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Predictive value of neoadjuvant chemotherapy failure in breast cancer using FDG–PET after the first course
The aim of this study was to prospectively evaluate the predictive value of 18 F-fluorodeoxyglucose–positron emission tomography (FDG–PET) to detect the absence of pathological response to preoperative chemotherapy in patients (pts) with breast cancer. 63 consecutive pts with non-metastatic, non-inf...
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Published in: | Breast cancer research and treatment 2012-01, Vol.131 (2), p.517-525 |
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description | The aim of this study was to prospectively evaluate the predictive value of
18
F-fluorodeoxyglucose–positron emission tomography (FDG–PET) to detect the absence of pathological response to preoperative chemotherapy in patients (pts) with breast cancer. 63 consecutive pts with non-metastatic, non-inflammatory breast cancer, eligible for neoadjuvant chemotherapy (3 FEC 100 followed by 3 Docetaxel) were enrolled. FDG–PET was performed just before the first as well as before the second course. Metabolic activity (tumour FDG uptake) was measured by standardised uptake value (SUV
max
). Pts were classified as non-responders (NR) when the decrease of SUV
max
in the primary tumour was less than 15% at the time of the second PET (EORTC 1999 criteria). The metabolic response in FDG–PET was correlated with WHO criteria (clinical evaluation and ultrasound and/or mammography) evaluated after three cycles, pathological complete response (pCR) after surgery (according to Sataloff classification) and 4-year relapse-free survival (RFS). The mean SUV
max
decrease according to histological response was −52 ± 21% in case of pCR (Sataloff A) and 25 ± 34% in other cases (Sataloff B + C + D). Out of the 16 pts with no PET response (SUV decrease less than 15%), only one had a clinical response after the third cycle, and no pCR was observed. The 4-year RFS rate was significantly longer for metabolic responders than for NR (respectively, 85 vs. 44%;
P
= 0.01). This prospective study shows that a decrease in the SUV of less than 15% after the first chemotherapy course is a very potent predictor for failure of neoadjuvant chemotherapy, especially of pCR. It is interesting to note that this was shown despite the fact that the chemotherapy regimen was changed after the third course. |
doi_str_mv | 10.1007/s10549-011-1832-4 |
format | article |
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18
F-fluorodeoxyglucose–positron emission tomography (FDG–PET) to detect the absence of pathological response to preoperative chemotherapy in patients (pts) with breast cancer. 63 consecutive pts with non-metastatic, non-inflammatory breast cancer, eligible for neoadjuvant chemotherapy (3 FEC 100 followed by 3 Docetaxel) were enrolled. FDG–PET was performed just before the first as well as before the second course. Metabolic activity (tumour FDG uptake) was measured by standardised uptake value (SUV
max
). Pts were classified as non-responders (NR) when the decrease of SUV
max
in the primary tumour was less than 15% at the time of the second PET (EORTC 1999 criteria). The metabolic response in FDG–PET was correlated with WHO criteria (clinical evaluation and ultrasound and/or mammography) evaluated after three cycles, pathological complete response (pCR) after surgery (according to Sataloff classification) and 4-year relapse-free survival (RFS). The mean SUV
max
decrease according to histological response was −52 ± 21% in case of pCR (Sataloff A) and 25 ± 34% in other cases (Sataloff B + C + D). Out of the 16 pts with no PET response (SUV decrease less than 15%), only one had a clinical response after the third cycle, and no pCR was observed. The 4-year RFS rate was significantly longer for metabolic responders than for NR (respectively, 85 vs. 44%;
P
= 0.01). This prospective study shows that a decrease in the SUV of less than 15% after the first chemotherapy course is a very potent predictor for failure of neoadjuvant chemotherapy, especially of pCR. It is interesting to note that this was shown despite the fact that the chemotherapy regimen was changed after the third course.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-011-1832-4</identifier><identifier>PMID: 22037787</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adjuvant treatment ; Adult ; Aged ; Biological and medical sciences ; Breast cancer ; Breast Neoplasms - diagnostic imaging ; Breast Neoplasms - drug therapy ; Breast Neoplasms - mortality ; Cancer ; Cancer research ; Cancer therapies ; Chemotherapy ; Clinical Trial ; Docetaxel ; Failure ; Female ; Fluorodeoxyglucose F18 ; Gynecology. Andrology. Obstetrics ; Humans ; Mammary gland diseases ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Neoadjuvant Therapy ; Neoplasm Staging ; Oncology ; PET imaging ; Positron-Emission Tomography ; Predictions ; Prognosis ; Sport-utility vehicles ; Survival Analysis ; Tomography ; Treatment Failure ; Tumors</subject><ispartof>Breast cancer research and treatment, 2012-01, Vol.131 (2), p.517-525</ispartof><rights>Springer Science+Business Media, LLC. 2011</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2012 Springer</rights><rights>Springer Science+Business Media, LLC. 