Clonal Evolution of Resistance to Imatinib in Patients with Metastatic Gastrointestinal Stromal Tumors
Purpose: Resistance to imatinib mesylate is emerging as a clinical challenge in patients with metastatic gastrointestinal stromal tumors (GIST). Novel patterns of progression have been noted in a number of these patients. The objective of this study was to correlate molecular and radiologic patterns...
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creator | SHAH JAYESH DESAI, Neil P SHANKAR, Sridhar SILVERRNAN, Stuart G VAN DEN ABBEELE, Annick D VAN SONNENBERG, Eric DEMETRI, George D HEINRICH, Michael C FLETCHER, Jonathan A FLETCHER, Christopher D MANOLA, Judi MORGAN, Jeffrey A CORLESS, Christopher L GEORGE, Suzanne TUNCALI, Kernal |
description | Purpose: Resistance to imatinib mesylate is emerging as a clinical challenge in patients with metastatic gastrointestinal stromal
tumors (GIST). Novel patterns of progression have been noted in a number of these patients. The objective of this study was
to correlate molecular and radiologic patterns of imitinib-refractory disease with existing conventional criteria for disease
progression.
Experimental Design: Patients with metastatic GIST treated with imatinib were followed with serial computed tomography/magnetic resonance imaging
and [ 18 F]fluoro-2-deoxy- d -glucose positron emission tomography. Where feasible, biopsies were done to document disease progression.
Results: A total of 89 patients were followed for a median of 43 months. Forty-eight patients developed progressive disease. A unique
“resistant clonal nodule” pattern (defined as a new enhancing nodular focus enclosed within a preexisting tumor mass) was
seen in 23 of 48 patients and was thought to represent emergence of clones resistant to imatinib. Nodules were demonstrable
a median of 5 months (range, 0-13 months) before objective progression defined by tumor size criteria and were the first sign
of progression in 18 of 23 patients. Median survival among patients whose first progression was nodular was 35.1 months, compared
with 44.6 months for patients whose first progression met Southwest Oncology Group criteria ( P = 0.31). Comparative tumor biopsies were done in 10 patients at baseline and from progressing nodules. Genotypic analyses
of KIT and PDGFRA kinases were done, revealing new activating kinase mutations in 80% (8 of 10) of these patients.
Conclusion: The resistant clonal nodule is a unique pattern of disease progression seen in patients with GISTs after an initial response
to imatinib and reflects the emergence of imatinib-resistant clones. Conventional tumor measurements (Southwest Oncology Group/Response
Evaluation Criteria in Solid Tumors) do not detect this subtle finding. A new enhancing nodule growing within a preexisting
tumor mass should be classified as a new lesion and be regarded, at least, as partial progression of GIST. |
doi_str_mv | 10.1158/1078-0432.CCR-06-0858 |
format | Article |
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tumors (GIST). Novel patterns of progression have been noted in a number of these patients. The objective of this study was
to correlate molecular and radiologic patterns of imitinib-refractory disease with existing conventional criteria for disease
progression.
Experimental Design: Patients with metastatic GIST treated with imatinib were followed with serial computed tomography/magnetic resonance imaging
and [ 18 F]fluoro-2-deoxy- d -glucose positron emission tomography. Where feasible, biopsies were done to document disease progression.
Results: A total of 89 patients were followed for a median of 43 months. Forty-eight patients developed progressive disease. A unique
“resistant clonal nodule” pattern (defined as a new enhancing nodular focus enclosed within a preexisting tumor mass) was
seen in 23 of 48 patients and was thought to represent emergence of clones resistant to imatinib. Nodules were demonstrable
a median of 5 months (range, 0-13 months) before objective progression defined by tumor size criteria and were the first sign
of progression in 18 of 23 patients. Median survival among patients whose first progression was nodular was 35.1 months, compared
with 44.6 months for patients whose first progression met Southwest Oncology Group criteria ( P = 0.31). Comparative tumor biopsies were done in 10 patients at baseline and from progressing nodules. Genotypic analyses
of KIT and PDGFRA kinases were done, revealing new activating kinase mutations in 80% (8 of 10) of these patients.
