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Proteomic detection of a large amount of SCGFα in the stroma of GISTs after imatinib therapy
Gastrointestinal stromal tumors (GISTs) are the most frequent mesenchymal tumors to develop in the digestive tract. These tumors are highly resistant to conventional chemotherapy and only the introduction of imatinib mesylate has improved the prognosis of patients. However, Response Evaluation Crite...
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Published in: | Journal of translational medicine 2011-09, Vol.9 (1), p.158-158, Article 158 |
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creator | Da Riva, Luca Bozzi, Fabio Mondellini, Piera Miccichè, Francesca Fumagalli, Elena Vaghi, Elena Tarantino, Eva Huber, Veronica Gronchi, Alessandro Tamborini, Elena Pierotti, Marco A Pilotti, Silvana Bongarzone, Italia |
description | Gastrointestinal stromal tumors (GISTs) are the most frequent mesenchymal tumors to develop in the digestive tract. These tumors are highly resistant to conventional chemotherapy and only the introduction of imatinib mesylate has improved the prognosis of patients. However, Response Evaluation Criteria in Solid Tumors are inappropriate for assessing tumor response, and the histological/pathological response to imatinib is variable, heterogeneous, and does not associate with clinical response. The effects of imatinib on responding GISTs are still being explored, and few studies correlate the clinical response with the histological response after pharmacological treatment. Recently, apoptosis and autophagy were suggested as possible alternative mechanisms of pharmacological response.
Here, we used a proteomic approach, combined with other analyses, to identify some molecular stromal components related to the response/behavior of resected, high-risk GISTs after neoadiuvant imatinib therapy.
Our proteomic results indicate an elevated concentration of Stem Cell Growth Factor (SCGF), a hematopoietic growth factor having a role in the development of erythroid and myeloid progenitors, in imatinib-responsive tumor areas. SCGFα expression was detected by mass spectrometry, immunohistochemistry and/or western blot and attributed to acellular matrix of areas scored negative for KIT (CD117). RT-PCR results indicated that GIST samples did not express SCGF transcripts. The recently reported demonstration by Gundacker et al. 1 of the secretion of SCGF in mature pro-inflammatory dendritic cells would indicate a potential importance of SCGF in tissue inflammatory response. Accordingly, inflammatory infiltrates were detected in imatinib-affected areas and the CD68-positivity of the SCGF-positive and KIT-negative areas suggested previous infiltration of monocytes/macrophages into these regions. Thus, chronic inflammation subsequent to imatinib treatment may determine monocyte/macrophage recruitment in imatinib-damaged areas; these areas also feature prominent tumor-cell loss that is replaced by dense hyalinization and fibrosis.
Our studies highlight a possible role of SCGFα in imatinib-induced changes of GIST structure, consistent with a therapeutic response. |
doi_str_mv | 10.1186/1479-5876-9-158 |
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Here, we used a proteomic approach, combined with other analyses, to identify some molecular stromal components related to the response/behavior of resected, high-risk GISTs after neoadiuvant imatinib therapy.
Our proteomic results indicate an elevated concentration of Stem Cell Growth Factor (SCGF), a hematopoietic growth factor having a role in the development of erythroid and myeloid progenitors, in imatinib-responsive tumor areas. SCGFα expression was detected by mass spectrometry, immunohistochemistry and/or western blot and attributed to acellular matrix of areas scored negative for KIT (CD117). RT-PCR results indicated that GIST samples did not express SCGF transcripts. The recently reported demonstration by Gundacker et al. 1 of the secretion of SCGF in mature pro-inflammatory dendritic cells would indicate a potential importance of SCGF in tissue inflammatory response. Accordingly, inflammatory infiltrates were detected in imatinib-affected areas and the CD68-positivity of the SCGF-positive and KIT-negative areas suggested previous infiltration of monocytes/macrophages into these regions. Thus, chronic inflammation subsequent to imatinib treatment may determine monocyte/macrophage recruitment in imatinib-damaged areas; these areas also feature prominent tumor-cell loss that is replaced by dense hyalinization and fibrosis.
