Effects of KRAS, STK11, KEAP1, and TP53 mutations on the clinical outcomes of immune checkpoint inhibitors among patients with lung adenocarcinoma
This study aimed to identify the associations between individual KRAS, STK11, KEAP1, or TP53 mutations, as well as the comutation status of these genes, and the tumor mutation burden (TMB) with clinical outcomes of lung adenocarcinoma patients treated with immune checkpoint inhibitors (ICIs). We col...
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| creator | Liang, Yao Maeda, Osamu Kondo, Chiaki Nishida, Kazuki Ando, Yuichi |
| description | This study aimed to identify the associations between individual KRAS, STK11, KEAP1, or TP53 mutations, as well as the comutation status of these genes, and the tumor mutation burden (TMB) with clinical outcomes of lung adenocarcinoma patients treated with immune checkpoint inhibitors (ICIs).
We collected data from patients with lung adenocarcinoma treated with ICIs from the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database between June 2019 and August 2023. The main endpoints were the treatment response and overall survival (OS).
Among 343 patients with lung adenocarcinoma, 61 (18%), 69 (20%), 41 (12%), and 222 (65%) patients had KRAS, STK11, KEAP1, and TP53 mutations, respectively. An overall objective response was observed in 94 of 338 patients (28%), including 2 (1%) who achieved a complete response and 92 (27%) who achieved a partial response. Patients with STK11, KEAP1, or TP53 mutations had a significantly greater TMB (P |
| doi_str_mv | 10.1371/journal.pone.0307580 |
| format | Article |
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We collected data from patients with lung adenocarcinoma treated with ICIs from the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database between June 2019 and August 2023. The main endpoints were the treatment response and overall survival (OS).
Among 343 patients with lung adenocarcinoma, 61 (18%), 69 (20%), 41 (12%), and 222 (65%) patients had KRAS, STK11, KEAP1, and TP53 mutations, respectively. An overall objective response was observed in 94 of 338 patients (28%), including 2 (1%) who achieved a complete response and 92 (27%) who achieved a partial response. Patients with STK11, KEAP1, or TP53 mutations had a significantly greater TMB (P<0.001). According to the univariate analysis, the treatment response was significantly correlated with TP53 mutation in both the general (P = 0.041) and KRAS wild-type (P = 0.009) populations. KEAP1 and TP53 mutations were associated with worse OS among assessable patients (hazard ratio (HR) = 2.027, P = 0.002; HR = 1.673, P = 0.007, respectively) and among patients without KRAS mutations (HR = 1.897, P = 0.012; HR = 1.908, P = 0.004, respectively). According to the multivariate analysis, KEAP1 (HR = 1.890, P = 0.008) and TP53 (HR = 1.735, P = 0.011) mutations were found to be independent factors for OS.
STK11, KEAP1, and TP53 mutations are significantly associated with a high TMB. TP53 mutation could affect the treatment response to some degree, and both KEAP1 and TP53 mutations resulted in inferior OS in the general patient population and in those with KRAS-wild-type lung adenocarcinoma, indicating that KEAP1 and TP53 mutations might act as prognostic factors for ICI treatment in lung adenocarcinoma patients.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0307580</identifier><identifier>PMID: 39037971</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenocarcinoma ; Adenocarcinoma of Lung - drug therapy ; Adenocarcinoma of Lung - genetics ; Adenocarcinoma of Lung - mortality ; Adenocarcinoma of Lung - pathology ; Adult ; Aged ; Aged, 80 and over ; AMP-Activated Protein Kinase Kinases ; Biology and Life Sciences ; Biomarkers ; Cancer ; Care and treatment ; Cell cycle ; Chemotherapy ; Clinical outcomes ; Female ; Genes ; Genetic aspects ; Genomics ; Humans ; Immune checkpoint inhibitors ; Immune Checkpoint Inhibitors - therapeutic use ; Inhibitors ; K-Ras protein ; Kelch-Like ECH-Associated Protein 1 - genetics ; Kinases ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - mortality ; Lungs ; Male ; Medicine and Health Sciences ; Middle Aged ; Multivariate analysis ; Mutation ; p53 Protein ; Patient outcomes ; Patients ; Protein