Type I interferons in the treatment of pancreatic cancer : Mechanisms of action and role of related receptors
We evaluated the role of type I interferons (IFNs) and IFN receptors in the regulation of cell growth in 3 human pancreatic adenocarcinoma cell lines (BxPC-3, MiaPaCa-2, and Panc-1). Chemotherapy and radiotherapy have a marginal role in the management of pancreatic adenocarcinoma. The addition of IF...
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| Veröffentlicht in: | Annals of surgery 2007-08, Vol.246 (2), p.259-268 |
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| creator | VITALE, Giovanni VAN EIJCK, Casper H. J LAMBERTS, Steven W. J HOFLAND, Leo J VAN KOETSVELD ING, Peter M ERDMANN, Joris I SPEEL, Ernst Jan M VAN DER WANSEM ING, Katy MOOIJ, Diana M COLAO, Annamaria LOMBARDI, Gaetano CROZE, Ed |
| description | We evaluated the role of type I interferons (IFNs) and IFN receptors in the regulation of cell growth in 3 human pancreatic adenocarcinoma cell lines (BxPC-3, MiaPaCa-2, and Panc-1).
Chemotherapy and radiotherapy have a marginal role in the management of pancreatic adenocarcinoma. The addition of IFN-alpha showed promising results in early clinical trials.
Cell proliferation and apoptosis were evaluated by DNA measurement and DNA fragmentation, respectively. Type I IFN receptor (IFNAR-1 and IFNAR-2 subunits) was determined by quantitative RT-PCR and immunocytochemistry. Cell cycle distribution was evaluated by propidium iodide staining and flow-cytometric analysis.
The incubation with IFN-beta for 6 days showed a potent inhibitory effect on the proliferation of BxPC-3 (IC(50), 14 IU/mL) and MiaPaCa-2 (IC(50), 64 IU/mL). The inhibitory effect of IFN-beta was stronger than IFN-alpha in all 3 cell lines and mainly modulated by the stimulation of apoptosis, although cell cycle arrest was induced as well. The expression of the type I IFN receptors was significantly higher in BxPC-3 (the most sensitive cell line to IFN) and mainly localized on the membrane, whereas in Panc-1 (the most resistant cell line) about 60% to 70% of cells were negative for IFNAR-2c with a mainly cytoplasmic staining for IFNAR-2c.
The antitumor activity of IFN-beta is more potent than IFN-alpha in pancreatic cancer cell lines through the induction of apoptosis. Further studies should investigate in vivo whether the intensity and distribution of IFNAR-1 and IFNAR-2c may predict the response to therapy with IFN-alpha and IFN-beta in pancreatic cancer. |
| doi_str_mv | 10.1097/01.sla.0000261460.07110.f2 |
| format | Article |
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Chemotherapy and radiotherapy have a marginal role in the management of pancreatic adenocarcinoma. The addition of IFN-alpha showed promising results in early clinical trials.
Cell proliferation and apoptosis were evaluated by DNA measurement and DNA fragmentation, respectively. Type I IFN receptor (IFNAR-1 and IFNAR-2 subunits) was determined by quantitative RT-PCR and immunocytochemistry. Cell cycle distribution was evaluated by propidium iodide staining and flow-cytometric analysis.
The incubation with IFN-beta for 6 days showed a potent inhibitory effect on the proliferation of BxPC-3 (IC(50), 14 IU/mL) and MiaPaCa-2 (IC(50), 64 IU/mL). The inhibitory effect of IFN-beta was stronger than IFN-alpha in all 3 cell lines and mainly modulated by the stimulation of apoptosis, although cell cycle arrest was induced as well. The expression of the type I IFN receptors was significantly higher in BxPC-3 (the most sensitive cell line to IFN) and mainly localized on the membrane, whereas in Panc-1 (the most resistant cell line) about 60% to 70% of cells were negative for IFNAR-2c with a mainly cytoplasmic staining for IFNAR-2c.
