Prognostic relevance of KRAS genotype in metastatic colorectal cancer patients unfit for FIr-B/FOx intensive regimen
First-line triplet chemotherapy plus bevacizumab (FIr-B/FOx) can improve efficacy of metastatic colorectal cancer (MCRC), KRAS wild-type and mutant. Prognostic relevance of KRAS genotype was evaluated in patients unfit for FIr-B/FOx, treated with conventional medical treatments. Consecutive MCRC pat...
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| Veröffentlicht in: | International journal of oncology 2014-06, Vol.44 (6), p.1820-1830 |
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| creator | BRUERA, GEMMA CANNITA, KATIA GIORDANO, ALDO VICTOR VICENTINI, ROBERTO FICORELLA, CORRADO RICEVUTO, ENRICO |
| description | First-line triplet chemotherapy plus bevacizumab (FIr-B/FOx) can improve efficacy of metastatic colorectal cancer (MCRC), KRAS wild-type and mutant. Prognostic relevance of KRAS genotype was evaluated in patients unfit for FIr-B/FOx, treated with conventional medical treatments. Consecutive MCRC patients not eligible for FIr-B/FOx regimen due to age (≥75 years) and/or comorbidities were treated with tailored conventional first-line treatments. KRAS codon 12/13 mutations were screened by direct sequencing. Activity and efficacy were evaluated and compared according to medical treatments, age (non-elderly and elderly ≥65 years), comorbidity stage (Cumulative Illness Rating Scale), metastatic extension (liver-limited and other/multiple metastatic), and KRAS genotype, using log-rank. Selected first line treatments were medical in 37 patients (92.5%), and surgical in 3 patients (7.5%). Medical treatment regimens: triplet, 18 (45%); doublet, 15 (37.5%); mono-therapy, 4 (10%). At median follow-up of 8 months, objective response rate (ORR) was 37%, median progression-free survival (PFS) 7 months, liver metastasectomies 8% (liver-limited disease 37.5%), median overall survival (OS) 13 months. Triplet regimens failed to significantly affect clinical outcome, compared to doublet. According to KRAS genotype, ORR, PFS and OS were, respectively: wild-type 50%, 8 months, 13 months; mutant 25%, 6 months, 9 months. KRAS genotype wild-type compared to mutant significantly affected PFS, while not OS. KRAS c.35 G>A mutation (G12D) significantly affected worse PFS and OS compared to wild-type and/or other mutations. KRAS genotype, specifically the c.35 G>A KRAS mutation, may indicate poor prognosis in MCRC patients unfit for intensive medical treatments. |
| doi_str_mv | 10.3892/ijo.2014.2369 |
| format | Article |
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Prognostic relevance of KRAS genotype was evaluated in patients unfit for FIr-B/FOx, treated with conventional medical treatments. Consecutive MCRC patients not eligible for FIr-B/FOx regimen due to age (≥75 years) and/or comorbidities were treated with tailored conventional first-line treatments. KRAS codon 12/13 mutations were screened by direct sequencing. Activity and efficacy were evaluated and compared according to medical treatments, age (non-elderly and elderly ≥65 years), comorbidity stage (Cumulative Illness Rating Scale), metastatic extension (liver-limited and other/multiple metastatic), and KRAS genotype, using log-rank. Selected first line treatments were medical in 37 patients (92.5%), and surgical in 3 patients (7.5%). Medical treatment regimens: triplet, 18 (45%); doublet, 15 (37.5%); mono-therapy, 4 (10%). At median follow-up of 8 months, objective response rate (ORR) was 37%, median progression-free survival (PFS) 7 months, liver metastasectomies 8% (liver-limited disease 37.5%), median overall survival (OS) 13 months. Triplet regimens failed to significantly affect clinical outcome, compared to doublet. According to KRAS genotype, ORR, PFS and OS were, respectively: wild-type 50%, 8 months, 13 months; mutant 25%, 6 months, 9 months. KRAS genotype wild-type compared to mutant significantly affected PFS, while not OS. KRAS c.35 G>A mutation (G12D) significantly affected worse PFS and OS compared to wild-type and/or other mutations. KRAS genotype, specifically the c.35 G>A KRAS mutation, may indicate poor prognosis in MCRC patients unfit for intensive medical treatments.