Our studies highlight a possible role of SCGFα in imatinib-induced changes of GIST structure, consistent with a therapeutic response.</description><identifier>ISSN: 1479-5876</identifier><identifier>EISSN: 1479-5876</identifier><identifier>DOI: 10.1186/1479-5876-9-158</identifier><identifier>PMID: 21943129</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Benzamides ; Blotting, Western ; Cell Line, Tumor ; Electrophoresis, Polyacrylamide Gel ; Gastrointestinal Stromal Tumors - drug therapy ; Gastrointestinal Stromal Tumors - genetics ; Gastrointestinal Stromal Tumors - metabolism ; Gastrointestinal Stromal Tumors - pathology ; Gene Expression Regulation, Neoplastic ; Glycosylation ; Hematopoietic Cell Growth Factors - genetics ; Hematopoietic Cell Growth Factors - metabolism ; Humans ; Imatinib Mesylate ; Immunohistochemistry ; Lectins, C-Type - genetics ; Lectins, C-Type - metabolism ; Piperazines - therapeutic use ; Proteomics - methods ; Pyrimidines - therapeutic use ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Stromal Cells - metabolism ; Stromal Cells - pathology</subject><ispartof>Journal of translational medicine, 2011-09, Vol.9 (1), p.158-158, Article 158</ispartof><rights>Copyright ©2011 Da Riva et al; licensee BioMed Central Ltd. 2011 Da Riva et al; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b517t-8cd06f72cda6ea5abad1092f0148d8fdef77ca57d52dc064c9471d80045962e63</citedby><cites>FETCH-LOGICAL-b517t-8cd06f72cda6ea5abad1092f0148d8fdef77ca57d52dc064c9471d80045962e63</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/PMC3192683/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192683/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,37013,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21943129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Da Riva, Luca</creatorcontrib><creatorcontrib>Bozzi, Fabio</creatorcontrib><creatorcontrib>Mondellini, Piera</creatorcontrib><creatorcontrib>Miccichè, Francesca</creatorcontrib><creatorcontrib>Fumagalli, Elena</creatorcontrib><creatorcontrib>Vaghi, Elena</creatorcontrib><creatorcontrib>Tarantino, Eva</creatorcontrib><creatorcontrib>Huber, Veronica</creatorcontrib><creatorcontrib>Gronchi, Alessandro</creatorcontrib><creatorcontrib>Tamborini, Elena</creatorcontrib><creatorcontrib>Pierotti, Marco A</creatorcontrib><creatorcontrib>Pilotti, Silvana</creatorcontrib><creatorcontrib>Bongarzone, Italia</creatorcontrib><title>Proteomic detection of a large amount of SCGFα in the stroma of GISTs after imatinib therapy</title><title>Journal of translational medicine</title><addtitle>J Transl Med</addtitle><description>Gastrointestinal stromal tumors (GISTs) are the most frequent mesenchymal tumors to develop in the digestive tract. These tumors are highly resistant to conventional chemotherapy and only the introduction of imatinib mesylate has improved the prognosis of patients. However, Response Evaluation Criteria in Solid Tumors are inappropriate for assessing tumor response, and the histological/pathological response to imatinib is variable, heterogeneous, and does not associate with clinical response. The effects of imatinib on responding GISTs are still being explored, and few studies correlate the clinical response with the histological response after pharmacological treatment. Recently, apoptosis and autophagy were suggested as possible alternative mechanisms of pharmacological response.
Here, we used a proteomic approach, combined with other analyses, to identify some molecular stromal components related to the response/behavior of resected, high-risk GISTs after neoadiuvant imatinib therapy.
Our proteomic results indicate an elevated concentration of Stem Cell Growth Factor (SCGF), a hematopoietic growth factor having a role in the development of erythroid and myeloid progenitors, in imatinib-responsive tumor areas. SCGFα expression was detected by mass spectrometry, immunohistochemistry and/or western blot and attributed to acellular matrix of areas scored negative for KIT (CD117). RT-PCR results indicated that GIST samples did not express SCGF transcripts. The recently reported demonstration by Gundacker et al. 1 of the secretion of SCGF in mature pro-inflammatory dendritic cells would indicate a potential importance of SCGF in tissue inflammatory response. Accordingly, inflammatory infiltrates were detected in imatinib-affected areas and the CD68-positivity of the SCGF-positive and KIT-negative areas suggested previous infiltration of monocytes/macrophages into these regions. Thus, chronic inflammation subsequent to imatinib treatment may determine monocyte/macrophage recruitment in imatinib-damaged areas; these areas also feature prominent tumor-cell loss that is replaced by dense hyalinization and fibrosis.
