Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer
Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patie...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
HE Jingyi [verfasserIn] WU Fang [verfasserIn] HU Chunhong [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Chinesisch |
| Erschienen: |
2019 |
|---|
| Schlagwörter: |
|---|
| Übergeordnetes Werk: |
In: Zhongliu Fangzhi Yanjiu - Magazine House of Cancer Research on Prevention and Treatment, 2019, 46(2019), 10, Seite 938-945 |
|---|---|
| Übergeordnetes Werk: |
volume:46 ; year:2019 ; number:10 ; pages:938-945 |
| Links: |
Link aufrufen |
|---|
| DOI / URN: |
10.3971/j.issn.1000-8578.2019.19.0169 |
|---|
| Katalog-ID: |
DOAJ038116944 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | DOAJ038116944 | ||
| 003 | DE-627 | ||
| 005 | 20230308015541.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 230227s2019 xx |||||o 00| ||chi c | ||
| 024 | 7 | |a 10.3971/j.issn.1000-8578.2019.19.0169 |2 doi | |
| 035 | |a (DE-627)DOAJ038116944 | ||
| 035 | |a (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a chi | ||
| 050 | 0 | |a RC254-282 | |
| 100 | 0 | |a HE Jingyi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer |
| 264 | 1 | |c 2019 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 520 | |a Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. | ||
| 650 | 4 | |a egfr | |
| 650 | 4 | |a the third-generation egfr-tkis | |
| 650 | 4 | |a osimertinib | |
| 650 | 4 | |a non-small cell lung cancer | |
| 650 | 4 | |a resistance mechanisms | |
| 653 | 0 | |a Neoplasms. Tumors. Oncology. Including cancer and carcinogens | |
| 700 | 0 | |a WU Fang |e verfasserin |4 aut | |
| 700 | 0 | |a HU Chunhong |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i In |t Zhongliu Fangzhi Yanjiu |d Magazine House of Cancer Research on Prevention and Treatment, 2019 |g 46(2019), 10, Seite 938-945 |w (DE-627)176063638X |x 10008578 |7 nnns |
| 773 | 1 | 8 | |g volume:46 |g year:2019 |g number:10 |g pages:938-945 |
| 856 | 4 | 0 | |u https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 |z kostenfrei |
| 856 | 4 | 0 | |u https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d |z kostenfrei |
| 856 | 4 | 0 | |u http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm |z kostenfrei |
| 856 | 4 | 2 | |u https://doaj.org/toc/1000-8578 |y Journal toc |z kostenfrei |
| 856 | 4 | 2 | |u https://doaj.org/toc/1000-8578 |y Journal toc |z kostenfrei |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a SYSFLAG_A | ||
| 912 | |a GBV_DOAJ | ||
| 951 | |a AR | ||
| 952 | |d 46 |j 2019 |e 10 |h 938-945 | ||
| author_variant |
h j hj w f wf h c hc |
|---|---|
| matchkey_str |
article:10008578:2019----::eerhrgesneitneehnssnoecmnsrtgettideeaingrks |
| hierarchy_sort_str |
2019 |
| callnumber-subject-code |
RC |
| publishDate |
2019 |
| allfields |
10.3971/j.issn.1000-8578.2019.19.0169 doi (DE-627)DOAJ038116944 (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d DE-627 ger DE-627 rakwb chi RC254-282 HE Jingyi verfasserin aut Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms Neoplasms. Tumors. Oncology. Including cancer and carcinogens WU Fang verfasserin aut HU Chunhong verfasserin aut In Zhongliu Fangzhi Yanjiu Magazine House of Cancer Research on Prevention and Treatment, 2019 46(2019), 10, Seite 938-945 (DE-627)176063638X 10008578 nnns volume:46 year:2019 number:10 pages:938-945 https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 kostenfrei https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d kostenfrei http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 46 2019 10 938-945 |
| spelling |
10.3971/j.issn.1000-8578.2019.19.0169 doi (DE-627)DOAJ038116944 (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d DE-627 ger DE-627 rakwb chi RC254-282 HE Jingyi verfasserin aut Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms Neoplasms. Tumors. Oncology. Including cancer and carcinogens WU Fang verfasserin aut HU Chunhong verfasserin aut In Zhongliu Fangzhi Yanjiu Magazine House of Cancer Research on Prevention and Treatment, 2019 46(2019), 10, Seite 938-945 (DE-627)176063638X 10008578 nnns volume:46 year:2019 number:10 pages:938-945 https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 kostenfrei https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d kostenfrei http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 46 2019 10 938-945 |
| allfields_unstemmed |
10.3971/j.issn.1000-8578.2019.19.0169 doi (DE-627)DOAJ038116944 (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d DE-627 ger DE-627 rakwb chi RC254-282 HE Jingyi verfasserin aut Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms Neoplasms. Tumors. Oncology. Including cancer and carcinogens WU Fang verfasserin aut HU Chunhong verfasserin aut In Zhongliu Fangzhi Yanjiu Magazine House of Cancer Research on Prevention and Treatment, 2019 46(2019), 10, Seite 938-945 (DE-627)176063638X 10008578 nnns volume:46 year:2019 number:10 pages:938-945 https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 kostenfrei https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d kostenfrei http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 46 2019 10 938-945 |
| allfieldsGer |
