JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation
Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression in LTRs facilitates activation of JCV...
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| Veröffentlicht in: | Clinical cancer research 2008-10, Vol.14 (20), p.6717-6721 |
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| creator | SELGRAD, Michael KOORNSTRA, Jan Jacob GOEL, Ajay WILLIAMS, Sharenda L MEYER, Richard L HAAGSMA, Elizabeth B RICCIARDIELLO, Luigi BOLAND, C. Richard FINI, Lucia BLOM, Marloes RONG HUANG DEVOL, Edward B BOERSMA-VAN EK, Wytske DIJKSTRA, Gerard VERDONK, Robert C DE JONG, Steven |
| description | Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is
unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression
in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia.
Experimental Design: JCV TAg DNA and protein expression were determined in normal colonic epithelium ( n = 15) and adenomatous polyps ( n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively.
Results: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal
mucosa ( P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas.
JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls ( P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 ± 3.2% versus 42.7
± 2.8%, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 ± 0.08% versus 0.39 ± 0.06%, P = 0.05).
Conclusions: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents,
suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of
colorectal neoplasia in LTRs. |
| doi_str_mv | 10.1158/1078-0432.CCR-08-0961 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2846598</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>18927316</sourcerecordid><originalsourceid>FETCH-LOGICAL-c473t-32bed93d751a5fe37eab41b54d3650f7896daed56375270cd587d947c4fb25a63</originalsourceid><addsrcrecordid>eNpVkM1O3DAUhS3UigHaRwB500UXATv-SzZIKC1_GoGEpt1aN87NxFVIRnYYxNvXwwyUbuxj-bvH1kfIMWennKvijDNTZEyK_LSqHjKWcqn5HjngSplM5Fp9SvmNmZHDGP8wxiVncp_MeFHmRnB9QBa3Ff3tw1OkN0OLbvLjQP1Aq7EfQzpCT-9wXPUQPdBFBxP9gWvsx1Wk0E4Y6Nyv07oIMMREDRNsGr6Qzy30Eb_u9iPy6_LnorrO5vdXN9XFPHPSiCn9ssamFI1RHFSLwiDUktdKNkIr1pqi1A1go7QwKjfMNaowTSmNk22dK9DiiJxve1dP9SM2DocpQG9XwT9CeLEjePv_zeA7uxzXNi-kVmWRCtS2wIUxxoDt-yxndqPZbhTajUKbNFuWctKc5k4-Pvxvauc1Ad92AEQHfZv8OB_fuZwVMuev3Pct1_ll9-wDWpdIDAEjQnCd5TLBVhtuxF8MtZW8</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>SELGRAD, Michael ; KOORNSTRA, Jan Jacob ; GOEL, Ajay ; WILLIAMS, Sharenda L ; MEYER, Richard L ; HAAGSMA, Elizabeth B ; RICCIARDIELLO, Luigi ; BOLAND, C. Richard ; FINI, Lucia ; BLOM, Marloes ; RONG HUANG ; DEVOL, Edward B ; BOERSMA-VAN EK, Wytske ; DIJKSTRA, Gerard ; VERDONK, Robert C ; DE JONG, Steven</creator><creatorcontrib>SELGRAD, Michael ; KOORNSTRA, Jan Jacob ; GOEL, Ajay ; WILLIAMS, Sharenda L ; MEYER, Richard L ; HAAGSMA, Elizabeth B ; RICCIARDIELLO, Luigi ; BOLAND, C. Richard ; FINI, Lucia ; BLOM, Marloes ; RONG HUANG ; DEVOL, Edward B ; BOERSMA-VAN EK, Wytske ; DIJKSTRA, Gerard ; VERDONK, Robert C ; DE JONG, Steven</creatorcontrib><description>Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is
unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression
in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia.
Experimental Design: JCV TAg DNA and protein expression were determined in normal colonic epithelium ( n = 15) and adenomatous polyps ( n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively.
Results: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal
mucosa ( P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas.
JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls ( P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 ± 3.2% versus 42.7
± 2.8%, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 ± 0.08% versus 0.39 ± 0.06%, P = 0.05).
