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KRAS G12C-Mutant Non-Small Cell Lung Cancer

1. Disease Information

2026-05-09
Falcon MONDO:0005061 Model: Edison Scientific Literature 29 citations

1. Disease Information

Concise overview

KRAS G12C‑mutant NSCLC refers to NSCLC (most commonly lung adenocarcinoma) in which tumor cells harbor a somatic KRAS p.G12C substitution (glycine→cysteine at codon 12). This is a driver oncogene alteration that has become clinically actionable through covalent “OFF‑state” KRAS G12C inhibitors such as sotorasib and adagrasib. (mina2025emergingtargetedtherapies pages 2-4, sreter2024resistancetokras pages 1-2)

Key identifiers and terminologies

  • Disease ontology identifiers available from retrieved evidence:
  • NSCLC: EFO_0003060 (Open Targets evidence) (OpenTargets Search: non-small cell lung carcinoma-KRAS)
  • Lung adenocarcinoma: EFO_0000571 (Open Targets evidence) (OpenTargets Search: non-small cell lung carcinoma-KRAS)
  • MeSH / ICD‑10 / ICD‑11 / Orphanet / OMIM: Not explicitly provided in the retrieved sources for this molecular subtype; therefore not asserted here.

Common synonyms / alternative names

Evidence provenance (individual vs aggregated)

Most information below is derived from: - Aggregated clinical-trial evidence (CodeBreaK 100/200; KRYSTAL‑1 and later analyses) (dy2023longtermoutcomesand pages 2-3, langen2023sotorasibversusdocetaxel pages 8-10) - Real‑world observational datasets (claims/registry cohorts) (sultan2024realworldevaluationof pages 1-2, gecgel2025krasg12cmutation pages 9-11) - Preclinical model studies and mechanistic reviews (resistance/combination rationale) (sreter2024resistancetokras pages 1-2, shaverdashvili2025advancesinthe pages 2-3)

2. Etiology

Disease causal factors

Risk factors

  • Smoking association: KRAS mutations are reported as more frequent in smokers than nonsmokers (example values: 30% vs 11%) and more common in Western vs Asian populations (26% vs 11%) in a 2024 overview review. (tenekeci2024anupdatedoverview pages 2-3)

Protective factors

No protective genetic or environmental factors specific to developing KRAS G12C‑mutant NSCLC were identified in the retrieved evidence.

Gene–environment interactions

The retrieved evidence supports a correlation between smoking exposure and KRAS mutation frequency, consistent with a gene–environment relationship; however, specific quantitative interaction models were not captured in the retrieved sources. (tenekeci2024anupdatedoverview pages 2-3)

3. Phenotypes

Clinical phenotype (NSCLC context)

The retrieved evidence is focused on molecular stratification and treatment outcomes rather than detailed symptom frequencies. As a molecular subtype of NSCLC, phenotypes are generally those of advanced NSCLC; however, phenotype frequencies and HPO mappings were not reported in the retrieved clinical-trial excerpts.

Suggested HPO terms (knowledge-base suggestions; not extracted from the above trials)

Because the phenotype spectrum is not explicitly described in the retrieved sources, the following are standard NSCLC‑relevant HPO suggestions for a knowledge base entry (flagged as suggestions rather than evidence‑extracted): - Cough (HP:0012735) - Dyspnea (HP:0002094) - Chest pain (HP:0100749) - Hemoptysis (HP:0002105) - Weight loss (HP:0001824) - Fatigue (HP:0012378) - Metastatic lesions (HP:0033006; broad)

4. Genetic / Molecular Information

Causal gene

  • KRAS (KRAS proto‑oncogene, GTPase) is strongly associated with NSCLC and lung adenocarcinoma in Open Targets evidence. (OpenTargets Search: non-small cell lung carcinoma-KRAS)

Pathogenic variant

Co-mutations / molecular modifiers (prognostic and predictive)

Co‑alterations shape prognosis and response to KRAS G12C inhibitors. - In a clinico‑genomic analysis of adagrasib‑treated KRAS G12C NSCLC (KRYSTAL‑1), KEAP1 and STK11 co‑mutations were associated with markedly worse outcomes: - KEAP1: PFS 4.1 vs 9.9 months; OS 5.4 vs 19.0 months (HRs ~2.7–3.6; P<0.01) (negrao2025impactofcomutations pages 1-2) - STK11: PFS 4.2 vs 11.0 months; OS 9.8 months vs not reached (HRs ~2.2–2.6; P<0.01) (negrao2025impactofcomutations pages 1-2) - High NRF2 signaling (including KEAP1/NRF2 axis activation) correlated with shorter survival on adagrasib even in KEAP1WT tumors. (negrao2025impactofcomutations pages 1-2) - A favorable molecular group (KEAP1WT/STK11WT/NRF2LOW) represented ~32% of adagrasib‑treated patients and showed longer PFS and OS than comparison groups in that analysis. (negrao2025impactofcomutations pages 1-2)

