Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer. Müller, C., B., De Bastiani, M., A., Becker, M., França, F., S., Branco, M., A., Castro, M., A., A., & Klamt, F. Oncotarget, 6(6):3531-9, Impact Journals, LLC, 2015. Website abstract bibtex Current challenge in oncology is to establish the concept of personalized medicine in clinical practice. In this context, non-small-cell lung cancer (NSCLC) presents clinical, histological and molecular heterogeneity, being one of the most genomically diverse of all cancers. Recent advances added Epidermal Growth Factor Receptor (EGFR) as a predictive biomarker for patients with advanced NSCLC. In tumors with activating EGFR mutations, tyrosine kinase inhibitors (TKI) are indicated as first-line treatment, although restricted to a very small target population. In this context, cofilin-1 (a cytosolic protein involved with actin dynamics) has been widely studied as a biomarker of an aggressive phenotype in tumors, and overexpression of cofilin-1 is associated with cisplatin resistance and poor prognosis in NSCLC. Here, we gather information about the predictive potential of cofilin-1 and reviewed the crosstalk between cofilin-1/EGFR pathways. We aimed to highlight new perspectives of how these interactions might affect cisplatin resistance in NSCLC. We propose that cofilin-1 quantification in clinical samples in combination with presence/absence of EGFR mutation could be used to select patients that would benefit from TKI's treatment. This information is of paramount importance and could result in a possibility of guiding more effective treatments to NSCLC patients.
@article{
title = {Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer},
type = {article},
year = {2015},
identifiers = {[object Object]},
keywords = {2014,2015,accepted,chemotherapy resistance,cofilin-1,december 02,egfr,february 28,january 22,nsclc,personalized medicine,published,received},
pages = {3531-9},
volume = {6},
websites = {http://www.ncbi.nlm.nih.gov/pubmed/25784483%5Cnhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4414134},
publisher = {Impact Journals, LLC},
id = {3dfa69f9-a850-362a-832c-3c71ca53af81},
created = {2019-02-04T15:29:32.786Z},
file_attached = {false},
profile_id = {81a97cb0-31b8-3385-bd0e-efcfffedaada},
group_id = {b954b4a7-36ce-39f9-9501-2e3795a979e9},
last_modified = {2019-02-04T15:29:32.786Z},
read = {false},
starred = {false},
authored = {false},
confirmed = {true},
hidden = {false},
citation_key = {Muller2015},
source_type = {Article},
private_publication = {false},
abstract = {Current challenge in oncology is to establish the concept of personalized medicine in clinical practice. In this context, non-small-cell lung cancer (NSCLC) presents clinical, histological and molecular heterogeneity, being one of the most genomically diverse of all cancers. Recent advances added Epidermal Growth Factor Receptor (EGFR) as a predictive biomarker for patients with advanced NSCLC. In tumors with activating EGFR mutations, tyrosine kinase inhibitors (TKI) are indicated as first-line treatment, although restricted to a very small target population. In this context, cofilin-1 (a cytosolic protein involved with actin dynamics) has been widely studied as a biomarker of an aggressive phenotype in tumors, and overexpression of cofilin-1 is associated with cisplatin resistance and poor prognosis in NSCLC. Here, we gather information about the predictive potential of cofilin-1 and reviewed the crosstalk between cofilin-1/EGFR pathways. We aimed to highlight new perspectives of how these interactions might affect cisplatin resistance in NSCLC. We propose that cofilin-1 quantification in clinical samples in combination with presence/absence of EGFR mutation could be used to select patients that would benefit from TKI's treatment. This information is of paramount importance and could result in a possibility of guiding more effective treatments to NSCLC patients.},
bibtype = {article},
author = {Müller, Carolina Beatriz and De Bastiani, Marco Antônio and Becker, Matheus and França, Fernanda Stapenhorst and Branco, Mariane Araujo and Castro, Mauro Antônio Alves and Klamt, Fabio},
journal = {Oncotarget},
number = {6}
}
Downloads: 0
{"_id":"9fkMf5STGHreLAjhS","bibbaseid":"mller-debastiani-becker-frana-branco-castro-klamt-potentialcrosstalkbetweencofilin1andegfrpathwaysincisplatinresistanceofnonsmallcelllungcancer-2015","authorIDs":[],"author_short":["Müller, C., B.","De Bastiani, M., A.","Becker, M.","França, F., S.","Branco, M., A.","Castro, M., A., A.","Klamt, F."],"bibdata":{"title":"Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer","type":"article","year":"2015","identifiers":"[object Object]","keywords":"2014,2015,accepted,chemotherapy resistance,cofilin-1,december 02,egfr,february 28,january 22,nsclc,personalized medicine,published,received","pages":"3531-9","volume":"6","websites":"http://www.ncbi.nlm.nih.gov/pubmed/25784483%5Cnhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4414134","publisher":"Impact Journals, LLC","id":"3dfa69f9-a850-362a-832c-3c71ca53af81","created":"2019-02-04T15:29:32.786Z","file_attached":false,"profile_id":"81a97cb0-31b8-3385-bd0e-efcfffedaada","group_id":"b954b4a7-36ce-39f9-9501-2e3795a979e9","last_modified":"2019-02-04T15:29:32.786Z","read":false,"starred":false,"authored":false,"confirmed":"true","hidden":false,"citation_key":"Muller2015","source_type":"Article","private_publication":false,"abstract":"Current