Our studies highlight a possible role of SCGFα in imatinib-induced changes of GIST structure, consistent with a therapeutic response.</description><subject>Benzamides</subject><subject>Blotting, Western</subject><subject>Cell Line, Tumor</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Gastrointestinal Stromal Tumors - drug therapy</subject><subject>Gastrointestinal Stromal Tumors - genetics</subject><subject>Gastrointestinal Stromal Tumors - metabolism</subject><subject>Gastrointestinal Stromal Tumors - pathology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycosylation</subject><subject>Hematopoietic Cell Growth Factors - genetics</subject><subject>Hematopoietic Cell Growth Factors - metabolism</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Immunohistochemistry</subject><subject>Lectins, C-Type - genetics</subject><subject>Lectins, C-Type - metabolism</subject><subject>Piperazines - therapeutic use</subject><subject>Proteomics - methods</subject><subject>Pyrimidines - therapeutic use</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</subject><subject>Stromal Cells - metabolism</subject><subject>Stromal Cells - pathology</subject><issn>1479-5876</issn><issn>1479-5876</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp1kl1rFDEUhgex2Fq99k5y59XYZCafN4Iudl0oWGh7KeHkY7YpM5M1yRb6s_wj_iZn3Lp0wUIg4T0vzznhPVX1juCPhEh-RqhQNZOC16omTL6oTvbKyyfv4-p1zncYN5RR9ao6boiiLWnUSfXjMsXi4xAscr54W0IcUewQoB7S2iMY4nYss3K1WJ7__oXCiMqtR7mkOMCsL1dX1xlBV3xCYYASxmBmS4LNw5vqqIM--7eP92l1c_71evGtvvi-XC0-X9SGEVFqaR3mnWisA-6BgQFHsGo6TKh0snO-E8ICE441zmJOraKCOIkxZYo3nren1WrHdRHu9CZNc6QHHSHov0JMaw2pBNt7Dd44xsESpQQlrZPOGGM5ng5tLKYT69OOtdmawTvrx5KgP4AeVsZwq9fxXrdENVy2E-DLDmBCfAZwWLFx0HNUeo5KKz0FOUE-PE6R4s-tz0UPIVvf9zD6uM1aKskwVq2anGc7p00x5-S7fSeC9bwk_2G_f_rDvf_fVrR_AJ5ZueE</recordid><startdate>20110923</startdate><enddate>20110923</enddate><creator>Da Riva, Luca</creator><creator>Bozzi, Fabio</creator><creator>Mondellini, Piera</creator><creator>Miccichè, Francesca</creator><creator>Fumagalli, Elena</creator><creator>Vaghi, Elena</creator><creator>Tarantino, Eva</creator><creator>Huber, Veronica</creator><creator>Gronchi, Alessandro</creator><creator>Tamborini, Elena</creator><creator>Pierotti, Marco A</creator><creator>Pilotti, Silvana</creator><creator>Bongarzone, Italia</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20110923</creationdate><title>Proteomic detection of a large amount of SCGFα in the stroma of GISTs after imatinib therapy</title><author>Da Riva, Luca ; Bozzi, Fabio ; Mondellini, Piera ; Miccichè, Francesca ; Fumagalli, Elena ; Vaghi, Elena ; Tarantino, Eva ; Huber, Veronica ; Gronchi, Alessandro ; Tamborini, Elena ; Pierotti, Marco A ; Pilotti, Silvana ; Bongarzone, Italia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b517t-8cd06f72cda6ea5abad1092f0148d8fdef77ca57d52dc064c9471d80045962e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Benzamides</topic><topic>Blotting, Western</topic><topic>Cell Line, Tumor</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Gastrointestinal Stromal Tumors - drug therapy</topic><topic>Gastrointestinal Stromal Tumors - genetics</topic><topic>Gastrointestinal Stromal Tumors - metabolism</topic><topic>Gastrointestinal Stromal Tumors - pathology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glycosylation</topic><topic>Hematopoietic Cell Growth Factors - genetics</topic><topic>Hematopoietic Cell Growth Factors - metabolism</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Immunohistochemistry</topic><topic>Lectins, C-Type - genetics</topic><topic>Lectins, C-Type - metabolism</topic><topic>Piperazines - therapeutic use</topic><topic>Proteomics - methods</topic><topic>Pyrimidines - therapeutic use</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization</topic><topic>Stromal Cells - metabolism</topic><topic>Stromal Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Da Riva, Luca</creatorcontrib><creatorcontrib>Bozzi, Fabio</creatorcontrib><creatorcontrib>Mondellini, Piera</creatorcontrib><creatorcontrib>Miccichè, Francesca</creatorcontrib><creatorcontrib>Fumagalli, Elena</creatorcontrib><creatorcontrib>Vaghi, Elena</creatorcontrib><creatorcontrib>Tarantino, Eva</creatorcontrib><creatorcontrib>Huber, Veronica</creatorcontrib><creatorcontrib>Gronchi, Alessandro</creatorcontrib><creatorcontrib>Tamborini, Elena</creatorcontrib><creatorcontrib>Pierotti, Marco