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2014.2369</identifier><identifier>PMID: 24715238</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Age ; Aged ; Aged, 80 and over ; Antineoplastic Agents - administration & dosage ; Antineoplastic Agents - therapeutic use ; Antineoplastic Combined Chemotherapy Protocols - administration & dosage ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; c.35 G>A KRAS mutation ; Cancer therapies ; Chemotherapy ; Clinical decision making ; Clinical outcomes ; Colorectal cancer ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - secondary ; Decision making ; Development and progression ; elderly ; Female ; FIr-B/FOx ; Frailty ; Gene mutations ; Genetic aspects ; Genotype ; Genotype & phenotype ; Health aspects ; Humans ; Identification and classification ; Immunotherapy ; KRAS genotype ; Liver ; Male ; Medical prognosis ; Medical treatment ; Metastasis ; metastatic colorectal cancer ; Middle Aged ; Monoclonal antibodies ; Morbidity ; Mortality ; Mutation ; Neoplasm Metastasis - drug therapy ; Neoplasm Metastasis - genetics ; Patients ; Prognosis ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins p21(ras) ; ras Proteins - genetics ; Retrospective Studies ; Targeted cancer therapy ; Treatment Outcome ; triplet chemotherapy plus bevacizumab</subject><ispartof>International journal of oncology, 2014-06, Vol.44 (6), p.1820-1830</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><rights>Copyright © 2014, Spandidos Publications 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c545t-222c7b25803b11e1102bd8da744b283acf478a606db709f566fdec167f74ecc3</citedby><cites>FETCH-LOGICAL-c545t-222c7b25803b11e1102bd8da744b283acf478a606db709f566fdec167f74ecc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24715238$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BRUERA, GEMMA</creatorcontrib><creatorcontrib>CANNITA, KATIA</creatorcontrib><creatorcontrib>GIORDANO, ALDO VICTOR</creatorcontrib><creatorcontrib>VICENTINI, ROBERTO</creatorcontrib><creatorcontrib>FICORELLA, CORRADO</creatorcontrib><creatorcontrib>RICEVUTO, ENRICO</creatorcontrib><title>Prognostic relevance of KRAS genotype in metastatic colorectal cancer patients unfit for FIr-B/FOx intensive regimen</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>First-line triplet chemotherapy plus bevacizumab (FIr-B/FOx) can improve efficacy of metastatic colorectal cancer (MCRC), KRAS wild-type and mutant. Prognostic relevance of KRAS genotype was evaluated in patients unfit for FIr-B/FOx, treated with conventional medical treatments. Consecutive MCRC patients not eligible for FIr-B/FOx regimen due to age (≥75 years) and/or comorbidities were treated with tailored conventional first-line treatments. KRAS codon 12/13 mutations were screened by direct sequencing. Activity and efficacy were evaluated and compared according to medical treatments, age (non-elderly and elderly ≥65 years), comorbidity stage (Cumulative Illness Rating Scale), metastatic extension (liver-limited and other/multiple metastatic), and KRAS genotype, using log-rank. Selected first line treatments were medical in 37 patients (92.5%), and surgical in 3 patients (7.5%). Medical treatment regimens: triplet, 18 (45%); doublet, 15 (37.5%); mono-therapy, 4 (10%). At median follow-up of 8 months, objective response rate (ORR) was 37%, median progression-free survival (PFS) 7 months, liver metastasectomies 8% (liver-limited disease 37.5%), median overall survival (OS) 13 months. Triplet regimens failed to significantly affect clinical outcome, compared to doublet. According to KRAS genotype, ORR, PFS and OS were, respectively: wild-type 50%, 8 months, 13 months; mutant 25%, 6 months, 9 months. KRAS genotype wild-type compared to mutant significantly affected PFS, while not OS. KRAS c.35 G>A mutation (G12D) significantly affected worse PFS and OS compared to wild-type and/or other mutations. KRAS genotype, specifically the c.35 G>A KRAS mutation, may indicate poor prognosis in MCRC patients unfit for intensive medical treatments.