Conclusion: The resistant clonal nodule is a unique pattern of disease progression seen in patients with GISTs after an initial response
to imatinib and reflects the emergence of imatinib-resistant clones. Conventional tumor measurements (Southwest Oncology Group/Response
Evaluation Criteria in Solid Tumors) do not detect this subtle finding. A new enhancing nodule growing within a preexisting
tumor mass should be classified as a new lesion and be regarded, at least, as partial progression of GIST.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-06-0858</identifier><identifier>PMID: 17875769</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Antineoplastic agents ; Antineoplastic Agents - therapeutic use ; Benzamides ; Biological and medical sciences ; Clone Cells - pathology ; Drug Resistance, Neoplasm - genetics ; Evolution, Molecular ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gastrointestinal Stromal Tumor ; Gastrointestinal Stromal Tumors - diagnostic imaging ; Gastrointestinal Stromal Tumors - drug therapy ; Gastrointestinal Stromal Tumors - pathology ; Humans ; Imatinib Mesylate ; Male ; Medical sciences ; Middle Aged ; Pharmacology. Drug treatments ; Piperazines - therapeutic use ; Protein tyrosine kinases ; Proto-Oncogene Proteins c-kit - genetics ; Pyrimidines - therapeutic use ; Radiography ; Receptor, Platelet-Derived Growth Factor alpha - genetics ; Resistance ; Sequence Deletion ; Signal transduction ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Survival Analysis ; Tumors</subject><ispartof>Clinical cancer research, 2007-09, Vol.13 (18), p.5398-5405</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371t-c91321a9ee227b7f0c8a71a6cb5bf22d6fb54470cd0219fa6b26295000dca88e3</citedby><cites>FETCH-LOGICAL-c371t-c91321a9ee227b7f0c8a71a6cb5bf22d6fb54470cd0219fa6b26295000dca88e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19164042$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17875769$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHAH JAYESH DESAI, Neil P</creatorcontrib><creatorcontrib>SHANKAR, Sridhar</creatorcontrib><creatorcontrib>SILVERRNAN, Stuart G</creatorcontrib><creatorcontrib>VAN DEN ABBEELE, Annick D</creatorcontrib><creatorcontrib>VAN SONNENBERG, Eric</creatorcontrib><creatorcontrib>DEMETRI, George D</creatorcontrib><creatorcontrib>HEINRICH, Michael C</creatorcontrib><creatorcontrib>FLETCHER, Jonathan A</creatorcontrib><creatorcontrib>FLETCHER, Christopher D</creatorcontrib><creatorcontrib>MANOLA, Judi</creatorcontrib><creatorcontrib>MORGAN, Jeffrey A</creatorcontrib><creatorcontrib>CORLESS, Christopher L</creatorcontrib><creatorcontrib>GEORGE, Suzanne</creatorcontrib><creatorcontrib>TUNCALI, Kernal</creatorcontrib><title>Clonal Evolution of Resistance to Imatinib in Patients with Metastatic Gastrointestinal Stromal Tumors</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Resistance to imatinib mesylate is emerging as a clinical challenge in patients with metastatic gastrointestinal stromal
tumors (GIST). Novel patterns of progression have been noted in a number of these patients. The objective of this study was
to correlate molecular and radiologic patterns of imitinib-refractory disease with existing conventional criteria for disease
progression.
Experimental Design: Patients with metastatic GIST treated with imatinib were followed with serial computed tomography/magnetic resonance imaging
and [ 18 F]fluoro-2-deoxy- d -glucose positron emission tomography. Where feasible, biopsies were done to document disease progression.
Results: A total of 89 patients were followed for a median of 43 months. Forty-eight patients developed progressive disease. A unique
“resistant clonal nodule” pattern (defined as a new enhancing nodular focus enclosed within a preexisting tumor mass) was
seen in 23 of 48 patients and was thought to represent emergence of clones resistant to imatinib. Nodules were demonstrable
a median of 5 months (range, 0-13 months) before objective progression defined by tumor size criteria and were the first sign
of progression in 18 of 23 patients. Median survival among patients whose first progression was nodular was 35.1 months, compared
with 44.6 months for patients whose first progression met Southwest Oncology Group criteria ( P = 0.31). Comparative tumor biopsies were done in 10 patients at baseline and from progressing nodules. Genotypic analyses
of KIT and PDGFRA kinases were done, revealing new activating kinase mutations in 80% (8 of 10) of these patients.
