KRAS-G12C Mutation Is Associated with Poor Outcome in Surgically Resected Lung Adenocarcinoma

Nadal, Ernest; Chen, Guoan; Prensner, John R.; Shiratsuchi, Hiroe; Sam, Christine; Zhao, Lili; Kalemkerian, Gregory P.; Brenner, Dean E.; Lin, Jules; Reddy, Rishindra M.; Chang, Andrew C.; Capellà, Gabriel; Cardenal, Felipe; Beer, David G.; Ramnath, Nithya

doi:10.1097/jto.0000000000000305

Cited by 115 publications

(93 citation statements)

References 44 publications

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“…1 In our manuscript, we performed a multivariate analysis comparing KRAS-G12C and nonG12C versus KRAS wild-type, as shown in the Supplementary Table S4, but we agree with Dr. Smit that we did not present the multivariate analysis comparing KRAS-G12C with the other KRAS codon variants. Here, we show the results from the multivariate Cox analysis for overall survival according to KRAS amino acid substitution using each subtype of KRAS-nonG12C as a reference: G12D vs. G12C, HR = 2.81 (1.07 – 7.36, p = 0.035); G12A vs. G12C, HR = 5.99 (1.39 – 25.7, p = 0.016); G12V vs. G12C, HR = 1.62 (0.70 – 3.76, p = 0.259).…”

Section: In Responsementioning

confidence: 76%

KRAS-G12C Mutation is Associated with Poor Outcome in Surgically Resected Lung Adenocarcinoma

Nadal

Beer

Ramnath

2015

Journal of Thoracic Oncology

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Section: In Responsementioning

confidence: 76%

KRAS-G12C Mutation is Associated with Poor Outcome in Surgically Resected Lung Adenocarcinoma

Nadal

Beer

Ramnath

2015

Journal of Thoracic Oncology

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“…Nadal et al . reported that KRAS-G12C mutants overexpress EMT genes in surgically resected lung adenocarcinoma 37 . Activation of KRAS signaling could stimulate EMT pathways via extracellular signal–regulated kinase (ERK)1/2 in lung cancer cells 38 .…”

Section: Discussionmentioning

confidence: 99%

Prognostic Significance of EDIL3 Expression and Correlation with Mesenchymal Phenotype and Microvessel Density in Lung Adenocarcinoma

Jeong

Ban

et al. 2017

Sci Rep

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We examined the prognostic significance of Epidermal Growth Factor-like repeats and Discoidin I-Like Domains 3 (EDIL3) expression and its correlations with mesenchymal phenotype and microvessel density in non-small cell lung carcinoma (NSCLC). A total of 268 NSCLC specimens were evaluated retrospectively by immunohistochemical staining for EDIL3, EMT markers (e-cadherin, β-catenin, and vimentin), and CD31 to measure microvessel density. EDIL3, e-cadherin, β-catenin, and vimentin were expressed in 16%, 22.8%, 3.7%, and 10.1% of the specimens, respectively. The mRNA level of EDIL3 in tumor was correlated with the level of EDIL3 protein expression using immunohistochemistry. In lung adenocarcinoma patients, EDIL3 expression was significantly correlated with low e-cadherin expression, high vimentin expression, and increased microvessel density (P < 0.001, P = 0.001, and P = 0.023, respectively). In lung squamous cell carcinoma patients, EDIL3 expression was significantly correlated with low e-cadherin expression and high vimentin expression (P = 0.021 and P = 0.002, respectively). In lung adenocarcinoma patients, EDIL3 was an independent prognostic factor for overall survival in a multivariate analysis (hazard ratio: 2.552, P = 0.004). EDIL3 is significantly correlated with mesenchymal phenotype, angiogenesis, and tumor progression in lung adenocarcinoma.

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“… 12 Nadal and colleagues showed in 179 resected lung adenocarcinoma that patients with KRAS -G12C mutant tumors had significantly shorter disease-free survival (DFS) compared with tumors harboring other KRAS mutations or KRAS wild-type tumors. 22 In contrast, Izar and colleagues identified improved OS and DFS for G12C and G12V patients in 127 patients. 23 Similarly, Renaud and colleagues showed that KRAS G12V patients had significantly higher risk of recurrence, lower median OS and lower time to recurrence when compared with non- KRAS G12V, EGFR mutated or wild-type patients in 841 surgically treated French patients.…”

Section: Prognostic Role Of Kras Mutations In Nsclmentioning

confidence: 94%

Treating KRAS-mutant NSCLC: latest evidence and clinical consequences

et al. 2017

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KRAS mutations represent one of the most prevalent oncogenic driver mutations in non-small cell lung cancer (NSCLC). For many years we have unsuccessfully addressed KRAS mutation as a unique disease. The recent widespread use of comprehensive genomic profiling has identified different subgroups with prognostic implications. Moreover, recent data recognizing the distinct biology and therapeutic vulnerabilities of different KRAS subgroups have allowed us to explore different treatment approaches. Small molecules that selectively inhibit KRAS G12C or use of immune checkpoint inhibitors based on co-mutation status are some examples which anticipate that personalized treatment for this challenging disease is finally on the horizon.

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KRAS-G12C Mutation Is Associated with Poor Outcome in Surgically Resected Lung Adenocarcinoma

Abstract: KRAS-G12C mutation is associated with worse DFS and OS in resected lung AC. Gene-expression profiles in lung cancer cell lines and surgically resected lung AC revealed that KRAS-G12C mutants had an epithelial to mesenchymal transition and a KRAS-independent phenotype.

Cited by 115 publications

References 44 publications

KRAS-G12C Mutation is Associated with Poor Outcome in Surgically Resected Lung Adenocarcinoma

KRAS-G12C Mutation is Associated with Poor Outcome in Surgically Resected Lung Adenocarcinoma

Prognostic Significance of EDIL3 Expression and Correlation with Mesenchymal Phenotype and Microvessel Density in Lung Adenocarcinoma

Treating KRAS-mutant NSCLC: latest evidence and clinical consequences

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