Large-scale clinico-genomic profile of non-small cell lung cancer with KRAS G12C: Results from LC-SCRUM-Asia study
•The frequency of KRAS G12C was 4.0% in Asian patients with NSCLC.•KRAS G12C tumor had higher tumor mutation burden and higher PD-L1 expression.•KRAS G12C-positive NSCLC showed potential sensitivity to ICIs. KRAS G12C is an oncogenic driver mutation, accounting for approximately 14% of Caucasian pat...
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| Veröffentlicht in: | Lung cancer (Amsterdam, Netherlands) Netherlands), 2023-02, Vol.176, p.103-111 |
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| creator | Tamiya, Yutaro Matsumoto, Shingo Zenke, Yoshitaka Yoh, Kiyotaka Ikeda, Takaya Shibata, Yuji Kato, Terufumi Nishino, Kazumi Nakamura, Atsushi Furuya, Naoki Miyamoto, Shingo Kuyama, Shoichi Nomura, Shogo Ikeno, Takashi Udagawa, Hibiki Sugiyama, Eri Nosaki, Kaname Izumi, Hiroki Sakai, Tetsuya Hashimoto, Naozumi Goto, Koichi |
| description | •The frequency of KRAS G12C was 4.0% in Asian patients with NSCLC.•KRAS G12C tumor had higher tumor mutation burden and higher PD-L1 expression.•KRAS G12C-positive NSCLC showed potential sensitivity to ICIs.
KRAS G12C is an oncogenic driver mutation, accounting for approximately 14% of Caucasian patients with non-small cell lung cancer (NSCLC). Recently, several KRAS G12C-targeted drugs have been developed; however, the clinico-genomic characteristics of NSCLC patients with KRAS G12C remain unclear.
Based on the large-scale prospective lung cancer genomic screening project (LC-SCRUM-Asia) database, the clinico-genomic characteristics and therapeutic outcomes of NSCLC patients with KRAS G12C were evaluated.
From March 2015 to March 2021, 10,023 NSCLC patients were enrolled in LC-SCRUM-Asia. KRAS mutations were detected in 1258 patients (14 %), including G12C in 376 (4.0 %), G12D in 289 (3.1 %) and G12V in 251 (2.7 %). The proportions of males and smokers were higher in patients with KRAS G12C than in those with KRAS non-G12C mutations (males: 73 % vs 63 %, p |
| doi_str_mv | 10.1016/j.lungcan.2022.12.019 |
| format | Article |
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KRAS G12C is an oncogenic driver mutation, accounting for approximately 14% of Caucasian patients with non-small cell lung cancer (NSCLC). Recently, several KRAS G12C-targeted drugs have been developed; however, the clinico-genomic characteristics of NSCLC patients with KRAS G12C remain unclear.
Based on the large-scale prospective lung cancer genomic screening project (LC-SCRUM-Asia) database, the clinico-genomic characteristics and therapeutic outcomes of NSCLC patients with KRAS G12C were evaluated.
From March 2015 to March 2021, 10,023 NSCLC patients were enrolled in LC-SCRUM-Asia. KRAS mutations were detected in 1258 patients (14 %), including G12C in 376 (4.0 %), G12D in 289 (3.1 %) and G12V in 251 (2.7 %). The proportions of males and smokers were higher in patients with KRAS G12C than in those with KRAS non-G12C mutations (males: 73 % vs 63 %, p < 0.001; smokers: 89 % vs 76 %, p < 0.001). KRAS G12C-positive tumors showed a higher tumor mutation burden (TMB) (mean, 8.1 mut/Mb, p < 0.001) and a higher percentage of tumors with programmed cell death ligand-1 (PD-L1) expression ≥50 % (52 %, p = 0.08). The overall survival in patients with KRAS G12C (median, 24.6 months) was not different between patients with other mutation subtypes (G12V: 18.2 months, p = 0.23; G12D: 20.6 months, p = 0.65; other KRAS mutations: 18.3 months, p = 0.20). Among KRAS-mutated patients who received immune checkpoint inhibitors (ICIs), the progression-free survival in G12C-positive patients (median, 3.4 months) was similar to that in G12V-positive patients (4.2 months, p = 0.90), but significantly longer than that in G12D- (2.0 months, p = 0.02) and other KRAS mutation-positive patients (2.5 months, p = 0.02).
