzAQhC0EoqVw4QGQz0gpazuxnSOqaEH0T6WIo5W4GwhtkyhOBX0sXoRnIiW0R04rjb6ZHQ0hlwy6DIDfFGXuulwwzY5Im0GoPAA_OCZt4Ao8nwnVImfOvQPUOPBT0qp1ppXUbTKe5SukeUKrN6Tzcd_7_qIlWiyqvKTVtkDKaJ7R3YsqqpDaqLRplr9ihi51NM3oMsvtMt9UdJ1aPCcnSbRyePF3O-S5fzfv3XvDyeChdzv0rJCKeSEkOhCJiGXgSx4mWmMQK1-EWvsLy1SgQAuuJYs56MRCgJpJ9AO5sBjHCyk65LrJtXUxV2JiijJdR-XWMDC7UcyusfkdpYavGrjYxGtcHND9CjXAGuAjXeH2nygznU2e9qFe40ldhZ8HT1QujVRCBeZlPDBTCB_DEe-bkfgBgQd7Mg</recordid><startdate>201607</startdate><enddate>201607</enddate><creator>Galheigo, Maria Raquel Unterkircher</creator><creator>Cruz, Amanda Rodrigues</creator><creator>Cabral, Ágata Silva</creator><creator>Faria, Paulo Rogério</creator><creator>Cordeiro, Renato Simões</creator><creator>Silva, Marcelo José Barbosa</creator><creator>Tomiosso, Tatiana Carla</creator><creator>Gonçalves, Bianca Fachim</creator><creator>Pinto-Fochi, Maria Etelvina</creator><creator>Taboga, Sebastião Roberto</creator><creator>Góes, Rejane Maira</creator><creator>Ribeiro, Daniele Lisboa</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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></search><sort><creationdate>201607</creationdate><title>Role of the TNF-α receptor type 1 on prostate carcinogenesis in knockout mice</title><author>Galheigo, Maria Raquel Unterkircher ; Cruz, Amanda Rodrigues ; Cabral, Ágata Silva ; Faria, Paulo Rogério ; Cordeiro, Renato Simões ; Silva, Marcelo José Barbosa ; Tomiosso, Tatiana Carla ; Gonçalves, Bianca Fachim ; Pinto-Fochi, Maria Etelvina ; Taboga, Sebastião Roberto ; Góes, Rejane Maira ; Ribeiro, Daniele Lisboa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3671-90f853f3b654629f88e5b7439884dc17570832861b208fc05e816e456dcebbd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenocarcinoma - pathology</topic><topic>AKT/mTOR</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>carcinogenesis</topic><topic>Carcinogenesis - pathology</topic><topic>Cell Proliferation</topic><topic>Cell Survival</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>NF-kappa B - metabolism</topic><topic>Proliferating Cell Nuclear Antigen - analysis</topic><topic>prostate</topic><topic>Prostatic Intraepithelial Neoplasia - pathology</topic><topic>Prostatic Neoplasms - chemistry</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptors, Androgen - analysis</topic><topic>Receptors, Tumor Necrosis Factor, Type I - deficiency</topic><topic>Receptors, Tumor Necrosis Factor, Type I - genetics</topic><topic>Receptors, Tumor Necrosis Factor, Type I - physiology</topic><topic>TNF-α</topic><topic>TNFR-1</topic><topic>TOR Serine-Threonine Kinases - analysis</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Transcription Factor RelA - analysis</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Galheigo, Maria Raquel Unterkircher</creatorcontrib><creatorcontrib>Cruz, Amanda Rodrigues</creatorcontrib><creatorcontrib>Cabral, Ágata Silva</creatorcontrib><creatorcontrib>Faria, Paulo Rogério</creatorcontrib><creatorcontrib>Cordeiro, Renato Simões</creatorcontrib><creatorcontrib>Silva, Marcelo José Barbosa</creatorcontrib><creatorcontrib>Tomiosso, Tatiana Carla</creatorcontrib><creatorcontrib>Gonçalves, Bianca Fachim</creatorcontrib><creatorcontrib>Pinto-Fochi, Maria Etelvina</creatorcontrib><creatorcontrib>Taboga, Sebastião Roberto</creatorcontrib><creatorcontrib>Góes, Rejane Maira</creatorcontrib><creatorcontrib>Ribeiro, Daniele Lisboa</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galheigo, Maria Raquel Unterkircher</au><au>Cruz, Amanda Rodrigues</au><au>Cabral, Ágata Silva</au><au>Faria, Paulo Rogério</au><au>Cordeiro, Renato Simões</au><au>Silva, Marcelo José