1265P IMpower150: A post hoc analysis of efficacy outcomes in patients with KRAS, STK11 and KEAP1 mutations

West, Howard; Cappuzzo, Federico; Reck, Martin; Mok, Tony; Jotte, Robert M.; Nishio, Makoto; Kim, E.; Morris, Stefanie; Shankar, Geetha; Wu, Zhongze; Shames, D.; McCleland, Mark L.; Socinski, Mark A.

doi:10.1016/j.annonc.2020.08.1579

Cited by 16 publications

(20 citation statements)

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“…Several retrospective studies of patients with previously treated advanced NSCLC compared outcomes of patients with KRAS and STK11 co-mutations with outcomes of patients with only an STK11 mutation. In these studies, patients with the co-mutations had poorer outcomes [63][64][65][66][67]. In an analysis from IMpower150, STK11 was shown to be a major driver of primary resistance to PD-1/PD-L1 checkpoint blockade in patients with KRAS mutations [64][65][66]68].…”

Section: Co-mutations Of Special Interestmentioning

confidence: 99%

“…In an analysis from IMpower150, STK11 was shown to be a major driver of primary resistance to PD-1/PD-L1 checkpoint blockade in patients with KRAS mutations [64][65][66]68]. In this study, median OS in patients with KRAS, STK11, and/or KEAP1 mutations who received the combination of atezolizumab, J o u r n a l P r e -p r o o f bevacizumab, and chemotherapy was 11.1 months, as compared with 8.67 months in those receiving the combination of bevacizumab and chemotherapy (HR for death, 0.50); PFS in the 2 groups was 6 and 3.35 months, respectively [64,67].…”

Section: Co-mutations Of Special Interestmentioning

confidence: 99%

See 1 more Smart Citation

Targeting KRAS in non-small-cell lung cancer: recent progress and new approaches

Reck¹,

Carbone²,

Garassino³

et al. 2021

Annals of Oncology

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170

144

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Co-mutations Of Special Interestmentioning

confidence: 99%

Section: Co-mutations Of Special Interestmentioning

confidence: 99%

Targeting KRAS in non-small-cell lung cancer: recent progress and new approaches

Reck¹,

Carbone²,

Garassino³

et al. 2021

Annals of Oncology

Self Cite

170

144

View full text Add to dashboard Cite

show abstract

“…Also, for KRAS G12C mutations, OS HR was 1.14 (95% CI: 0.45-2.92) [22]. In the IM-POWER150 study, in the population with KRAS mutations, ABCP showed more benefit in OS and PFS than ACP or BCP; in the KRAS-WT population, comparing with BCP, the improvement in OS of ABCP or ACP was limited [23].…”

Section: Anti-pd-l(1) Combined Chemotherapymentioning

confidence: 97%

KRAS-Mutant Non–Small Cell Lung Cancer: Recent Progress

shu¹,

Liu²,

Zhou³

2021

Preprint

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The KRAS mutant population has been undruggable for 40 years. G12C inhibitors and immunotherapy are the beginning of success. It is necessary to summarize the successful experience of the existing treatment model and explore the direction of the next treatment. In this review, we discuss the latest developments in targeted therapy and immunotherapy for KRAS-mutation NSCLC, aiming to provide direction or enlightenment for future treatment strategies.

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“…The relationship between VEGF and KRAS has been identified in previous studies, which showed that VEGF was upregulated by oncogenic KRAS [ 72 , 73 ] and that VEGF promoter activity was upregulated by activation of the PI3K-AKT signaling pathway [ 74 ]. Of note, a recent clinical study demonstrated that the addition of the anti-VEGF antibody bevacizumab to a regimen including the anti-PD-L1 antibody atezolizumab plus carboplatin and paclitaxel (ABCP) produced longer progression-free survival and a greater overall survival benefit than atezolizumab plus carboplatin and paclitaxel (ACP), or bevacizumab plus carboplatin and paclitaxel (BCP), in patients with metastatic nonsquamous NSCLC with KRAS mutations [ 75 ]. Moreover, a greater survival benefit was achieved with ABCP compared with ACP or BCP in patients with tumors carrying KRAS / LKB1 / KEAP1 comutations.…”

Section: Oncogenic Kras Regulates the Tumor Microenvironment (Tme)mentioning

confidence: 99%

Targeting Oncogenic KRAS in Non-Small-Cell Lung Cancer

Sunaga

Miura

Kasahara

et al. 2021

Cancers

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Recent advances in molecular biology and the resultant identification of driver oncogenes have achieved major progress in precision medicine for non-small-cell lung cancer (NSCLC). v-Ki-ras2 Kirsten rat sarcoma viral oncogene (KRAS) is the most common driver in NSCLC, and targeting KRAS is considerably important. The recent discovery of covalent KRAS G12C inhibitors offers hope for improving the prognosis of NSCLC patients, but the development of combination therapies corresponding to tumor characteristics is still required given the vast heterogeneity of KRAS-mutated NSCLC. In this review, we summarize the current understanding of KRAS mutations regarding the involvement of malignant transformation and describe the preclinical and clinical evidence for targeting KRAS-mutated NSCLC. We also discuss the mechanisms of resistance to KRAS G12C inhibitors and possible combination treatment strategies to overcome this drug resistance.

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1265P IMpower150: A post hoc analysis of efficacy outcomes in patients with KRAS, STK11 and KEAP1 mutations

Cited by 16 publications

References 0 publications

Targeting KRAS in non-small-cell lung cancer: recent progress and new approaches

Targeting KRAS in non-small-cell lung cancer: recent progress and new approaches

KRAS-Mutant Non–Small Cell Lung Cancer: Recent Progress

Targeting Oncogenic KRAS in Non-Small-Cell Lung Cancer

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