The antitumor activity of IFN-beta is more potent than IFN-alpha in pancreatic cancer cell lines through the induction of apoptosis. Further studies should investigate in vivo whether the intensity and distribution of IFNAR-1 and IFNAR-2c may predict the response to therapy with IFN-alpha and IFN-beta in pancreatic cancer.</description><identifier>ISSN: 0003-4932</identifier><identifier>EISSN: 1528-1140</identifier><identifier>DOI: 10.1097/01.sla.0000261460.07110.f2</identifier><identifier>PMID: 17667505</identifier><identifier>CODEN: ANSUA5</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Antineoplastic Agents - therapeutic use ; Apoptosis - drug effects ; Biological and medical sciences ; Biomarkers, Tumor - biosynthesis ; Biomarkers, Tumor - genetics ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Flow Cytometry ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; General aspects ; Humans ; Immunohistochemistry ; Interferon Type I - therapeutic use ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; Original ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Prognosis ; Receptor, Interferon alpha-beta - biosynthesis ; Receptor, Interferon alpha-beta - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Tumors</subject><ispartof>Annals of surgery, 2007-08, Vol.246 (2), p.259-268</ispartof><rights>2007 INIST-CNRS</rights><rights>2007 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c345t-47e88d6cef7ce08d8538145a3033b8dff91be9edca74ad7bd1884caee7a60c563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933574/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933574/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18939962$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17667505$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VITALE, Giovanni</creatorcontrib><creatorcontrib>VAN EIJCK, Casper H. J</creatorcontrib><creatorcontrib>LAMBERTS, Steven W. J</creatorcontrib><creatorcontrib>HOFLAND, Leo J</creatorcontrib><creatorcontrib>VAN KOETSVELD ING, Peter M</creatorcontrib><creatorcontrib>ERDMANN, Joris I</creatorcontrib><creatorcontrib>SPEEL, Ernst Jan M</creatorcontrib><creatorcontrib>VAN DER WANSEM ING, Katy</creatorcontrib><creatorcontrib>MOOIJ, Diana M</creatorcontrib><creatorcontrib>COLAO, Annamaria</creatorcontrib><creatorcontrib>LOMBARDI, Gaetano</creatorcontrib><creatorcontrib>CROZE, Ed</creatorcontrib><title>Type I interferons in the treatment of pancreatic cancer : Mechanisms of action and role of related receptors</title><title>Annals of surgery</title><addtitle>Ann Surg</addtitle><description>We evaluated the role of type I interferons (IFNs) and IFN receptors in the regulation of cell growth in 3 human pancreatic adenocarcinoma cell lines (BxPC-3, MiaPaCa-2, and Panc-1).
Chemotherapy and radiotherapy have a marginal role in the management of pancreatic adenocarcinoma. The addition of IFN-alpha showed promising results in early clinical trials.
Cell proliferation and apoptosis were evaluated by DNA measurement and DNA fragmentation, respectively. Type I IFN receptor (IFNAR-1 and IFNAR-2 subunits) was determined by quantitative RT-PCR and immunocytochemistry. Cell cycle distribution was evaluated by propidium iodide staining and flow-cytometric analysis.
The incubation with IFN-beta for 6 days showed a potent inhibitory effect on the proliferation of BxPC-3 (IC(50), 14 IU/mL) and MiaPaCa-2 (IC(50), 64 IU/mL). The inhibitory effect of IFN-beta was stronger than IFN-alpha in all 3 cell lines and mainly modulated by the stimulation of apoptosis, although cell cycle arrest was induced as well. The expression of the type I IFN receptors was significantly higher in BxPC-3 (the most sensitive cell line to IFN) and mainly localized on the membrane, whereas in Panc-1 (the most resistant cell line) about 60% to 70% of cells were negative for IFNAR-2c with a mainly cytoplasmic staining for IFNAR-2c.
The antitumor activity of IFN-beta is more potent than IFN-alpha in pancreatic cancer cell lines through the induction of apoptosis. Further studies should investigate in vivo whether the intensity and distribution of IFNAR-1 and IFNAR-2c may predict the response to therapy with IFN-alpha and IFN-beta in pancreatic cancer.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - biosynthesis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Flow Cytometry</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>General aspects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Interferon Type I - therapeutic use</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>Original</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Prognosis</subject><subject>Receptor, Interferon alpha-beta - biosynthesis</subject><subject>Receptor, Interferon alpha-beta - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Tumors</subject><issn>0003-4932</issn><issn>1528-1140</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkd9vFCEQx4mxsWf1XzDERN_2CgsLbB9MTOOPJm36Up_JHDt4mN1lBc6k_72svXjKCzPMZ74DfAl5y9mWs15fMr7NI2xZXa3iUrEt07wWffuMbHjXmoZzyZ6TTQVEI3vRnpOXOf9gjEvD9AtyzrVSumPdhkwPjwvSGxrmgsljinOuMS17pCUhlAnnQqOnC8xuzYOjroaY6BW9Q7eHOeQprwS4EuJMYR5oiiOuRwlHKFhzdLiUmPIrcuZhzPj6uF-Qb58_PVx_bW7vv9xcf7xtnJBdaaRGYwbl0GuHzAymE4bLDgQTYmcG73u-wx4HB1rCoHcDN0Y6QNSgmOuUuCAfnnSXw26qXH1EgtEuKUyQHm2EYP-vzGFvv8dflvdCdFpWgfdHgRR_HjAXO4XscBxhxnjIVhneCsHaCl49gS7FnBP6v0M4s6tblnFb3bInt-wft6xfm9_8e81T69GeCrw7ApAdjD7Vrw_5xJle9L1qxW_UdaHa</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>VITALE, Giovanni</creator><creator>VAN EIJCK, Casper H. 