Conclusions: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents,
suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of
colorectal neoplasia in LTRs.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-08-0961</identifier><identifier>PMID: 18927316</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenocarcinoma - therapy ; Adenocarcinoma - virology ; Adenoma - therapy ; Adenoma - virology ; Adenomatous Polyps - therapy ; Adenomatous Polyps - virology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Antigens, Viral, Tumor - analysis ; Antineoplastic agents ; Biological and medical sciences ; Case-Control Studies ; colorectal neoplasia ; Colorectal Neoplasms - virology ; DNA, Viral - analysis ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Immunosuppression ; Infectious diseases ; JC virus ; JC Virus - isolation & purification ; JC Virus - physiology ; Liver Transplantation ; Male ; Medical sciences ; Middle Aged ; Pharmacology. Drug treatments ; Polymerase Chain Reaction ; Polyomavirus Infections - virology ; Prognosis ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; T antigen ; Tumor Virus Infections - virology ; Tumors ; Viral diseases ; Virus Activation ; Young Adult</subject><ispartof>Clinical cancer research, 2008-10, Vol.14 (20), p.6717-6721</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c473t-32bed93d751a5fe37eab41b54d3650f7896daed56375270cd587d947c4fb25a63</citedby><cites>FETCH-LOGICAL-c473t-32bed93d751a5fe37eab41b54d3650f7896daed56375270cd587d947c4fb25a63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20842116$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18927316$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SELGRAD, Michael</creatorcontrib><creatorcontrib>KOORNSTRA, Jan Jacob</creatorcontrib><creatorcontrib>GOEL, Ajay</creatorcontrib><creatorcontrib>WILLIAMS, Sharenda L</creatorcontrib><creatorcontrib>MEYER, Richard L</creatorcontrib><creatorcontrib>HAAGSMA, Elizabeth B</creatorcontrib><creatorcontrib>RICCIARDIELLO, Luigi</creatorcontrib><creatorcontrib>BOLAND, C. Richard</creatorcontrib><creatorcontrib>FINI, Lucia</creatorcontrib><creatorcontrib>BLOM, Marloes</creatorcontrib><creatorcontrib>RONG HUANG</creatorcontrib><creatorcontrib>DEVOL, Edward B</creatorcontrib><creatorcontrib>BOERSMA-VAN EK, Wytske</creatorcontrib><creatorcontrib>DIJKSTRA, Gerard</creatorcontrib><creatorcontrib>VERDONK, Robert C</creatorcontrib><creatorcontrib>DE JONG, Steven</creatorcontrib><title>JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is
unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression
in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia.
Experimental Design: JCV TAg DNA and protein expression were determined in normal colonic epithelium ( n = 15) and adenomatous polyps ( n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively.
Results: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal
mucosa ( P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas.
JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls ( P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 ± 3.2% versus 42.7
± 2.8%, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 ± 0.08% versus 0.39 ± 0.06%, P = 0.05).
Conclusions: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents,
suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of
colorectal neoplasia in LTRs.</description><subject>Adenocarcinoma - therapy</subject><subject>Adenocarcinoma - virology</subject><subject>Adenoma - therapy</subject><subject>Adenoma - virology</subject><subject>Adenomatous Polyps - therapy</subject><subject>Adenomatous Polyps - virology</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antigens, Viral, Tumor - analysis</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>colorectal neoplasia</subject><subject>Colorectal Neoplasms - virology</subject><subject>DNA, Viral - analysis</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Immunosuppression</subject><subject>Infectious diseases</subject><subject>JC virus</subject><subject>JC Virus - isolation & purification</subject><subject>JC Virus - physiology</subject><subject>Liver Transplantation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymerase Chain Reaction</subject><subject>Polyomavirus Infections - virology</subject><subject>Prognosis</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>T antigen</subject><subject>Tumor Virus Infections - virology</subject><subject>Tumors</subject><subject>Viral diseases</subject><subject>Virus Activation</subject><subject>Young Adult</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkM1O3DAUhS3UigHaRwB500UXATv-SzZIKC1_GoGEpt1aN87NxFVIRnYYxNvXwwyUbuxj-bvH1kfIMWennKvijDNTZEyK_LSqHjKWcqn5HjngSplM5Fp9SvmNmZHDGP8wxiVncp_MeFHmRnB9QBa3Ff3tw1OkN0OLbvLjQP1Aq7EfQzpCT-9wXPUQPdBFBxP9gWvsx1Wk0E4Y6Nyv07oIMMREDRNsGr6Qzy30Eb_u9iPy6_LnorrO5vdXN9XFPHPSiCn9ssamFI1RHFSLwiDUktdKNkIr1pqi1A1go7QwKjfMNaowTSmNk22dK9DiiJxve1dP9SM2DocpQG9XwT9CeLEjePv_zeA7uxzXNi-kVmWRCtS2wIUxxoDt-yxndqPZbhTajUKbNFuWctKc5k4-Pvxvauc1Ad92AEQHfZv8OB_fuZwVMuev3Pct1_ll9-wDWpdIDAEjQnCd5TLBVhtuxF8MtZW8</recordid><startdate>20081015</startdate><enddate>20081015</enddate><creator>SELGRAD, Michael</creator><creator>KOORNSTRA, Jan Jacob</creator><creator>GOEL, Ajay</creator><creator>WILLIAMS, Sharenda L</creator><creator>MEYER, Richard L</creator><creator>HAAGSMA, Elizabeth B</creator><creator>RICCIARDIELLO, Luigi</creator><creator>BOLAND, C. Richard</creator><creator>FINI, Lucia</creator><creator>BLOM, Marloes</creator><creator>RONG