Conclusion: The resistant clonal nodule is a unique pattern of disease progression seen in patients with GISTs after an initial response
to imatinib and reflects the emergence of imatinib-resistant clones. Conventional tumor measurements (Southwest Oncology Group/Response
Evaluation Criteria in Solid Tumors) do not detect this subtle finding. A new enhancing nodule growing within a preexisting
tumor mass should be classified as a new lesion and be regarded, at least, as partial progression of GIST.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Benzamides</subject><subject>Biological and medical sciences</subject><subject>Clone Cells - pathology</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Evolution, Molecular</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gastrointestinal Stromal Tumor</subject><subject>Gastrointestinal Stromal Tumors - diagnostic imaging</subject><subject>Gastrointestinal Stromal Tumors - drug therapy</subject><subject>Gastrointestinal Stromal Tumors - pathology</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Piperazines - therapeutic use</subject><subject>Protein tyrosine kinases</subject><subject>Proto-Oncogene Proteins c-kit - genetics</subject><subject>Pyrimidines - therapeutic use</subject><subject>Radiography</subject><subject>Receptor, Platelet-Derived Growth Factor alpha - genetics</subject><subject>Resistance</subject><subject>Sequence Deletion</subject><subject>Signal transduction</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Survival Analysis</subject><subject>Tumors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtv1TAQRi0Eog_4CSBvQOoiZcaJH1miqJRKRaBS1pbja3ONkrjYDhX_Hkf3oq7mG-nMQ4eQNwiXiFx9QJCqga5ll8Nw14BoQHH1jJwi57JpmeDPa_7PnJCznH8BYIfQvSQnKJXkUvSnxA9TXMxEr_7EaS0hLjR6eudyyMUs1tES6c1sSljCSMNCv9XolpLpYyh7-sUVU7kSLL2uIcWwFJcrXBd-r-1c6_06x5RfkRfeTNm9PtZz8uPT1f3wubn9en0zfLxtbCuxNLbHlqHpnWNMjtKDVUaiEXbko2dsJ_zIu06C3QHD3hsxMsF6DgA7a5Ry7Tl5f9j7kOLvtf6i55CtmyazuLhmLRRTrAOoID-ANsWck_P6IYXZpL8aQW-C9SZPb_J0FaxB6E1wnXt7PLCOs9s9TR2NVuDdETDZmsmnqjHkJ65H0UHHKndx4Pbh5_4xJKftJjwll51Jdq-x1ag0b3vV_gOS3ZNf</recordid><startdate>20070915</startdate><enddate>20070915</enddate><creator>SHAH JAYESH DESAI, Neil P</creator><creator>SHANKAR, Sridhar</creator><creator>SILVERRNAN, Stuart G</creator><creator>VAN DEN ABBEELE, Annick D</creator><creator>VAN SONNENBERG, Eric</creator><creator>DEMETRI, George D</creator><creator>HEINRICH, Michael C</creator><creator>FLETCHER, Jonathan A</creator><creator>FLETCHER, Christopher D</creator><creator>MANOLA, Judi</creator><creator>MORGAN, Jeffrey A</creator><creator>CORLESS, Christopher L</creator><creator>GEORGE, Suzanne</creator><creator>TUNCALI, Kernal</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>7X8</scope></search><sort><creationdate>20070915</creationdate><title>Clonal Evolution of Resistance to Imatinib in Patients with Metastatic Gastrointestinal Stromal Tumors</title><author>SHAH JAYESH DESAI, Neil P ; SHANKAR, Sridhar ; SILVERRNAN, Stuart G ; VAN DEN ABBEELE, Annick D ; VAN SONNENBERG, Eric ; DEMETRI, George D ; HEINRICH, Michael C ; FLETCHER, Jonathan A ; FLETCHER, Christopher D ; MANOLA, Judi ; MORGAN, Jeffrey A ; CORLESS, Christopher L ; GEORGE, Suzanne ; TUNCALI, Kernal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371t-c91321a9ee227b7f0c8a71a6cb5bf22d6fb54470cd0219fa6b26295000dca88e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Benzamides</topic><topic>Biological and medical sciences</topic><topic>Clone Cells - pathology</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Evolution, Molecular</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gastrointestinal Stromal Tumor</topic><topic>Gastrointestinal Stromal Tumors - diagnostic imaging</topic><topic>Gastrointestinal Stromal Tumors - drug therapy</topic><topic>Gastrointestinal Stromal Tumors - pathology</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Piperazines - therapeutic use</topic><topic>Protein tyrosine kinases</topic><topic>Proto-Oncogene Proteins c-kit - genetics</topic><topic>Pyrimidines - therapeutic use</topic><topic>Radiography</topic><topic>Receptor, Platelet-Derived Growth Factor alpha - genetics</topic><topic>Resistance</topic><topic>Sequence Deletion</topic><topic>Signal transduction</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Survival Analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHAH JAYESH DESAI, Neil P</creatorcontrib><creatorcontrib>SHANKAR, Sridhar</creatorcontrib><creatorcontrib>SILVERRNAN, Stuart G</creatorcontrib><creatorcontrib>VAN DEN ABBEELE, Annick D</creatorcontrib><creatorcontrib>VAN SONNENBERG, Eric</creatorcontrib><creatorcontrib>DEMETRI, George D</creatorcontrib><creatorcontrib>HEINRICH, Michael