The frequencies of KRAS G12C were lower in Asian than in Caucasian NSCLC patients. Among the KRAS-mutated NSCLC patients, G12C-positive tumors showed increased immunogenicity, such as high TMB and high PD-L1 expression, and potential sensitivity to ICIs.</description><identifier>ISSN: 0169-5002</identifier><identifier>EISSN: 1872-8332</identifier><identifier>DOI: 10.1016/j.lungcan.2022.12.019</identifier><identifier>PMID: 36634571</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>B7-H1 Antigen - genetics ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Humans ; KRAS G12C ; KRAS mutation ; Lung Neoplasms - drug therapy ; Male ; Mutation ; Next-generation sequencing ; Non-small cell lung cancer ; PD-L1 expression ; Prospective Studies ; Proto-Oncogene Proteins p21(ras) - genetics ; Tumor burden</subject><ispartof>Lung cancer (Amsterdam, Netherlands), 2023-02, Vol.176, p.103-111</ispartof><rights>2023 Elsevier B.V.</rights><rights>Copyright © 2023 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-b7caed67c6b13eda841f9c3b43e6c0210565f7a373998bb657a37a05117730393</citedby><cites>FETCH-LOGICAL-c412t-b7caed67c6b13eda841f9c3b43e6c0210565f7a373998bb657a37a05117730393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lungcan.2022.12.019$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36634571$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tamiya, Yutaro</creatorcontrib><creatorcontrib>Matsumoto, Shingo</creatorcontrib><creatorcontrib>Zenke, Yoshitaka</creatorcontrib><creatorcontrib>Yoh, Kiyotaka</creatorcontrib><creatorcontrib>Ikeda, Takaya</creatorcontrib><creatorcontrib>Shibata, Yuji</creatorcontrib><creatorcontrib>Kato, Terufumi</creatorcontrib><creatorcontrib>Nishino, Kazumi</creatorcontrib><creatorcontrib>Nakamura, Atsushi</creatorcontrib><creatorcontrib>Furuya, Naoki</creatorcontrib><creatorcontrib>Miyamoto, Shingo</creatorcontrib><creatorcontrib>Kuyama, Shoichi</creatorcontrib><creatorcontrib>Nomura, Shogo</creatorcontrib><creatorcontrib>Ikeno, Takashi</creatorcontrib><creatorcontrib>Udagawa, Hibiki</creatorcontrib><creatorcontrib>Sugiyama, Eri</creatorcontrib><creatorcontrib>Nosaki, Kaname</creatorcontrib><creatorcontrib>Izumi, Hiroki</creatorcontrib><creatorcontrib>Sakai, Tetsuya</creatorcontrib><creatorcontrib>Hashimoto, Naozumi</creatorcontrib><creatorcontrib>Goto, Koichi</creatorcontrib><title>Large-scale clinico-genomic profile of non-small cell lung cancer with KRAS G12C: Results from LC-SCRUM-Asia study</title><title>Lung cancer (Amsterdam, Netherlands)</title><addtitle>Lung Cancer</addtitle><description>•The frequency of KRAS G12C was 4.0% in Asian patients with NSCLC.•KRAS G12C tumor had higher tumor mutation burden and higher PD-L1 expression.•KRAS G12C-positive NSCLC showed potential sensitivity to ICIs.
KRAS G12C is an oncogenic driver mutation, accounting for approximately 14% of Caucasian patients with non-small cell lung cancer (NSCLC). Recently, several KRAS G12C-targeted drugs have been developed; however, the clinico-genomic characteristics of NSCLC patients with KRAS G12C remain unclear.
Based on the large-scale prospective lung cancer genomic screening project (LC-SCRUM-Asia) database, the clinico-genomic characteristics and therapeutic outcomes of NSCLC patients with KRAS G12C were evaluated.
From March 2015 to March 2021, 10,023 NSCLC patients were enrolled in LC-SCRUM-Asia. KRAS mutations were detected in 1258 patients (14 %), including G12C in 376 (4.0 %), G12D in 289 (3.1 %) and G12V in 251 (2.7 %). The proportions of males and smokers were higher in patients with KRAS G12C than in those with KRAS non-G12C mutations (males: 73 % vs 63 %, p < 0.001; smokers: 89 % vs 76 %, p < 0.001). KRAS G12C-positive tumors showed a higher tumor mutation burden (TMB) (mean, 8.1 mut/Mb, p < 0.001) and a higher percentage of tumors with programmed cell death ligand-1 (PD-L1) expression ≥50 % (52 %, p = 0.08). The overall survival in patients with KRAS G12C (median, 24.6 months) was not different between patients with other mutation subtypes (G12V: 18.2 months, p = 0.23; G12D: 20.6 months, p = 0.65; other KRAS mutations: 18.3 months, p = 0.20). Among KRAS-mutated patients who received immune checkpoint inhibitors (ICIs), the progression-free survival in G12C-positive patients (median, 3.4 months) was similar to that in G12V-positive patients (4.2 months, p = 0.90), but significantly longer than that in G12D- (2.0 months, p = 0.02) and other KRAS mutation-positive patients (2.5 months, p = 0.02).