Functional consequence (high-level)

The KRAS G12C mutation yields a KRAS protein state exploitable by covalent inhibitors that bind the cysteine at position 12 and stabilize the GDP‑bound (inactive) form. (mina2025emergingtargetedtherapies pages 2-4, tenekeci2024anupdatedoverview pages 2-3)

Suggested GO terms (mechanism-oriented; consistent with retrieved pathway statements)

5. Environmental Information

Key environmental/lifestyle factors

  • Tobacco smoke exposure is the most clearly supported lifestyle association in the retrieved evidence through its association with higher KRAS mutation frequency. (tenekeci2024anupdatedoverview pages 2-3)

No infectious agents specific to this molecular subtype were identified in the retrieved evidence.

6. Mechanism / Pathophysiology

Core signaling pathways

KRAS activation drives downstream oncogenic signaling including: - MAPK pathway (RAF–MEK–ERK axis) and - PI3K–AKT–mTOR axis as summarized in recent reviews of KRAS‑mutant NSCLC and KRAS inhibition resistance. (sreter2024resistancetokras pages 1-2, mina2025emergingtargetedtherapies pages 2-4)

Therapeutic mechanism of KRAS G12C inhibitors

Covalent KRAS G12C inhibitors exploit the mutant cysteine to bind KRAS in a state that reduces signaling output; nonetheless, clinical activity is often limited by adaptive and acquired resistance. (mina2025emergingtargetedtherapies pages 2-4, shaverdashvili2025advancesinthe pages 2-3)

Resistance mechanisms (current understanding)

The retrieved evidence emphasizes that resistance to KRAS G12C inhibition is frequent and can be: - On‑target (secondary KRAS alterations preventing drug binding) and - Off‑target / bypass (reactivation via alternative oncogenic nodes or pathways), including RTK‑driven upstream reactivation and downstream pathway rewiring. (shaverdashvili2025advancesinthe pages 2-3)

A high‑impact 2024 preclinical study supports a concrete combination rationale: - Co‑targeting SOS1 (using BI‑3406) plus the KRAS G12C inhibitor adagrasib produced stronger suppression of RAS–MAPK signaling, delayed acquired resistance, and restored responses in adagrasib‑resistant models; resistance was associated with MRAS activity, which SOS1 and SHP2 inhibition can suppress. (sreter2024resistancetokras pages 1-2)

Cell types (CL) and tissues (UBERON)

The evidence is primarily genotype/therapy focused; histology indicates most cases are lung adenocarcinoma (UBERON:0002048 lung; tissue subtype not explicitly curated in retrieved excerpts). (OpenTargets Search: non-small cell lung carcinoma-KRAS)

7. Anatomical Structures Affected

  • Primary organ: Lung (NSCLC; often lung adenocarcinoma). (OpenTargets Search: non-small cell lung carcinoma-KRAS)
  • Central nervous system involvement: CodeBreaK 100 included an intracranial efficacy subset (16 evaluable) with intracranial complete responses and high intracranial disease control on sotorasib, supporting clinically relevant CNS metastatic disease considerations in this population. (dy2023longtermoutcomesand pages 2-3)

Suggested ontology terms: - UBERON:0002048 (lung) - UBERON:0000955 (brain) for CNS metastasis context

8. Temporal Development

KRAS G12C‑mutant NSCLC is typically an adult-onset malignancy and frequently diagnosed in advanced stage, but stage-at-diagnosis distributions specific to this genotype were not extracted in the retrieved evidence.

In the therapeutic setting, acquired resistance typically emerges within months on KRAS G12C inhibitors, motivating combination strategies; the retrieved evidence emphasizes transience of response and rapid resistance emergence. (shaverdashvili2025advancesinthe pages 2-3)

9. Inheritance and Population

Inheritance pattern

This is overwhelmingly a somatic (tumor-acquired) driver alteration in NSCLC; no germline inheritance pattern is implied by the retrieved evidence.