HUANG</creator><creator>DEVOL, Edward B</creator><creator>BOERSMA-VAN EK, Wytske</creator><creator>DIJKSTRA, Gerard</creator><creator>VERDONK, Robert C</creator><creator>DE JONG, Steven</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>20081015</creationdate><title>JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation</title><author>SELGRAD, Michael ; KOORNSTRA, Jan Jacob ; GOEL, Ajay ; WILLIAMS, Sharenda L ; MEYER, Richard L ; HAAGSMA, Elizabeth B ; RICCIARDIELLO, Luigi ; BOLAND, C. Richard ; FINI, Lucia ; BLOM, Marloes ; RONG HUANG ; DEVOL, Edward B ; BOERSMA-VAN EK, Wytske ; DIJKSTRA, Gerard ; VERDONK, Robert C ; DE JONG, Steven</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c473t-32bed93d751a5fe37eab41b54d3650f7896daed56375270cd587d947c4fb25a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adenocarcinoma - therapy</topic><topic>Adenocarcinoma - virology</topic><topic>Adenoma - therapy</topic><topic>Adenoma - virology</topic><topic>Adenomatous Polyps - therapy</topic><topic>Adenomatous Polyps - virology</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antigens, Viral, Tumor - analysis</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>colorectal neoplasia</topic><topic>Colorectal Neoplasms - virology</topic><topic>DNA, Viral - analysis</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Immunosuppression</topic><topic>Infectious diseases</topic><topic>JC virus</topic><topic>JC Virus - isolation & purification</topic><topic>JC Virus - physiology</topic><topic>Liver Transplantation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymerase Chain Reaction</topic><topic>Polyomavirus Infections - virology</topic><topic>Prognosis</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>T antigen</topic><topic>Tumor Virus Infections - virology</topic><topic>Tumors</topic><topic>Viral diseases</topic><topic>Virus Activation</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SELGRAD, Michael</creatorcontrib><creatorcontrib>KOORNSTRA, Jan Jacob</creatorcontrib><creatorcontrib>GOEL, Ajay</creatorcontrib><creatorcontrib>WILLIAMS, Sharenda L</creatorcontrib><creatorcontrib>MEYER, Richard L</creatorcontrib><creatorcontrib>HAAGSMA, Elizabeth B</creatorcontrib><creatorcontrib>RICCIARDIELLO, Luigi</creatorcontrib><creatorcontrib>BOLAND, C. Richard</creatorcontrib><creatorcontrib>FINI, Lucia</creatorcontrib><creatorcontrib>BLOM, Marloes</creatorcontrib><creatorcontrib>RONG HUANG</creatorcontrib><creatorcontrib>DEVOL, Edward B</creatorcontrib><creatorcontrib>BOERSMA-VAN EK, Wytske</creatorcontrib><creatorcontrib>DIJKSTRA, Gerard</creatorcontrib><creatorcontrib>VERDONK, Robert C</creatorcontrib><creatorcontrib>DE JONG, Steven</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>SELGRAD, Michael</au><au>KOORNSTRA, Jan Jacob</au><au>GOEL, Ajay</au><au>WILLIAMS, Sharenda L</au><au>MEYER, Richard L</au><au>HAAGSMA, Elizabeth B</au><au>RICCIARDIELLO, Luigi</au><au>BOLAND, C. Richard</au><au>FINI, Lucia</au><au>BLOM, Marloes</au><au>RONG HUANG</au><au>DEVOL, Edward B</au><au>BOERSMA-VAN EK, Wytske</au><au>DIJKSTRA, Gerard</au><au>VERDONK, Robert C</au><au>DE JONG, Steven</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2008-10-15</date><risdate>2008</risdate><volume>14</volume><issue>20</issue><spage>6717</spage><epage>6721</epage><pages>6717-6721</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is
unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression
in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia.
Experimental Design: JCV TAg DNA and protein expression were determined in normal colonic epithelium ( n = 15) and adenomatous polyps ( n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively.
Results: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal
mucosa ( P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas.
JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls ( P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 ± 3.2% versus 42.7
± 2.8%, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 ± 0.08% versus 0.39 ± 0.06%, P = 0.05).
Conclusions: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents,
suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of
colorectal neoplasia in LTRs.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>18927316</pmid><doi>10.1158/1078-0432.CCR-08-0961</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical cancer research, 2008-10, Vol.14 (20), p.6717-6721 |
| issn | 1078-0432 1557-3265 |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adenocarcinoma - therapy Adenocarcinoma - virology Adenoma - therapy Adenoma - virology Adenomatous Polyps - therapy Adenomatous Polyps - virology Adolescent Adult Aged Aged, 80 and over Antigens, Viral, Tumor - analysis Antineoplastic agents Biological and medical sciences Case-Control Studies colorectal neoplasia Colorectal Neoplasms - virology DNA, Viral - analysis Female Gastroenterology. Liver. Pancreas. Abdomen Humans Immunosuppression Infectious diseases JC virus JC Virus - isolation & purification JC Virus - physiology Liver Transplantation Male Medical sciences Middle Aged Pharmacology. Drug treatments Polymerase Chain Reaction Polyomavirus Infections - virology Prognosis Stomach. Duodenum. Small intestine. Colon. Rectum. Anus T antigen Tumor Virus Infections - virology Tumors Viral diseases Virus Activation Young Adult |
| title | JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation |
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