The frequencies of KRAS G12C were lower in Asian than in Caucasian NSCLC patients. Among the KRAS-mutated NSCLC patients, G12C-positive tumors showed increased immunogenicity, such as high TMB and high PD-L1 expression, and potential sensitivity to ICIs.</description><subject>B7-H1 Antigen - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Humans</subject><subject>KRAS G12C</subject><subject>KRAS mutation</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Male</subject><subject>Mutation</subject><subject>Next-generation sequencing</subject><subject>Non-small cell lung cancer</subject><subject>PD-L1 expression</subject><subject>Prospective Studies</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>Tumor burden</subject><issn>0169-5002</issn><issn>1872-8332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFu3CAURVHVKpmm-YRWLLvB5YFtxtlEIytJq05VadKsEcbPU0a2ScBOlb8v1ky67QYQOpfLO4R8BJ4Bh_LLIevncW_NmAkuRAYi41C9IStYK8HWUoq3ZJW4ihWci3PyPsYD56CAV2fkXJalzAsFKxK2JuyRRWt6pLZ3o7Oe7XH0g7P0MfjOpXvf0dGPLA6m76nFtCzdNJVbDPSPm37T77vNPb0DUV_RHca5nyLtgh_otmb39e7hB9tEZ2ic5vblA3nXmT7i5Wm_IA-3N7_qr2z78-5bvdkym4OYWKOswbZUtmxAYmvWOXSVlU0usbRcAC_KolNGKllV66Ypi-VseAGglOSykhfk8_HdNMbTjHHSg4vL782Ifo5aqJRRQqk8ocURtcHHGLDTj8ENJrxo4HrRrQ_6pFsvujUInXSn3KdTxdwM2P5LvfpNwPURwDTos8Ogo3WYtLUuoJ10691_Kv4CDLmR1A</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Tamiya, Yutaro</creator><creator>Matsumoto, Shingo</creator><creator>Zenke, Yoshitaka</creator><creator>Yoh, Kiyotaka</creator><creator>Ikeda, Takaya</creator><creator>Shibata, Yuji</creator><creator>Kato, Terufumi</creator><creator>Nishino, Kazumi</creator><creator>Nakamura, Atsushi</creator><creator>Furuya, Naoki</creator><creator>Miyamoto, Shingo</creator><creator>Kuyama, Shoichi</creator><creator>Nomura, Shogo</creator><creator>Ikeno, Takashi</creator><creator>Udagawa, Hibiki</creator><creator>Sugiyama, Eri</creator><creator>Nosaki, Kaname</creator><creator>Izumi, Hiroki</creator><creator>Sakai, Tetsuya</creator><creator>Hashimoto, Naozumi</creator><creator>Goto, Koichi</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>202302</creationdate><title>Large-scale clinico-genomic profile of non-small cell lung cancer with KRAS G12C: Results from LC-SCRUM-Asia study</title><author>Tamiya, Yutaro ; Matsumoto, Shingo ; Zenke, Yoshitaka ; Yoh, Kiyotaka ; Ikeda, Takaya ; Shibata, Yuji ; Kato, Terufumi ; Nishino, Kazumi ; Nakamura, Atsushi ; Furuya, Naoki ; Miyamoto, Shingo ; Kuyama, Shoichi ; Nomura, Shogo ; Ikeno, Takashi ; Udagawa, Hibiki ; Sugiyama, Eri ; Nosaki, Kaname ; Izumi, Hiroki ; Sakai, Tetsuya ; Hashimoto, Naozumi ; Goto, Koichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-b7caed67c6b13eda841f9c3b43e6c0210565f7a373998bb657a37a05117730393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>B7-H1 Antigen - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Humans</topic><topic>KRAS G12C</topic><topic>KRAS mutation</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Male</topic><topic>Mutation</topic><topic>Next-generation sequencing</topic><topic>Non-small cell lung cancer</topic><topic>PD-L1 expression</topic><topic>Prospective Studies</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>Tumor burden</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tamiya, Yutaro</creatorcontrib><creatorcontrib>Matsumoto, Shingo</creatorcontrib><creatorcontrib>Zenke, Yoshitaka</creatorcontrib><creatorcontrib>Yoh, Kiyotaka</creatorcontrib><creatorcontrib>Ikeda, Takaya</creatorcontrib><creatorcontrib>Shibata, Yuji</creatorcontrib><creatorcontrib>Kato, Terufumi</creatorcontrib><creatorcontrib>Nishino, Kazumi</creatorcontrib><creatorcontrib>Nakamura, Atsushi</creatorcontrib><creatorcontrib>Furuya, Naoki</creatorcontrib><creatorcontrib>Miyamoto, Shingo</creatorcontrib><creatorcontrib>Kuyama, Shoichi</creatorcontrib><creatorcontrib>Nomura, Shogo</creatorcontrib><creatorcontrib>Ikeno, Takashi</creatorcontrib><creatorcontrib>Udagawa, Hibiki</creatorcontrib><creatorcontrib>Sugiyama, Eri</creatorcontrib><creatorcontrib>Nosaki, Kaname</creatorcontrib><creatorcontrib>Izumi, Hiroki</creatorcontrib><creatorcontrib>Sakai, Tetsuya</creatorcontrib><creatorcontrib>Hashimoto, Naozumi</creatorcontrib><creatorcontrib>Goto, Koichi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Lung