Serine-Threonine Kinases - genetics ; Proto-Oncogene Proteins p21(ras) - genetics ; Research and Analysis Methods ; Respiratory agents ; Signal transduction ; Treatment Outcome ; Tumor proteins ; Tumor Suppressor Protein p53 - genetics</subject><ispartof>PloS one, 2024-07, Vol.19 (7), p.e0307580</ispartof><rights>Copyright: © 2024 Liang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2024 Public Library of Science</rights><rights>2024 Liang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Liang et al 2024 Liang et al</rights><rights>2024 Liang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c572t-b2fe7b03f8c773694134fd8e7c65c098b6f705cc22ca239e893a29be869f42ca3</cites><orcidid>0009-0005-2365-1513 ; 0000-0002-6849-2297</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11262633/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11262633/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39037971$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Galli, Alvaro</contributor><creatorcontrib>Liang, Yao</creatorcontrib><creatorcontrib>Maeda, Osamu</creatorcontrib><creatorcontrib>Kondo, Chiaki</creatorcontrib><creatorcontrib>Nishida, Kazuki</creatorcontrib><creatorcontrib>Ando, Yuichi</creatorcontrib><title>Effects of KRAS, STK11, KEAP1, and TP53 mutations on the clinical outcomes of immune checkpoint inhibitors among patients with lung adenocarcinoma</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>This study aimed to identify the associations between individual KRAS, STK11, KEAP1, or TP53 mutations, as well as the comutation status of these genes, and the tumor mutation burden (TMB) with clinical outcomes of lung adenocarcinoma patients treated with immune checkpoint inhibitors (ICIs).
We collected data from patients with lung adenocarcinoma treated with ICIs from the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database between June 2019 and August 2023. The main endpoints were the treatment response and overall survival (OS).
Among 343 patients with lung adenocarcinoma, 61 (18%), 69 (20%), 41 (12%), and 222 (65%) patients had KRAS, STK11, KEAP1, and TP53 mutations, respectively. An overall objective response was observed in 94 of 338 patients (28%), including 2 (1%) who achieved a complete response and 92 (27%) who achieved a partial response. Patients with STK11, KEAP1, or TP53 mutations had a significantly greater TMB (P<0.001). According to the univariate analysis, the treatment response was significantly correlated with TP53 mutation in both the general (P = 0.041) and KRAS wild-type (P = 0.009) populations. KEAP1 and TP53 mutations were associated with worse OS among assessable patients (hazard ratio (HR) = 2.027, P = 0.002; HR = 1.673, P = 0.007, respectively) and among patients without KRAS mutations (HR = 1.897, P = 0.012; HR = 1.908, P = 0.004, respectively). According to the multivariate analysis, KEAP1 (HR = 1.890, P = 0.008) and TP53 (HR = 1.735, P = 0.011) mutations were found to be independent factors for OS.
STK11, KEAP1, and TP53 mutations are significantly associated with a high TMB. TP53 mutation could affect the treatment response to some degree, and both KEAP1 and TP53 mutations resulted in inferior OS in the general patient population and in those with KRAS-wild-type lung adenocarcinoma, indicating that KEAP1 and TP53 mutations might act as prognostic factors for ICI treatment in lung adenocarcinoma patients.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma of Lung - drug therapy</subject><subject>Adenocarcinoma of Lung - genetics</subject><subject>Adenocarcinoma of Lung - mortality</subject><subject>Adenocarcinoma of Lung - pathology</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>AMP-Activated Protein Kinase Kinases</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Chemotherapy</subject><subject>Clinical outcomes</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomics</subject><subject>Humans</subject><subject>Immune checkpoint inhibitors</subject><subject>Immune Checkpoint Inhibitors - therapeutic use</subject><subject>Inhibitors</subject><subject>K-Ras protein</subject><subject>Kelch-Like ECH-Associated Protein 1 - genetics</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - mortality</subject><subject>Lungs</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Middle