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-d66795745db096d7e9a3e441e81bd2f6ec8172d51795f1b5a75a0b373616f46e3</citedby><cites>FETCH-LOGICAL-c498t-d66795745db096d7e9a3e441e81bd2f6ec8172d51795f1b5a75a0b373616f46e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25422620$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22037787$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kolesnikov-Gauthier, Hélène</creatorcontrib><creatorcontrib>Vanlemmens, Laurence</creatorcontrib><creatorcontrib>Baranzelli, Marie-Christine</creatorcontrib><creatorcontrib>Vennin, Philippe</creatorcontrib><creatorcontrib>Servent, Véronique</creatorcontrib><creatorcontrib>Fournier, Charles</creatorcontrib><creatorcontrib>Carpentier, Philippe</creatorcontrib><creatorcontrib>Bonneterre, Jacques</creatorcontrib><title>Predictive value of neoadjuvant chemotherapy failure in breast cancer using FDG–PET after the first course</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>The aim of this study was to prospectively evaluate the predictive value of
18
F-fluorodeoxyglucose–positron emission tomography (FDG–PET) to detect the absence of pathological response to preoperative chemotherapy in patients (pts) with breast cancer. 63 consecutive pts with non-metastatic, non-inflammatory breast cancer, eligible for neoadjuvant chemotherapy (3 FEC 100 followed by 3 Docetaxel) were enrolled. FDG–PET was performed just before the first as well as before the second course. Metabolic activity (tumour FDG uptake) was measured by standardised uptake value (SUV
max
). Pts were classified as non-responders (NR) when the decrease of SUV
max
in the primary tumour was less than 15% at the time of the second PET (EORTC 1999 criteria). The metabolic response in FDG–PET was correlated with WHO criteria (clinical evaluation and ultrasound and/or mammography) evaluated after three cycles, pathological complete response (pCR) after surgery (according to Sataloff classification) and 4-year relapse-free survival (RFS). The mean SUV
max
decrease according to histological response was −52 ± 21% in case of pCR (Sataloff A) and 25 ± 34% in other cases (Sataloff B + C + D). Out of the 16 pts with no PET response (SUV decrease less than 15%), only one had a clinical response after the third cycle, and no pCR was observed. The 4-year RFS rate was significantly longer for metabolic responders than for NR (respectively, 85 vs. 44%;
P
= 0.01). This prospective study shows that a decrease in the SUV of less than 15% after the first chemotherapy course is a very potent predictor for failure of neoadjuvant chemotherapy, especially of pCR. It is interesting to note that this was shown despite the fact that the chemotherapy regimen was changed after the third course.</description><subject>Adjuvant treatment</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - diagnostic imaging</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - mortality</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Chemotherapy</subject><subject>Clinical Trial</subject><subject>Docetaxel</subject><subject>Failure</subject><subject>Female</subject><subject>Fluorodeoxyglucose F18</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neoadjuvant Therapy</subject><subject>Neoplasm Staging</subject><subject>Oncology</subject><subject>PET imaging</subject><subject>Positron-Emission Tomography</subject><subject>Predictions</subject><subject>Prognosis</subject><subject>Sport-utility vehicles</subject><subject>Survival Analysis</subject><subject>Tomography</subject><subject>Treatment Failure</subject><subject>Tumors</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp1kstu1DAUhi0EosPAA7BBFhWwSvEltpNlVdqCVIkuytpynOMZjzLOYCcjdcc78IY8CY4ybSkCeWHJ5_uPz-VH6DUlJ5QQ9TFRIsq6IJQWtOKsKJ-gBRWKF4pR9RQtCJWqkBWRR-hFShtCSK1I_RwdMUa4UpVaoO46Quvt4PeA96YbAfcOB-hNuxn3JgzYrmHbD2uIZneLnfHdGAH7gJsIJuWwCRYiHpMPK3zx6fLXj5_X5zfYuCG_Zhl2Pk5YP8YEL9EzZ7oErw73En27OL85-1xcfb38cnZ6VdiyroailVLVQpWibUgtWwW14VCWFCratMxJsBVVrBU0U442wihhSMMVl1S6UgJfog9z3l3sv4-QBr31yULXmdzZmHRNuWKkJDKTb_8iN7nSkIubIE5rkce5RMcztDIdaB9cP0Rjp5T6lAspKkoUz9TJP6h8Wth62wdwPr8_Erz_Q7AG0w3r1Hfj4PuQHoN0Bm3sU4rg9C76rYm3mhI9GUHPRtDZCHoygi6z5s2hsbHZQnuvuNt8Bt4dAJOs6VzMi_TpgRMlYzLDS8RmLuVQWEF8mND_f_8NZ6zIhA</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Kolesnikov-Gauthier, Hélène</creator><creator>Vanlemmens, Laurence</creator><creator>Baranzelli, Marie-Christine</creator><creator>Vennin, Philippe</creator><creator>Servent, Véronique</creator><creator>Fournier, Charles</creator><creator>Carpentier, Philippe</creator><creator>Bonneterre, Jacques</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120101</creationdate><title>Predictive value of neoadjuvant chemotherapy failure in breast cancer using FDG–PET after the first