10.3971/j.issn.1000-8578.2019.19.0169 doi (DE-627)DOAJ038116944 (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d DE-627 ger DE-627 rakwb chi RC254-282 HE Jingyi verfasserin aut Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms Neoplasms. Tumors. Oncology. Including cancer and carcinogens WU Fang verfasserin aut HU Chunhong verfasserin aut In Zhongliu Fangzhi Yanjiu Magazine House of Cancer Research on Prevention and Treatment, 2019 46(2019), 10, Seite 938-945 (DE-627)176063638X 10008578 nnns volume:46 year:2019 number:10 pages:938-945 https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 kostenfrei https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d kostenfrei http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 46 2019 10 938-945 |
| allfieldsSound |
10.3971/j.issn.1000-8578.2019.19.0169 doi (DE-627)DOAJ038116944 (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d DE-627 ger DE-627 rakwb chi RC254-282 HE Jingyi verfasserin aut Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms Neoplasms. Tumors. Oncology. Including cancer and carcinogens WU Fang verfasserin aut HU Chunhong verfasserin aut In Zhongliu Fangzhi Yanjiu Magazine House of Cancer Research on Prevention and Treatment, 2019 46(2019), 10, Seite 938-945 (DE-627)176063638X 10008578 nnns volume:46 year:2019 number:10 pages:938-945 https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 kostenfrei https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d kostenfrei http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei https://doaj.org/toc/1000-8578 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 46 2019 10 938-945 |
| language |
Chinese |
| source |
In Zhongliu Fangzhi Yanjiu 46(2019), 10, Seite 938-945 volume:46 year:2019 number:10 pages:938-945 |
| sourceStr |
In Zhongliu Fangzhi Yanjiu 46(2019), 10, Seite 938-945 volume:46 year:2019 number:10 pages:938-945 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| isfreeaccess_bool |
true |
| container_title |
Zhongliu Fangzhi Yanjiu |
| authorswithroles_txt_mv |
HE Jingyi @@aut@@ WU Fang @@aut@@ HU Chunhong @@aut@@ |
| publishDateDaySort_date |
2019-01-01T00:00:00Z |
| hierarchy_top_id |
176063638X |
| id |
DOAJ038116944 |
| language_de |
chinesisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ038116944</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308015541.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2019 xx |||||o 00| ||chi c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3971/j.issn.1000-8578.2019.19.0169</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ038116944</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">chi</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC254-282</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">HE Jingyi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">egfr</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">the third-generation egfr-tkis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">osimertinib</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">non-small cell lung cancer</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">resistance mechanisms</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. Including cancer and carcinogens</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">WU Fang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">HU Chunhong</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Zhongliu Fangzhi Yanjiu</subfield><subfield code="d">Magazine House of Cancer Research on Prevention and Treatment, 2019</subfield><subfield code="g">46(2019), 10, Seite 938-945</subfield><subfield code="w">(DE-627)176063638X</subfield><subfield code="x">10008578</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:46</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:10</subfield><subfield code="g">pages:938-945</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1000-8578</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1000-8578</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">46</subfield><subfield code="j">2019</subfield><subfield code="e">10</subfield><subfield code="h">938-945</subfield></datafield></record></collection>
|
| callnumber-first |
R - Medicine |
| author |
HE Jingyi |
| spellingShingle |
HE Jingyi misc RC254-282 misc egfr misc the third-generation egfr-tkis misc osimertinib misc non-small cell lung cancer misc resistance mechanisms misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer |
| authorStr |
HE Jingyi |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)176063638X |
| format |
electronic Article |
| delete_txt_mv |
keep |
| author_role |
aut aut aut |
| collection |
DOAJ |
| remote_str |
true |
| callnumber-label |
RC254-282 |
| illustrated |
Not Illustrated |
| issn |
10008578 |
| topic_title |
RC254-282 Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer egfr the third-generation egfr-tkis osimertinib non-small cell lung cancer resistance mechanisms |
| topic |
misc RC254-282 misc egfr misc the third-generation egfr-tkis misc osimertinib misc non-small cell lung cancer misc resistance mechanisms misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| topic_unstemmed |
misc RC254-282 misc egfr misc the third-generation egfr-tkis misc osimertinib misc non-small cell lung cancer misc resistance mechanisms misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| topic_browse |
misc RC254-282 misc egfr misc the third-generation egfr-tkis misc osimertinib misc non-small cell lung cancer misc resistance mechanisms misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
cr |
| hierarchy_parent_title |
Zhongliu Fangzhi Yanjiu |
| hierarchy_parent_id |