challenge in oncology is to establish the concept of personalized medicine in clinical practice. In this context, non-small-cell lung cancer (NSCLC) presents clinical, histological and molecular heterogeneity, being one of the most genomically diverse of all cancers. Recent advances added Epidermal Growth Factor Receptor (EGFR) as a predictive biomarker for patients with advanced NSCLC. In tumors with activating EGFR mutations, tyrosine kinase inhibitors (TKI) are indicated as first-line treatment, although restricted to a very small target population. In this context, cofilin-1 (a cytosolic protein involved with actin dynamics) has been widely studied as a biomarker of an aggressive phenotype in tumors, and overexpression of cofilin-1 is associated with cisplatin resistance and poor prognosis in NSCLC. Here, we gather information about the predictive potential of cofilin-1 and reviewed the crosstalk between cofilin-1/EGFR pathways. We aimed to highlight new perspectives of how these interactions might affect cisplatin resistance in NSCLC. We propose that cofilin-1 quantification in clinical samples in combination with presence/absence of EGFR mutation could be used to select patients that would benefit from TKI's treatment. This information is of paramount importance and could result in a possibility of guiding more effective treatments to NSCLC patients.","bibtype":"article","author":"Müller, Carolina Beatriz and De Bastiani, Marco Antônio and Becker, Matheus and França, Fernanda Stapenhorst and Branco, Mariane Araujo and Castro, Mauro Antônio Alves and Klamt, Fabio","journal":"Oncotarget","number":"6","bibtex":"@article{\n title = {Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer},\n type = {article},\n year = {2015},\n identifiers = {[object Object]},\n keywords = {2014,2015,accepted,chemotherapy resistance,cofilin-1,december 02,egfr,february 28,january 22,nsclc,personalized medicine,published,received},\n pages = {3531-9},\n volume = {6},\n websites = {http://www.ncbi.nlm.nih.gov/pubmed/25784483%5Cnhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4414134},\n publisher = {Impact Journals, LLC},\n id = {3dfa69f9-a850-362a-832c-3c71ca53af81},\n created = {2019-02-04T15:29:32.786Z},\n file_attached = {false},\n profile_id = {81a97cb0-31b8-3385-bd0e-efcfffedaada},\n group_id = {b954b4a7-36ce-39f9-9501-2e3795a979e9},\n last_modified = {2019-02-04T15:29:32.786Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {true},\n hidden = {false},\n citation_key = {Muller2015},\n source_type = {Article},\n private_publication = {false},\n abstract = {Current challenge in oncology is to establish the concept of personalized medicine in clinical practice. In this context, non-small-cell lung cancer (NSCLC) presents clinical, histological and molecular heterogeneity, being one of the most genomically diverse of all cancers. Recent advances added Epidermal Growth Factor Receptor (EGFR) as a predictive biomarker for patients with advanced NSCLC. In tumors with activating EGFR mutations, tyrosine kinase inhibitors (TKI) are indicated as first-line treatment, although restricted to a very small target population. In this context, cofilin-1 (a cytosolic protein involved with actin dynamics) has been widely studied as a biomarker of an aggressive phenotype in tumors, and overexpression of cofilin-1 is associated with cisplatin resistance and poor prognosis in NSCLC. Here, we gather information about the predictive potential of cofilin-1 and reviewed the crosstalk between cofilin-1/EGFR pathways. We aimed to highlight new perspectives of how these interactions might affect cisplatin resistance in NSCLC. We propose that cofilin-1 quantification in clinical samples in combination with presence/absence of EGFR mutation could be used to select patients that would benefit from TKI's treatment. This information is of paramount importance and could result in a possibility of guiding more effective treatments to NSCLC patients.},\n bibtype = {article},\n author = {Müller, Carolina Beatriz and De Bastiani, Marco Antônio and Becker, Matheus and França, Fernanda Stapenhorst and Branco, Mariane Araujo and Castro, Mauro Antônio Alves and Klamt, Fabio},\n journal = {Oncotarget},\n number = {6}\n}","author_short":["Müller, C., B.","De Bastiani, M., A.","Becker, M.","França, F., S.","Branco, M., A.","Castro, M., A., A.","Klamt, F."],"urls":{"Website":"http://www.ncbi.nlm.nih.gov/pubmed/25784483%5Cnhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4414134"},"bibbaseid":"mller-debastiani-becker-frana-branco-castro-klamt-potentialcrosstalkbetweencofilin1andegfrpathwaysincisplatinresistanceofnonsmallcelllungcancer-2015","role":"author","keyword":["2014","2015","accepted","chemotherapy resistance","cofilin-1","december 02","egfr","february 28","january 22","nsclc","personalized medicine","published","received"],"downloads":0},"bibtype":"article","creationDate":"2020-04-24T03:45:31.846Z","downloads":0,"keywords":["2014","2015","accepted","chemotherapy resistance","cofilin-1","december 02","egfr","february 28","january 22","nsclc","personalized medicine","published","received"],"search_terms":["potential","crosstalk","between","cofilin","egfr","pathways","cisplatin","resistance","non","small","cell","lung","cancer","müller","de bastiani","becker","frança","branco","castro","klamt"],"title":"Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer","year":2015}