Aged</subject><subject>Multivariate analysis</subject><subject>Mutation</subject><subject>p53 Protein</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>Research and Analysis Methods</subject><subject>Respiratory agents</subject><subject>Signal transduction</subject><subject>Treatment Outcome</subject><subject>Tumor proteins</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBYmoRAWos_kti5QtVUoOqkTWvh1nIcu3FJ7BI7fPwNfjFum00t2gXyha3j57zHfu2TJC8RHCNC0fu16zsrmvHGWTWGBNKMwUfJKSoIHuUYkscH65PkmfdrCDPC8vxpckIKSGhB0WnyZ6q1ksEDp8H8drK4AIvlHKELMJ9ObuIkbAWWNxkBbR9EMM5G0oJQKyAbY40UDXB9kK5VOwnTtr2Ne7WS3zbO2ACMrU1pgus8EK2zK7CJMsrGij9NqEHTx5ColHVSdNJY14rnyRMtGq9eDPNZ8uXjdHn5eXR1_Wl2ObkayYziMCqxVrSERDNJKcmLFJFUV0xRmWcSFqzMNYWZlBhLgUmhWEEELkrF8kKnMUbOktd73U3jPB_s9JxARnJCU1pEYrYnKifWfNOZVnS_uROG7wKuW3HRBSMbxTHMNZYVFalM02g5U5ksJWOIKoYw1FHrw1CtL1tVyWhBJ5oj0eMda2q-cj84QjjHOSFR4e2g0LnvvfKBt8ZL1TTCKtcPB6eQEhrR83_Qh683UCsRb2CsdrGw3IryCYMYY5ghFqnxA1QclWqNjJ9Pmxg_Snh3lBCZoH6Flei957PF7f-z11-P2TcHbK1EE2rvmn73K4_BdA_KznnfKX3vMoJ82zt3bvBt7_Chd2Laq8MXuk-6axbyF-7DEvQ</recordid><startdate>20240722</startdate><enddate>20240722</enddate><creator>Liang, Yao</creator><creator>Maeda, Osamu</creator><creator>Kondo, Chiaki</creator><creator>Nishida, Kazuki</creator><creator>Ando, Yuichi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0009-0005-2365-1513</orcidid><orcidid>https://orcid.org/0000-0002-6849-2297</orcidid></search><sort><creationdate>20240722</creationdate><title>Effects of KRAS, STK11, KEAP1, and TP53 mutations on the clinical outcomes of immune checkpoint inhibitors among patients with lung adenocarcinoma</title><author>Liang, Yao ; Maeda, Osamu ; Kondo, Chiaki ; Nishida, Kazuki ; Ando, Yuichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c572t-b2fe7b03f8c773694134fd8e7c65c098b6f705cc22ca239e893a29be869f42ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma of Lung - drug therapy</topic><topic>Adenocarcinoma of Lung - genetics</topic><topic>Adenocarcinoma of Lung - mortality</topic><topic>Adenocarcinoma of Lung - pathology</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>AMP-Activated Protein Kinase Kinases</topic><topic>Biology and Life Sciences</topic><topic>Biomarkers</topic><topic>Cancer</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Chemotherapy</topic><topic>Clinical outcomes</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genomics</topic><topic>Humans</topic><topic>Immune checkpoint inhibitors</topic><topic>Immune Checkpoint Inhibitors - therapeutic use</topic><topic>Inhibitors</topic><topic>K-Ras protein</topic><topic>Kelch-Like ECH-Associated Protein 1 - genetics</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - mortality</topic><topic>Lungs</topic><topic>Male</topic><topic>Medicine and Health Sciences</topic><topic>Middle Aged</topic><topic>Multivariate analysis</topic><topic>Mutation</topic><topic>p53 Protein</topic><topic>Patient outcomes</topic><topic>Patients</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>Research and Analysis Methods</topic><topic>Respiratory agents</topic><topic>Signal transduction</topic><topic>Treatment Outcome</topic><topic>Tumor proteins</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liang, Yao</creatorcontrib><creatorcontrib>Maeda, Osamu</creatorcontrib><creatorcontrib>Kondo, Chiaki</creatorcontrib><creatorcontrib>Nishida, Kazuki</creatorcontrib><creatorcontrib>Ando, Yuichi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liang, Yao</au><au>Maeda, Osamu</au><au>Kondo, Chiaki</au><au>Nishida, Kazuki</au><au>Ando, Yuichi</au><au>Galli, Alvaro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of KRAS, STK11, KEAP1, and TP53 mutations on the clinical outcomes of immune checkpoint inhibitors among patients with lung adenocarcinoma</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2024-07-22</date><risdate>2024</risdate><volume>19</volume><issue>7</issue><spage>e0307580</spage><pages>e0307580-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>This study aimed to identify the associations between individual KRAS, STK11, KEAP1, or TP53 mutations, as well as the comutation status of these genes, and the tumor mutation burden (TMB) with clinical outcomes of lung adenocarcinoma patients treated with immune checkpoint inhibitors (ICIs).