cancer (Amsterdam, Netherlands)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tamiya, Yutaro</au><au>Matsumoto, Shingo</au><au>Zenke, Yoshitaka</au><au>Yoh, Kiyotaka</au><au>Ikeda, Takaya</au><au>Shibata, Yuji</au><au>Kato, Terufumi</au><au>Nishino, Kazumi</au><au>Nakamura, Atsushi</au><au>Furuya, Naoki</au><au>Miyamoto, Shingo</au><au>Kuyama, Shoichi</au><au>Nomura, Shogo</au><au>Ikeno, Takashi</au><au>Udagawa, Hibiki</au><au>Sugiyama, Eri</au><au>Nosaki, Kaname</au><au>Izumi, Hiroki</au><au>Sakai, Tetsuya</au><au>Hashimoto, Naozumi</au><au>Goto, Koichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Large-scale clinico-genomic profile of non-small cell lung cancer with KRAS G12C: Results from LC-SCRUM-Asia study</atitle><jtitle>Lung cancer (Amsterdam, Netherlands)</jtitle><addtitle>Lung Cancer</addtitle><date>2023-02</date><risdate>2023</risdate><volume>176</volume><spage>103</spage><epage>111</epage><pages>103-111</pages><issn>0169-5002</issn><eissn>1872-8332</eissn><abstract>•The frequency of KRAS G12C was 4.0% in Asian patients with NSCLC.•KRAS G12C tumor had higher tumor mutation burden and higher PD-L1 expression.•KRAS G12C-positive NSCLC showed potential sensitivity to ICIs.
KRAS G12C is an oncogenic driver mutation, accounting for approximately 14% of Caucasian patients with non-small cell lung cancer (NSCLC). Recently, several KRAS G12C-targeted drugs have been developed; however, the clinico-genomic characteristics of NSCLC patients with KRAS G12C remain unclear.
Based on the large-scale prospective lung cancer genomic screening project (LC-SCRUM-Asia) database, the clinico-genomic characteristics and therapeutic outcomes of NSCLC patients with KRAS G12C were evaluated.
From March 2015 to March 2021, 10,023 NSCLC patients were enrolled in LC-SCRUM-Asia. KRAS mutations were detected in 1258 patients (14 %), including G12C in 376 (4.0 %), G12D in 289 (3.1 %) and G12V in 251 (2.7 %). The proportions of males and smokers were higher in patients with KRAS G12C than in those with KRAS non-G12C mutations (males: 73 % vs 63 %, p < 0.001; smokers: 89 % vs 76 %, p < 0.001). KRAS G12C-positive tumors showed a higher tumor mutation burden (TMB) (mean, 8.1 mut/Mb, p < 0.001) and a higher percentage of tumors with programmed cell death ligand-1 (PD-L1) expression ≥50 % (52 %, p = 0.08). The overall survival in patients with KRAS G12C (median, 24.6 months) was not different between patients with other mutation subtypes (G12V: 18.2 months, p = 0.23; G12D: 20.6 months, p = 0.65; other KRAS mutations: 18.3 months, p = 0.20). Among KRAS-mutated patients who received immune checkpoint inhibitors (ICIs), the progression-free survival in G12C-positive patients (median, 3.4 months) was similar to that in G12V-positive patients (4.2 months, p = 0.90), but significantly longer than that in G12D- (2.0 months, p = 0.02) and other KRAS mutation-positive patients (2.5 months, p = 0.02).
The frequencies of KRAS G12C were lower in Asian than in Caucasian NSCLC patients. Among the KRAS-mutated NSCLC patients, G12C-positive tumors showed increased immunogenicity, such as high TMB and high PD-L1 expression, and potential sensitivity to ICIs.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>36634571</pmid><doi>10.1016/j.lungcan.2022.12.019</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | B7-H1 Antigen - genetics Carcinoma, Non-Small-Cell Lung - drug therapy Humans KRAS G12C KRAS mutation Lung Neoplasms - drug therapy Male Mutation Next-generation sequencing Non-small cell lung cancer PD-L1 expression Prospective Studies Proto-Oncogene Proteins p21(ras) - genetics Tumor burden |
| title | Large-scale clinico-genomic profile of non-small cell lung cancer with KRAS G12C: Results from LC-SCRUM-Asia study |
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