Epidemiology: frequency of KRAS and KRAS G12C in NSCLC

  • KRAS mutations occur in roughly ~29–32% of lung adenocarcinomas in a 2024 resistance review. (sreter2024resistancetokras pages 1-2)
  • Across KRAS point mutations in lung adenocarcinoma, G12C is the most common (~39%) in that review. (sreter2024resistancetokras pages 1-2)
  • Another 2024 overview reports KRAS mutations in ~20–40% of lung adenocarcinomas and that G12C comprises ~39–42% of KRAS variants in lung adenocarcinoma; it also reports higher KRAS mutation frequency in smokers and in Western populations. (tenekeci2024anupdatedoverview pages 2-3)

Real‑world demographic notes (example cohort)

  • In a Finnish real‑world registry cohort of advanced/unresectable or metastatic NSCLC undergoing NGS testing, all KRAS‑mutant patients were previous/current smokers; KRAS G12C was identified in n=35 (within KRAS‑mutant subgroup) and KRAS G12C was associated with poorer survival in that cohort (pre‑KRAS‑G12C inhibitor era context and access limitations may apply). (sultan2024realworldevaluationof pages 1-2)

10. Diagnostics

Molecular testing approaches and implementation

The evidence supports the clinical need for timely identification of KRAS G12C and co‑alterations.

  • Broad NGS testing and reflex workflows: A real‑world study of squamous NSCLC showed that broad DNA/RNA NGS can identify actionable alterations including KRAS G12C and argues for reflex testing across NSCLC histologies rather than restricting by smoking status/age. (mina2025emergingtargetedtherapies pages 2-4)
  • Turnaround time and rapid assays: A 2023 review notes NGS turnaround can be 12–15 days and describes the Idylla rapid oncology assay (<3 hours) to detect KRAS hotspot mutations from FFPE without DNA extraction, citing high concordance with NGS in studies it summarizes. (o’leary2023targetedtherapiesfor pages 4-5)
  • Tissue and plasma use in trials: CodeBreaK 200 exploratory analyses used tissue and/or plasma targeted NGS for genomic alteration analyses. (alharbi2024codebreak200study pages 2-4)

Biomarkers beyond KRAS G12C

  • Co‑mutation profiling (e.g., STK11, KEAP1, NRF2 pathway readouts) can stratify expected outcomes to KRAS G12C inhibitors, particularly for adagrasib in KRYSTAL‑1 analyses. (negrao2025impactofcomutations pages 1-2)

Liquid biopsy for resistance monitoring (expert interpretation supported by retrieved review statement)

A recent review explicitly highlights that “Tissue and liquid biopsies and genotyping of resistant clinical samples can elucidate resistance mechanisms and guide therapeutic decisions.” (shaverdashvili2025advancesinthe pages 2-3)

11. Outcome / Prognosis

Outcomes under KRAS G12C targeted therapy (key statistics)

Pivotal and long‑term trial outcomes for sotorasib in previously treated advanced KRAS G12C NSCLC: - CodeBreaK 200 (phase 3): sotorasib improved PFS vs docetaxel (median 5.6 vs 4.5 months, HR 0.66, p=0.0017), improved ORR (28.1% vs 13.2%), but did not improve OS (median 10.6 vs 11.3 months, HR 1.01). (langen2023sotorasibversusdocetaxel pages 8-10) - CodeBreaK 100 (2‑year update): ORR 41%, median DOR 12.3 months, median PFS 6.3 months, median OS 12.5 months, and 2‑year OS rate 33%; long‑term clinical benefit (PFS ≥12 months) in 23%. (dy2023longtermoutcomesand pages 2-3)

Prognostic modifiers

Co‑mutations (e.g., KEAP1, STK11, NRF2 signaling state) define distinct outcome strata under KRAS G12C inhibitor therapy in adagrasib‑treated patients. (negrao2025impactofcomutations pages 1-2)

Real‑world outcomes / utilization proxies

In a US claims‑based cohort receiving sotorasib (2L+), adherence was high (PDC 94.9%) and median treatment duration 4.3 months; median time to next treatment among those with subsequent therapy was 6.8 months, comparable in magnitude to PFS observed in trials (acknowledging TTNT is not a direct PFS measure). (sultan2024realworldevaluationof pages 1-2)

12. Treatment

12.1 Approved targeted therapies (current standard in previously treated setting)

Key practical safety consideration: hepatotoxicity risk can be higher when sotorasib is started soon after prior immunotherapy; pooled and comparative summaries highlight this clinically relevant sequencing issue. (higgins2025sotorasibforthe pages 3-4, speranza2025sexrelatedsafetysignals pages 9-11)