A</creatorcontrib><creatorcontrib>Pilotti, Silvana</creatorcontrib><creatorcontrib>Bongarzone, Italia</creatorcontrib><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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of translational medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Da Riva, Luca</au><au>Bozzi, Fabio</au><au>Mondellini, Piera</au><au>Miccichè, Francesca</au><au>Fumagalli, Elena</au><au>Vaghi, Elena</au><au>Tarantino, Eva</au><au>Huber, Veronica</au><au>Gronchi, Alessandro</au><au>Tamborini, Elena</au><au>Pierotti, Marco A</au><au>Pilotti, Silvana</au><au>Bongarzone, Italia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteomic detection of a large amount of SCGFα in the stroma of GISTs after imatinib therapy</atitle><jtitle>Journal of translational medicine</jtitle><addtitle>J Transl Med</addtitle><date>2011-09-23</date><risdate>2011</risdate><volume>9</volume><issue>1</issue><spage>158</spage><epage>158</epage><pages>158-158</pages><artnum>158</artnum><issn>1479-5876</issn><eissn>1479-5876</eissn><abstract>Gastrointestinal stromal tumors (GISTs) are the most frequent mesenchymal tumors to develop in the digestive tract. These tumors are highly resistant to conventional chemotherapy and only the introduction of imatinib mesylate has improved the prognosis of patients. However, Response Evaluation Criteria in Solid Tumors are inappropriate for assessing tumor response, and the histological/pathological response to imatinib is variable, heterogeneous, and does not associate with clinical response. The effects of imatinib on responding GISTs are still being explored, and few studies correlate the clinical response with the histological response after pharmacological treatment. Recently, apoptosis and autophagy were suggested as possible alternative mechanisms of pharmacological response.
Here, we used a proteomic approach, combined with other analyses, to identify some molecular stromal components related to the response/behavior of resected, high-risk GISTs after neoadiuvant imatinib therapy.
Our proteomic results indicate an elevated concentration of Stem Cell Growth Factor (SCGF), a hematopoietic growth factor having a role in the development of erythroid and myeloid progenitors, in imatinib-responsive tumor areas. SCGFα expression was detected by mass spectrometry, immunohistochemistry and/or western blot and attributed to acellular matrix of areas scored negative for KIT (CD117). RT-PCR results indicated that GIST samples did not express SCGF transcripts. The recently reported demonstration by Gundacker et al. 1 of the secretion of SCGF in mature pro-inflammatory dendritic cells would indicate a potential importance of SCGF in tissue inflammatory response. Accordingly, inflammatory infiltrates were detected in imatinib-affected areas and the CD68-positivity of the SCGF-positive and KIT-negative areas suggested previous infiltration of monocytes/macrophages into these regions. Thus, chronic inflammation subsequent to imatinib treatment may determine monocyte/macrophage recruitment in imatinib-damaged areas; these areas also feature prominent tumor-cell loss that is replaced by dense hyalinization and fibrosis.
Our studies highlight a possible role of SCGFα in imatinib-induced changes of GIST structure, consistent with a therapeutic response.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>21943129</pmid><doi>10.1186/1479-5876-9-158</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Benzamides Blotting, Western Cell Line, Tumor Electrophoresis, Polyacrylamide Gel Gastrointestinal Stromal Tumors - drug therapy Gastrointestinal Stromal Tumors - genetics Gastrointestinal Stromal Tumors - metabolism Gastrointestinal Stromal Tumors - pathology Gene Expression Regulation, Neoplastic Glycosylation Hematopoietic Cell Growth Factors - genetics Hematopoietic Cell Growth Factors - metabolism Humans Imatinib Mesylate Immunohistochemistry Lectins, C-Type - genetics Lectins, C-Type - metabolism Piperazines - therapeutic use Proteomics - methods Pyrimidines - therapeutic use RNA, Messenger - genetics RNA, Messenger - metabolism Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Stromal Cells - metabolism Stromal Cells - pathology |
title | Proteomic detection of a large amount of SCGFα in the stroma of GISTs after imatinib therapy |
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