Barbosa</au><au>Tomiosso, Tatiana Carla</au><au>Gonçalves, Bianca Fachim</au><au>Pinto-Fochi, Maria Etelvina</au><au>Taboga, Sebastião Roberto</au><au>Góes, Rejane Maira</au><au>Ribeiro, Daniele Lisboa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of the TNF-α receptor type 1 on prostate carcinogenesis in knockout mice</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2016-07</date><risdate>2016</risdate><volume>76</volume><issue>10</issue><spage>917</spage><epage>926</epage><pages>917-926</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><abstract>BACKGROUND
TNF‐α is a key cytokine involved in prostate carcinogenesis and is mediated by the TNF‐α receptor type 1 (TNFR‐1). This receptor triggers two opposite pathways: cell death or cell survival and presents a protective or stimulator role in cancer. Thus, the purpose of this study was to evaluate the role of TNF signaling in chemically induced prostate carcinogenesis in mice.
METHODS
C57bl/6 wild type (WT) and p55 TNFR‐1 knockout mice (KO) were treated with mineral oil (control) or N‐methyl N‐nitrosurea (MNU) in association with testosterone (MNU+T, single injection of 40 mg/kg and weekly injection 2 mg/kg, respectively) over the course of 6 months. After this induction period, prostate samples were processed for histological and biochemical analysis.
RESULTS
MNU+T treatment led to the development of prostate intraepithelial neoplasia (PIN) and adenocarcinoma (PCa) in both WT and KO animals; however, the incidence of PCa was lower in KO group than in WT. Cell proliferation analysis showed that PCNA levels were significantly lower in the KO group, even after carcinogenesis induction. Furthermore, the prostate of KO animals had lower levels of p65 and p‐mTOR after treatment with MNU+T than WT. There was also a decrease in prostate androgen receptor levels after induction of carcinogenesis in both KO and WT mice. Regarding the extracellular matrix in the prostate, KO mice had higher levels of fibronectin and lower levels of matrix metalloproteinase 2 (MMP2) after carcinogenesis. Finally, there was a similar increase in apoptosis in both groups after carcinogenesis, indicating that the TNAFr1 pathway in prostate carcinogenesis presented proliferative, and not apoptotic, stimuli.
CONCLUSIONS
TNF‐α, through its receptor TNFR‐1, promoted cell proliferation and cell survival in prostate by activation of the AKT/mTOR and NFKB pathway, which stimulated prostate carcinogenesis in chemically induced mice. Prostate 76: 917–926, 2016. © 2016 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>27018768</pmid><doi>10.1002/pros.23181</doi><tpages>10</tpages></addata></record> |
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subjects | Adenocarcinoma - pathology AKT/mTOR Animals Apoptosis carcinogenesis Carcinogenesis - pathology Cell Proliferation Cell Survival Male Mice Mice, Inbred C57BL Mice, Knockout NF-kappa B - metabolism Proliferating Cell Nuclear Antigen - analysis prostate Prostatic Intraepithelial Neoplasia - pathology Prostatic Neoplasms - chemistry Prostatic Neoplasms - pathology Proto-Oncogene Proteins c-akt - metabolism Receptors, Androgen - analysis Receptors, Tumor Necrosis Factor, Type I - deficiency Receptors, Tumor Necrosis Factor, Type I - genetics Receptors, Tumor Necrosis Factor, Type I - physiology TNF-α TNFR-1 TOR Serine-Threonine Kinases - analysis TOR Serine-Threonine Kinases - metabolism Transcription Factor RelA - analysis Tumor Necrosis Factor-alpha - physiology |
title | Role of the TNF-α receptor type 1 on prostate carcinogenesis in knockout mice |
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