12.2 Treatment sequencing and guideline‑adjacent expert framing

The retrieved evidence emphasizes that KRAS G12C inhibitors are widely positioned after progression on standard first‑line regimens (often immunotherapy‑based), with ongoing trials moving them into earlier lines and combinations. (tenekeci2024anupdatedoverview pages 2-3, o’leary2023targetedtherapiesfor pages 10-11)

12.3 Combination strategies (research frontier; mechanistic rationale)

  • KRAS G12C inhibitor + SOS1 inhibitor: stronger RAS–MAPK suppression and delayed resistance in preclinical KRAS G12C lung cancer models. (sreter2024resistancetokras pages 1-2)
  • Co‑mutation–informed combinations: adagrasib plus mTOR inhibition showed enhanced efficacy in STK11/KEAP1 co‑mutant preclinical models and is proposed as a rational approach for poor‑prognosis genomics. (negrao2025impactofcomutations pages 1-2)

12.4 Selected ongoing clinical trials (real‑world implementation pipeline)

From retrieved ClinicalTrials.gov records: - NCT06497556 (Phase 3): divarasib vs sotorasib or adagrasib in previously treated KRAS G12C‑positive advanced/metastatic NSCLC. (NCT06936644 chunk 1) - NCT05074810 (Phase 1/2): avutometinib (VS‑6766) + sotorasib with/without defactinib; includes KRAS G12C inhibitor‑naïve and previously exposed cohorts. (NCT05074810 chunk 1) - NCT06936644 (Phase 2, 1L): fulzerasib (IBI351) + ivonescimab (AK‑112) for first‑line advanced/metastatic KRAS G12C NSCLC. (NCT06936644 chunk 1) - NCT07198841 (Phase 2, 1L): IBI351 + cetuximab β in untreated advanced/metastatic KRAS G12C NSCLC. (NCT07198841 chunk 1) - NCT05504278 (Phase Ib/III, 1L): IBI351 monotherapy and combinations (with sintilimab; with pemetrexed/platinum; with cetuximab) in advanced/metastatic KRAS G12C nonsquamous NSCLC. (NCT05504278 chunk 1) - NCT05840510 (KRYSTAL‑19, Phase 1/2): adagrasib + nab‑sirolimus (terminated; enrolled 6). (NCT05840510 chunk 1)

Suggested MAXO terms (treatment actions; suggestions)

13. Prevention

No KRAS G12C‑specific primary prevention interventions were identified in the retrieved evidence. Prevention aligns with lung cancer prevention more generally (e.g., smoking reduction) and with secondary prevention via screening in eligible high‑risk populations, but guideline details were not retrieved here.

14. Other Species / Natural Disease

Not addressed in the retrieved evidence.

15. Model Organisms / Model Systems

The retrieved evidence base in this run contains limited KRAS G12C‑specific model system detail (beyond resistance/combination preclinical studies). However: - A high‑impact preclinical study used KRAS G12C mutant lung cancer models to demonstrate benefit of SOS1 inhibitor + adagrasib and implicated MRAS/SHOC2 biology in resistance and combination response. (sreter2024resistancetokras pages 1-2)

General model types referenced across evidence include cell lines and xenograft models used in clinico‑genomic correlates and resistance studies. (negrao2025impactofcomutations pages 1-2, sreter2024resistancetokras pages 1-2)

Key statistics (2023–2024 anchored) and evidence table

The following table compiles the major quantitative benchmarks used in contemporary practice and research:

Table (click to expand)
Study (year, journal) Population/line Treatment Key efficacy Key safety notes URL / PMID if mentioned
CodeBreaK 200 (2023, The Lancet) Previously treated KRAS G12C-mutant advanced NSCLC; randomized phase 3; n=171 sotorasib, n=174 docetaxel Sotorasib 960 mg daily vs docetaxel 75 mg/m² ORR 28.1% vs 13.2%; median PFS 5.6 vs 4.5 mo; PFS HR 0.66 (95% CI 0.51–0.86; p=0.0017); 12-mo PFS 24.8% vs 10.1%; median OS 10.6 vs 11.3 mo; OS HR 1.01 (95% CI 0.77–1.33); DOR 8.6 vs 6.8 mo; time to response 1.4 vs 2.8 mo (langen2023sotorasibversusdocetaxel pages 8-10, higgins2025sotorasibforthe pages 3-4, langen2023sotorasibversusdocetaxel media 446eaaec) Grade ≥3 TRAEs 33% vs 40%; serious TRAEs 11% vs 23%; common grade ≥3 with sotorasib: diarrhea 12%, ALT increase 8%, AST increase 5%; fatal TRAEs: 1 (<1%) vs 2 (1%); hepatotoxicity risk higher when started soon after prior immunotherapy (langen2023sotorasibversusdocetaxel pages 8-10, higgins2025sotorasibforthe pages 3-4, speranza2025sexrelatedsafetysignals pages 9-11) https://doi.org/10.1016/S0140-6736(23)00221-0
CodeBreaK 100 long-term update (2023, Journal of Clinical Oncology) Pretreated KRAS G12C-mutant advanced NSCLC; phase I/II; n=174 Sotorasib 960 mg daily ORR 41% (95% CI 33.3–48.4); DCR 84%; median DOR 12.3 mo; median PFS 6.3 mo; median OS 12.5 mo; 2-year OS 33%; long-term clinical benefit (PFS ≥12 mo) in 23% (dy2023longtermoutcomesand pages 1-2, dy2023longtermoutcomesand pages 2-3) Any-grade TRAEs 70%; grade 3 20%, grade 4 1%, no grade 5 new-onset TRAEs in long-term follow-up; common AEs: diarrhea 30%, ALT increase 18%, AST increase 18%; among >1-year treated patients, few late-onset toxicities (dy2023longtermoutcomesand pages 1-2, dy2023longtermoutcomesand pages 2-3) https://doi.org/10.1200/JCO.22.02524
KRYSTAL-1 phase II (2025 review summarizing trial data) Advanced KRAS G12C-mutant NSCLC; previously treated Adagrasib ORR 43% (48/112); median DOR 8.5 mo (95% CI 6.2–13.8); median PFS 6.5 mo; median OS 12.6 mo; intracranial ORR 42% (95% CI 20.3–66.5) (mina2025emergingtargetedtherapies pages 2-4) Signature AEs included nausea, diarrhea, fatigue, musculoskeletal pain, hepatotoxicity, renal impairment; separate review notes high-grade toxicity burden but exact phase II grade ≥3 rate not provided in the evidence snippet used here (mina2025emergingtargetedtherapies pages 2-4) https://doi.org/10.3390/cancers17030353
Real-world sotorasib claims study (2024, Advances in Therapy) US claims-based cohort; KRAS G12C-mutant NSCLC receiving sotorasib; 2L+ subset n=140 Sotorasib in routine practice Mean adherence (PDC) 94.9%; median treatment duration 4.3 mo; among those with subsequent treatment (n=31), median time to next treatment 6.8 mo; mean monthly costs US$23,063 during treatment vs US$25,541 pre-index (sultan2024realworldevaluationof pages 1-2) Resource utilization during treatment: mean 3.87 outpatient, 0.09 inpatient, 0.11 emergency visits/month; this study did not report trial-style grade ≥3 TRAEs (sultan2024realworldevaluationof pages 1-2) https://doi.org/10.1007/s12325-024-03020-7

Table: This table compacts the main quantitative clinical evidence for KRAS G12C-mutant NSCLC across pivotal sotorasib and adagrasib studies plus an early real-world sotorasib analysis. It highlights efficacy benchmarks, comparative outcomes, and the most clinically relevant safety signals for rapid reference.

Expert analysis (synthesis grounded in retrieved authoritative sources)

  1. Clinical benefit is real but modest in randomized evidence: CodeBreaK 200 demonstrates statistically significant PFS and ORR improvements versus docetaxel but no OS benefit, likely influenced by subsequent KRAS G12C inhibitor exposure and crossover. (langen2023sotorasibversusdocetaxel pages 8-10, langen2023sotorasibversusdocetaxel pages 37-39)
  2. Durable benefit occurs in a subset: Long‑term CodeBreaK 100 follow‑up shows a clinically meaningful tail with a 2‑year OS rate of 33% and 23% achieving PFS ≥12 months, supporting continued use while optimizing patient selection. (dy2023longtermoutcomesand pages 2-3)
  3. Co‑mutations are central to precision medicine for this subtype: KEAP1/STK11/NRF2 status stratifies outcomes with adagrasib and provides a rational basis for intensified or alternative strategies. (negrao2025impactofcomutations pages 1-2)
  4. Implementation requires robust molecular testing infrastructure: Real‑world testing gaps (e.g., community NGS rates and regional reimbursement variability) and the potential role of rapid assays highlight that access to genotyping is a rate‑limiting step for equitable delivery of KRAS G12C targeted therapy. (alharbi2024codebreak200study pages 2-4, o’leary2023targetedtherapiesfor pages 4-5)