C</creatorcontrib><creatorcontrib>FLETCHER, Jonathan A</creatorcontrib><creatorcontrib>FLETCHER, Christopher D</creatorcontrib><creatorcontrib>MANOLA, Judi</creatorcontrib><creatorcontrib>MORGAN, Jeffrey A</creatorcontrib><creatorcontrib>CORLESS, Christopher L</creatorcontrib><creatorcontrib>GEORGE, Suzanne</creatorcontrib><creatorcontrib>TUNCALI, Kernal</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><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHAH JAYESH DESAI, Neil P</au><au>SHANKAR, Sridhar</au><au>SILVERRNAN, Stuart G</au><au>VAN DEN ABBEELE, Annick D</au><au>VAN SONNENBERG, Eric</au><au>DEMETRI, George D</au><au>HEINRICH, Michael C</au><au>FLETCHER, Jonathan A</au><au>FLETCHER, Christopher D</au><au>MANOLA, Judi</au><au>MORGAN, Jeffrey A</au><au>CORLESS, Christopher L</au><au>GEORGE, Suzanne</au><au>TUNCALI, Kernal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clonal Evolution of Resistance to Imatinib in Patients with Metastatic Gastrointestinal Stromal Tumors</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2007-09-15</date><risdate>2007</risdate><volume>13</volume><issue>18</issue><spage>5398</spage><epage>5405</epage><pages>5398-5405</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Resistance to imatinib mesylate is emerging as a clinical challenge in patients with metastatic gastrointestinal stromal
tumors (GIST). Novel patterns of progression have been noted in a number of these patients. The objective of this study was
to correlate molecular and radiologic patterns of imitinib-refractory disease with existing conventional criteria for disease
progression.
Experimental Design: Patients with metastatic GIST treated with imatinib were followed with serial computed tomography/magnetic resonance imaging
and [ 18 F]fluoro-2-deoxy- d -glucose positron emission tomography. Where feasible, biopsies were done to document disease progression.
Results: A total of 89 patients were followed for a median of 43 months. Forty-eight patients developed progressive disease. A unique
“resistant clonal nodule” pattern (defined as a new enhancing nodular focus enclosed within a preexisting tumor mass) was
seen in 23 of 48 patients and was thought to represent emergence of clones resistant to imatinib. Nodules were demonstrable
a median of 5 months (range, 0-13 months) before objective progression defined by tumor size criteria and were the first sign
of progression in 18 of 23 patients. Median survival among patients whose first progression was nodular was 35.1 months, compared
with 44.6 months for patients whose first progression met Southwest Oncology Group criteria ( P = 0.31). Comparative tumor biopsies were done in 10 patients at baseline and from progressing nodules. Genotypic analyses
of KIT and PDGFRA kinases were done, revealing new activating kinase mutations in 80% (8 of 10) of these patients.
Conclusion: The resistant clonal nodule is a unique pattern of disease progression seen in patients with GISTs after an initial response
to imatinib and reflects the emergence of imatinib-resistant clones. Conventional tumor measurements (Southwest Oncology Group/Response
Evaluation Criteria in Solid Tumors) do not detect this subtle finding. A new enhancing nodule growing within a preexisting
tumor mass should be classified as a new lesion and be regarded, at least, as partial progression of GIST.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>17875769</pmid><doi>10.1158/1078-0432.CCR-06-0858</doi><tpages>8</tpages></addata></record> |
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source | MEDLINE; publisher website; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | Adolescent Adult Aged Aged, 80 and over Antineoplastic agents Antineoplastic Agents - therapeutic use Benzamides Biological and medical sciences Clone Cells - pathology Drug Resistance, Neoplasm - genetics Evolution, Molecular Female Gastroenterology. Liver. Pancreas. Abdomen Gastrointestinal Stromal Tumor Gastrointestinal Stromal Tumors - diagnostic imaging Gastrointestinal Stromal Tumors - drug therapy Gastrointestinal Stromal Tumors - pathology Humans Imatinib Mesylate Male Medical sciences Middle Aged Pharmacology. Drug treatments Piperazines - therapeutic use Protein tyrosine kinases Proto-Oncogene Proteins c-kit - genetics Pyrimidines - therapeutic use Radiography Receptor, Platelet-Derived Growth Factor alpha - genetics Resistance Sequence Deletion Signal transduction Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Survival Analysis Tumors |
title | Clonal Evolution of Resistance to Imatinib in Patients with Metastatic Gastrointestinal Stromal Tumors |
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