176063638X |
| hierarchy_top_title |
Zhongliu Fangzhi Yanjiu |
| isfreeaccess_txt |
true |
| familylinks_str_mv |
(DE-627)176063638X |
| title |
Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer |
| ctrlnum |
(DE-627)DOAJ038116944 (DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d |
| title_full |
Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer |
| author_sort |
HE Jingyi |
| journal |
Zhongliu Fangzhi Yanjiu |
| journalStr |
Zhongliu Fangzhi Yanjiu |
| callnumber-first-code |
R |
| lang_code |
chi |
| isOA_bool |
true |
| recordtype |
marc |
| publishDateSort |
2019 |
| contenttype_str_mv |
txt |
| container_start_page |
938 |
| author_browse |
HE Jingyi WU Fang HU Chunhong |
| container_volume |
46 |
| class |
RC254-282 |
| format_se |
Elektronische Aufsätze |
| author-letter |
HE Jingyi |
| doi_str_mv |
10.3971/j.issn.1000-8578.2019.19.0169 |
| author2-role |
verfasserin |
| title_sort |
research progress on resistance mechanisms and overcoming strategies to third-generation egfr-tkis in advanced non-small cell lung cancer |
| callnumber |
RC254-282 |
| title_auth |
Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer |
| abstract |
Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. |
| abstractGer |
Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. |
| abstract_unstemmed |
Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies. |
| collection_details |
GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ |
| container_issue |
10 |
| title_short |
Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer |
| url |
https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169 https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm https://doaj.org/toc/1000-8578 |
| remote_bool |
true |
| author2 |
WU Fang HU Chunhong |
| author2Str |
WU Fang HU Chunhong |
| ppnlink |
176063638X |
| callnumber-subject |
RC - Internal Medicine |
| mediatype_str_mv |
c |
| isOA_txt |
true |
| hochschulschrift_bool |
false |
| doi_str |
10.3971/j.issn.1000-8578.2019.19.0169 |
| callnumber-a |
RC254-282 |
| up_date |
2024-07-03T16:07:12.093Z |
| _version_ |
1803574661189992449 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ038116944</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308015541.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2019 xx |||||o 00| ||chi c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3971/j.issn.1000-8578.2019.19.0169</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ038116944</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJb411dd8ad20b4eb5af5986130e60281d</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">chi</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC254-282</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">HE Jingyi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Research Progress on Resistance Mechanisms and Overcoming Strategies to Third-generation EGFR-TKIs in Advanced Non-small Cell Lung Cancer</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as the first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The first- and second-generation EGFR-TKIs have shown significant efficacy in NSCLC patients with EGFR-sensitive mutations and EGFR T790M mutation is the main resistance mechanism of the first- and second-generation EGFR-TKIs. The third-generation EGFR-TKIs, represented by osimertinib, has been approved to overcome the EGFR T790M mutation in patients who are resistant to the first- or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. However, the development of acquired drug resistance is inevitable. In this review, we summarize the research progress in resistance mechanisms of advanced NSCLC to the third-generation EGFR-TKIs and the potential overcoming strategies.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">egfr</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">the third-generation egfr-tkis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">osimertinib</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">non-small cell lung cancer</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">resistance mechanisms</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. Including cancer and carcinogens</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">WU Fang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">HU Chunhong</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Zhongliu Fangzhi Yanjiu</subfield><subfield code="d">Magazine House of Cancer Research on Prevention and Treatment, 2019</subfield><subfield code="g">46(2019), 10, Seite 938-945</subfield><subfield code="w">(DE-627)176063638X</subfield><subfield code="x">10008578</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:46</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:10</subfield><subfield code="g">pages:938-945</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3971/j.issn.1000-8578.2019.19.0169</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/b411dd8ad20b4eb5af5986130e60281d</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://html.rhhz.net/ZLFZYJ/html/8578.2019.19.0169.htm</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1000-8578</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1000-8578</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">46</subfield><subfield code="j">2019</subfield><subfield code="e">10</subfield><subfield code="h">938-945</subfield></datafield></record></collection>
|
| score |
7.4011927 |