</description><subject>Age</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antineoplastic Agents - administration & dosage</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antineoplastic Combined Chemotherapy Protocols - administration & dosage</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>c.35 G>A KRAS mutation</subject><subject>Cancer therapies</subject><subject>Chemotherapy</subject><subject>Clinical decision making</subject><subject>Clinical outcomes</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - secondary</subject><subject>Decision making</subject><subject>Development and progression</subject><subject>elderly</subject><subject>Female</subject><subject>FIr-B/FOx</subject><subject>Frailty</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>Immunotherapy</subject><subject>KRAS genotype</subject><subject>Liver</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical treatment</subject><subject>Metastasis</subject><subject>metastatic colorectal cancer</subject><subject>Middle Aged</subject><subject>Monoclonal antibodies</subject><subject>Morbidity</subject><subject>Mortality</subject><subject>Mutation</subject><subject>Neoplasm Metastasis - drug therapy</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Patients</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins p21(ras)</subject><subject>ras Proteins - genetics</subject><subject>Retrospective Studies</subject><subject>Targeted cancer therapy</subject><subject>Treatment Outcome</subject><subject>triplet chemotherapy plus bevacizumab</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkt1rFDEUxQdRbK0--ioBQZ9mm6_5ehG2xdVioaJ9D5nMzWyWmWRMMov9782wde2C5CHh5nfOvQkny94SvGJ1Qy_Nzq0oJnxFWdk8y85J1ZCccsqepzMmTV5y1pxlr0LYYUyLApOX2RnlFSkoq8-z-N273roQjUIeBthLqwA5jb79WP9EPVgXHyZAxqIRogxRLqByg_OgohyQWniPplQHGwOarTYRaefR5sbnV5ebu99JHMEGs4fUoTcj2NfZCy2HAG8e94vsfvP5_vprfnv35eZ6fZurghcxp5SqqqVFjVlLCBCCadvVnaw4b2nNpNK8qmWJy66tcKOLstQdKFJWuuKgFLvIPh1sp7kdoVNpQC8HMXkzSv8gnDTi9MaarejdXnBcsoLVyeD9o4F3v2YIUezc7G0aWZCGUUYxx8U_qpcDCGO1S2ZqNEGJNWcVxrxhJFGr_1BpdTAa5Sxok-ongg9PBFuQQ9wGN8zROBtOwfwAKu9C8KCPLyRYLBkRKSNiyYhYMpL4d0-_5Uj_DUUCPh6AMEnbmc6FI5Occs5zXOakppj9AfDfxCo</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>BRUERA, GEMMA</creator><creator>CANNITA, KATIA</creator><creator>GIORDANO, ALDO VICTOR</creator><creator>VICENTINI, ROBERTO</creator><creator>FICORELLA, CORRADO</creator><creator>RICEVUTO, ENRICO</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20140601</creationdate><title>Prognostic relevance of KRAS genotype in metastatic colorectal cancer patients unfit for FIr-B/FOx intensive regimen</title><author>BRUERA, GEMMA ; CANNITA, KATIA ; GIORDANO, ALDO VICTOR ; VICENTINI, ROBERTO ; FICORELLA, CORRADO ; RICEVUTO, ENRICO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c545t-222c7b25803b11e1102bd8da744b283acf478a606db709f566fdec167f74ecc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Age</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antineoplastic Agents - administration & dosage</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antineoplastic Combined Chemotherapy Protocols - administration & dosage</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>c.35 G>A KRAS mutation</topic><topic>Cancer therapies</topic><topic>Chemotherapy</topic><topic>Clinical decision making</topic><topic>Clinical outcomes</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - secondary</topic><topic>Decision making</topic><topic>Development and progression</topic><topic>elderly</topic><topic>Female</topic><topic>FIr-B/FOx</topic><topic>Frailty</topic><topic>Gene mutations</topic><topic>Genetic aspects</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Identification and classification</topic><topic>Immunotherapy</topic><topic>KRAS genotype</topic><topic>Liver</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical treatment</topic><topic>Metastasis</topic><topic>metastatic colorectal cancer</topic><topic>Middle Aged</topic><topic>Monoclonal antibodies</topic><topic>Morbidity</topic><topic>Mortality</topic><topic>Mutation</topic><topic>Neoplasm Metastasis - drug therapy</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Patients</topic><topic>Prognosis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>ras Proteins - genetics</topic><topic>Retrospective Studies</topic><topic>Targeted cancer therapy</topic><topic>Treatment Outcome</topic><topic>triplet chemotherapy plus