course</title><author>Kolesnikov-Gauthier, Hélène ; Vanlemmens, Laurence ; Baranzelli, Marie-Christine ; Vennin, Philippe ; Servent, Véronique ; Fournier, Charles ; Carpentier, Philippe ; Bonneterre, Jacques</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-d66795745db096d7e9a3e441e81bd2f6ec8172d51795f1b5a75a0b373616f46e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adjuvant treatment</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - diagnostic imaging</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - mortality</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Cancer therapies</topic><topic>Chemotherapy</topic><topic>Clinical Trial</topic><topic>Docetaxel</topic><topic>Failure</topic><topic>Female</topic><topic>Fluorodeoxyglucose F18</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Neoadjuvant Therapy</topic><topic>Neoplasm Staging</topic><topic>Oncology</topic><topic>PET imaging</topic><topic>Positron-Emission Tomography</topic><topic>Predictions</topic><topic>Prognosis</topic><topic>Sport-utility vehicles</topic><topic>Survival Analysis</topic><topic>Tomography</topic><topic>Treatment Failure</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kolesnikov-Gauthier, Hélène</creatorcontrib><creatorcontrib>Vanlemmens, Laurence</creatorcontrib><creatorcontrib>Baranzelli, Marie-Christine</creatorcontrib><creatorcontrib>Vennin, Philippe</creatorcontrib><creatorcontrib>Servent, Véronique</creatorcontrib><creatorcontrib>Fournier, Charles</creatorcontrib><creatorcontrib>Carpentier, Philippe</creatorcontrib><creatorcontrib>Bonneterre, Jacques</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>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kolesnikov-Gauthier, Hélène</au><au>Vanlemmens, Laurence</au><au>Baranzelli, Marie-Christine</au><au>Vennin, Philippe</au><au>Servent, Véronique</au><au>Fournier, Charles</au><au>Carpentier, Philippe</au><au>Bonneterre, Jacques</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Predictive value of neoadjuvant chemotherapy failure in breast cancer using FDG–PET after the first course</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>131</volume><issue>2</issue><spage>517</spage><epage>525</epage><pages>517-525</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><coden>BCTRD6</coden><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><abstract>The aim of this study was to prospectively evaluate the predictive value of
18
F-fluorodeoxyglucose–positron emission tomography (FDG–PET) to detect the absence of pathological response to preoperative chemotherapy in patients (pts) with breast cancer. 63 consecutive pts with non-metastatic, non-inflammatory breast cancer, eligible for neoadjuvant chemotherapy (3 FEC 100 followed by 3 Docetaxel) were enrolled. FDG–PET was performed just before the first as well as before the second course. Metabolic activity (tumour FDG uptake) was measured by standardised uptake value (SUV
max
). Pts were classified as non-responders (NR) when the decrease of SUV
max
in the primary tumour was less than 15% at the time of the second PET (EORTC 1999 criteria). The metabolic response in FDG–PET was correlated with WHO criteria (clinical evaluation and ultrasound and/or mammography) evaluated after three cycles, pathological complete response (pCR) after surgery (according to Sataloff classification) and 4-year relapse-free survival (RFS). The mean SUV
max
decrease according to histological response was −52 ± 21% in case of pCR (Sataloff A) and 25 ± 34% in other cases (Sataloff B + C + D). Out of the 16 pts with no PET response (SUV decrease less than 15%), only one had a clinical response after the third cycle, and no pCR was observed. The 4-year RFS rate was significantly longer for metabolic responders than for NR (respectively, 85 vs. 44%;
P
= 0.01). This prospective study shows that a decrease in the SUV of less than 15% after the first chemotherapy course is a very potent predictor for failure of neoadjuvant chemotherapy, especially of pCR. It is interesting to note that this was shown despite the fact that the chemotherapy regimen was changed after the third course.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22037787</pmid><doi>10.1007/s10549-011-1832-4</doi><tpages>9</tpages></addata></record> |
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subjects | Adjuvant treatment Adult Aged Biological and medical sciences Breast cancer Breast Neoplasms - diagnostic imaging Breast Neoplasms - drug therapy Breast Neoplasms - mortality Cancer Cancer research Cancer therapies Chemotherapy Clinical Trial Docetaxel Failure Female Fluorodeoxyglucose F18 Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Medicine Medicine & Public Health Middle Aged Neoadjuvant Therapy Neoplasm Staging Oncology PET imaging Positron-Emission Tomography Predictions Prognosis Sport-utility vehicles Survival Analysis Tomography Treatment Failure Tumors |
title | Predictive value of neoadjuvant chemotherapy failure in breast cancer using FDG–PET after the first course |
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