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J ; HOFLAND, Leo J ; VAN KOETSVELD ING, Peter M ; ERDMANN, Joris I ; SPEEL, Ernst Jan M ; VAN DER WANSEM ING, Katy ; MOOIJ, Diana M ; COLAO, Annamaria ; LOMBARDI, Gaetano ; CROZE, Ed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c345t-47e88d6cef7ce08d8538145a3033b8dff91be9edca74ad7bd1884caee7a60c563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - biosynthesis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Flow Cytometry</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>General aspects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Interferon Type I - therapeutic use</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>Original</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Prognosis</topic><topic>Receptor, Interferon alpha-beta - biosynthesis</topic><topic>Receptor, Interferon alpha-beta - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VITALE, Giovanni</creatorcontrib><creatorcontrib>VAN EIJCK, Casper H. J</creatorcontrib><creatorcontrib>LAMBERTS, Steven W. J</creatorcontrib><creatorcontrib>HOFLAND, Leo J</creatorcontrib><creatorcontrib>VAN KOETSVELD ING, Peter M</creatorcontrib><creatorcontrib>ERDMANN, Joris I</creatorcontrib><creatorcontrib>SPEEL, Ernst Jan M</creatorcontrib><creatorcontrib>VAN DER WANSEM ING, Katy</creatorcontrib><creatorcontrib>MOOIJ, Diana M</creatorcontrib><creatorcontrib>COLAO, Annamaria</creatorcontrib><creatorcontrib>LOMBARDI, Gaetano</creatorcontrib><creatorcontrib>CROZE, Ed</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>PubMed Central (Full Participant titles)</collection><jtitle>Annals of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VITALE, Giovanni</au><au>VAN EIJCK, Casper H. J</au><au>LAMBERTS, Steven W. J</au><au>HOFLAND, Leo J</au><au>VAN KOETSVELD ING, Peter M</au><au>ERDMANN, Joris I</au><au>SPEEL, Ernst Jan M</au><au>VAN DER WANSEM ING, Katy</au><au>MOOIJ, Diana M</au><au>COLAO, Annamaria</au><au>LOMBARDI, Gaetano</au><au>CROZE, Ed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type I interferons in the treatment of pancreatic cancer : Mechanisms of action and role of related receptors</atitle><jtitle>Annals of surgery</jtitle><addtitle>Ann Surg</addtitle><date>2007-08-01</date><risdate>2007</risdate><volume>246</volume><issue>2</issue><spage>259</spage><epage>268</epage><pages>259-268</pages><issn>0003-4932</issn><eissn>1528-1140</eissn><coden>ANSUA5</coden><abstract>We evaluated the role of type I interferons (IFNs) and IFN receptors in the regulation of cell growth in 3 human pancreatic adenocarcinoma cell lines (BxPC-3, MiaPaCa-2, and Panc-1).
Chemotherapy and radiotherapy have a marginal role in the management of pancreatic adenocarcinoma. The addition of IFN-alpha showed promising results in early clinical trials.
Cell proliferation and apoptosis were evaluated by DNA measurement and DNA fragmentation, respectively. Type I IFN receptor (IFNAR-1 and IFNAR-2 subunits) was determined by quantitative RT-PCR and immunocytochemistry. Cell cycle distribution was evaluated by propidium iodide staining and flow-cytometric analysis.
The incubation with IFN-beta for 6 days showed a potent inhibitory effect on the proliferation of BxPC-3 (IC(50), 14 IU/mL) and MiaPaCa-2 (IC(50), 64 IU/mL). The inhibitory effect of IFN-beta was stronger than IFN-alpha in all 3 cell lines and mainly modulated by the stimulation of apoptosis, although cell cycle arrest was induced as well. The expression of the type I IFN receptors was significantly higher in BxPC-3 (the most sensitive cell line to IFN) and mainly localized on the membrane, whereas in Panc-1 (the most resistant cell line) about 60% to 70% of cells were negative for IFNAR-2c with a mainly cytoplasmic staining for IFNAR-2c.
The antitumor activity of IFN-beta is more potent than IFN-alpha in pancreatic cancer cell lines through the induction of apoptosis. Further studies should investigate in vivo whether the intensity and distribution of IFNAR-1 and IFNAR-2c may predict the response to therapy with IFN-alpha and IFN-beta in pancreatic cancer.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>17667505</pmid><doi>10.1097/01.sla.0000261460.07110.f2</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Annals of surgery, 2007-08, Vol.246 (2), p.259-268 |
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| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - metabolism Adenocarcinoma - pathology Antineoplastic Agents - therapeutic use Apoptosis - drug effects Biological and medical sciences Biomarkers, Tumor - biosynthesis Biomarkers, Tumor - genetics Cell Line, Tumor Cell Proliferation - drug effects Flow Cytometry Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic General aspects Humans Immunohistochemistry Interferon Type I - therapeutic use Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Original Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Prognosis Receptor, Interferon alpha-beta - biosynthesis Receptor, Interferon alpha-beta - genetics Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Tumors |
| title | Type I interferons in the treatment of pancreatic cancer : Mechanisms of action and role of related receptors |
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