bevacizumab</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BRUERA, GEMMA</creatorcontrib><creatorcontrib>CANNITA, KATIA</creatorcontrib><creatorcontrib>GIORDANO, ALDO VICTOR</creatorcontrib><creatorcontrib>VICENTINI, ROBERTO</creatorcontrib><creatorcontrib>FICORELLA, CORRADO</creatorcontrib><creatorcontrib>RICEVUTO, ENRICO</creatorcontrib><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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>PubMed Central (Full Participant titles)</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BRUERA, GEMMA</au><au>CANNITA, KATIA</au><au>GIORDANO, ALDO VICTOR</au><au>VICENTINI, ROBERTO</au><au>FICORELLA, CORRADO</au><au>RICEVUTO, ENRICO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prognostic relevance of KRAS genotype in metastatic colorectal cancer patients unfit for FIr-B/FOx intensive regimen</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>44</volume><issue>6</issue><spage>1820</spage><epage>1830</epage><pages>1820-1830</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>First-line triplet chemotherapy plus bevacizumab (FIr-B/FOx) can improve efficacy of metastatic colorectal cancer (MCRC), KRAS wild-type and mutant. Prognostic relevance of KRAS genotype was evaluated in patients unfit for FIr-B/FOx, treated with conventional medical treatments. Consecutive MCRC patients not eligible for FIr-B/FOx regimen due to age (≥75 years) and/or comorbidities were treated with tailored conventional first-line treatments. KRAS codon 12/13 mutations were screened by direct sequencing. Activity and efficacy were evaluated and compared according to medical treatments, age (non-elderly and elderly ≥65 years), comorbidity stage (Cumulative Illness Rating Scale), metastatic extension (liver-limited and other/multiple metastatic), and KRAS genotype, using log-rank. Selected first line treatments were medical in 37 patients (92.5%), and surgical in 3 patients (7.5%). Medical treatment regimens: triplet, 18 (45%); doublet, 15 (37.5%); mono-therapy, 4 (10%). At median follow-up of 8 months, objective response rate (ORR) was 37%, median progression-free survival (PFS) 7 months, liver metastasectomies 8% (liver-limited disease 37.5%), median overall survival (OS) 13 months. Triplet regimens failed to significantly affect clinical outcome, compared to doublet. According to KRAS genotype, ORR, PFS and OS were, respectively: wild-type 50%, 8 months, 13 months; mutant 25%, 6 months, 9 months. KRAS genotype wild-type compared to mutant significantly affected PFS, while not OS. KRAS c.35 G>A mutation (G12D) significantly affected worse PFS and OS compared to wild-type and/or other mutations. KRAS genotype, specifically the c.35 G>A KRAS mutation, may indicate poor prognosis in MCRC patients unfit for intensive medical treatments.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24715238</pmid><doi>10.3892/ijo.2014.2369</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2014-06, Vol.44 (6), p.1820-1830 |
| issn | 1019-6439 1791-2423 |
| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Age Aged Aged, 80 and over Antineoplastic Agents - administration & dosage Antineoplastic Agents - therapeutic use Antineoplastic Combined Chemotherapy Protocols - administration & dosage Antineoplastic Combined Chemotherapy Protocols - therapeutic use c.35 G>A KRAS mutation Cancer therapies Chemotherapy Clinical decision making Clinical outcomes Colorectal cancer Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - secondary Decision making Development and progression elderly Female FIr-B/FOx Frailty Gene mutations Genetic aspects Genotype Genotype & phenotype Health aspects Humans Identification and classification Immunotherapy KRAS genotype Liver Male Medical prognosis Medical treatment Metastasis metastatic colorectal cancer Middle Aged Monoclonal antibodies Morbidity Mortality Mutation Neoplasm Metastasis - drug therapy Neoplasm Metastasis - genetics Patients Prognosis Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins p21(ras) ras Proteins - genetics Retrospective Studies Targeted cancer therapy Treatment Outcome triplet chemotherapy plus bevacizumab |
| title | Prognostic relevance of KRAS genotype in metastatic colorectal cancer patients unfit for FIr-B/FOx intensive regimen |
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