We collected data from patients with lung adenocarcinoma treated with ICIs from the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database between June 2019 and August 2023. The main endpoints were the treatment response and overall survival (OS).
Among 343 patients with lung adenocarcinoma, 61 (18%), 69 (20%), 41 (12%), and 222 (65%) patients had KRAS, STK11, KEAP1, and TP53 mutations, respectively. An overall objective response was observed in 94 of 338 patients (28%), including 2 (1%) who achieved a complete response and 92 (27%) who achieved a partial response. Patients with STK11, KEAP1, or TP53 mutations had a significantly greater TMB (P<0.001). According to the univariate analysis, the treatment response was significantly correlated with TP53 mutation in both the general (P = 0.041) and KRAS wild-type (P = 0.009) populations. KEAP1 and TP53 mutations were associated with worse OS among assessable patients (hazard ratio (HR) = 2.027, P = 0.002; HR = 1.673, P = 0.007, respectively) and among patients without KRAS mutations (HR = 1.897, P = 0.012; HR = 1.908, P = 0.004, respectively). According to the multivariate analysis, KEAP1 (HR = 1.890, P = 0.008) and TP53 (HR = 1.735, P = 0.011) mutations were found to be independent factors for OS.
STK11, KEAP1, and TP53 mutations are significantly associated with a high TMB. TP53 mutation could affect the treatment response to some degree, and both KEAP1 and TP53 mutations resulted in inferior OS in the general patient population and in those with KRAS-wild-type lung adenocarcinoma, indicating that KEAP1 and TP53 mutations might act as prognostic factors for ICI treatment in lung adenocarcinoma patients.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>39037971</pmid><doi>10.1371/journal.pone.0307580</doi><tpages>e0307580</tpages><orcidid>https://orcid.org/0009-0005-2365-1513</orcidid><orcidid>https://orcid.org/0000-0002-6849-2297</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2024-07, Vol.19 (7), p.e0307580 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_3083637479 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adenocarcinoma Adenocarcinoma of Lung - drug therapy Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - mortality Adenocarcinoma of Lung - pathology Adult Aged Aged, 80 and over AMP-Activated Protein Kinase Kinases Biology and Life Sciences Biomarkers Cancer Care and treatment Cell cycle Chemotherapy Clinical outcomes Female Genes Genetic aspects Genomics Humans Immune checkpoint inhibitors Immune Checkpoint Inhibitors - therapeutic use Inhibitors K-Ras protein Kelch-Like ECH-Associated Protein 1 - genetics Kinases Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - mortality Lungs Male Medicine and Health Sciences Middle Aged Multivariate analysis Mutation p53 Protein Patient outcomes Patients Protein Serine-Threonine Kinases - genetics Proto-Oncogene Proteins p21(ras) - genetics Research and Analysis Methods Respiratory agents Signal transduction Treatment Outcome Tumor proteins Tumor Suppressor Protein p53 - genetics |
| title | Effects of KRAS, STK11, KEAP1, and TP53 mutations on the clinical outcomes of immune checkpoint inhibitors among patients with lung adenocarcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T11%3A46%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Effects%20of%20KRAS,%20STK11,%20KEAP1,%20and%20TP53%20mutations%20on%20the%20clinical%20outcomes%20of%20immune%20checkpoint%20inhibitors%20among%20patients%20with%20lung%20adenocarcinoma&rft.jtitle=PloS%20one&rft.au=Liang,%20Yao&rft.date=2024-07-22&rft.volume=19&rft.issue=7&rft.spage=e0307580&rft.pages=e0307580-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0307580&rft_dat=%3Cgale_plos_%3EA802220518%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3083637479&rft_id=info:pmid/39037971&rft_galeid=A802220518&rft_doaj_id=oai_doaj_org_article_206f2cd7a4c446208e5cbc8817e8120f&rfr_iscdi=true |