Visual evidence from pivotal trial publication

Cropped figures/tables from the CodeBreaK 200 Lancet trial show the key efficacy summaries (PFS HR/medians; OS; ORR) and are consistent with the numeric endpoints cited above. (langen2023sotorasibversusdocetaxel media 446eaaec, langen2023sotorasibversusdocetaxel media 3169850c, langen2023sotorasibversusdocetaxel media 9b269017, langen2023sotorasibversusdocetaxel media f94b5c79)

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  16. (NCT06936644 chunk 1): Zhong Runbo. A Multicenter, Single-arm Phase II Study to Evaluate the Efficacy and Safety of Fulzerasib (IBI351) in Combination With Ivonescimab (AK-112) in First-line Treatment of Advanced or Metastatic Non-small Cell Lung Cancer Patients With KRAS G12C Mutation. Shanghai Chest Hospital. 2025. ClinicalTrials.gov Identifier: NCT06936644

  17. (NCT05074810 chunk 1): Phase 1/2 Study of Avutometinib (VS-6766) + Sotorasib With or Without Defactinib in KRAS G12C NSCLC Patients. Verastem, Inc.. 2022. ClinicalTrials.gov Identifier: NCT05074810

  18. (NCT07198841 chunk 1): IBI351 Plus Cetuximab β in Untreated Advanced Non-small Cell Lung Cancer With KRAS G12C Mutation. Guangdong Association of Clinical Trials. 2025. ClinicalTrials.gov Identifier: NCT07198841

  19. (NCT05504278 chunk 1): Efficacy and Safety of IBI351 in Combination With Chemotherapy in Advanced Non-squamous Non-small Cell Lung Cancer Subjects With KRAS G12C Mutation. Innovent Biologics (Suzhou) Co. Ltd.. 2022. ClinicalTrials.gov Identifier: NCT05504278

  20. (NCT05840510 chunk 1): Adagrasib in Combination With Nab-Sirolimus in Patients With Advanced Solid Tumors and Non-Small Cell Lung Cancer With a KRAS G12C Mutation (KRYSTAL -19). Mirati Therapeutics Inc.. 2023. ClinicalTrials.gov Identifier: NCT05840510

  21. (langen2023sotorasibversusdocetaxel media 446eaaec): Adrianus Johannes de Langen, Melissa L Johnson, Julien Mazieres, Anne-Marie C Dingemans, Giannis Mountzios, Miklos Pless, Jürgen Wolf, Martin Schuler, Hervé Lena, Ferdinandos Skoulidis, Yasuto Yoneshima, Sang-We Kim, Helena Linardou, Silvia Novello, Anthonie J van der Wekken, Yuanbin Chen, Solange Peters, Enriqueta Felip, Benjamin J Solomon, Suresh S. Ramalingam, Christophe Dooms, Colin R Lindsay, Carlos Gil Ferreira, Normand Blais, Cynthia C Obiozor, Yang Wang, Bhakti Mehta, Tracy Varrieur, Gataree Ngarmchamnanrith, Björn Stollenwerk, David Waterhouse, and Luis Paz-Ares. Sotorasib versus docetaxel for previously treated non-small-cell lung cancer with krasg12c mutation: a randomised, open-label, phase 3 trial. The Lancet, 401:733-746, Mar 2023. URL: https://doi.org/10.1016/s0140-6736(23)00221-0, doi:10.1016/s0140-6736(23)00221-0. This article has 650 citations and is from a highest quality peer-reviewed journal.

  22. (dy2023longtermoutcomesand pages 1-2): Grace K. Dy, Ramaswamy Govindan, Vamsidhar Velcheti, Gerald S. Falchook, Antoine Italiano, Jürgen Wolf, Adrian G. Sacher, Toshiaki Takahashi, Suresh S. Ramalingam, Christophe Dooms, Dong-Wan Kim, Alfredo Addeo, Jayesh Desai, Martin Schuler, Pascale Tomasini, David S. Hong, Piro Lito, Qui Tran, Simon Jones, Abraham Anderson, Antreas Hindoyan, Wendy Snyder, Ferdinandos Skoulidis, and Bob T. Li. Long-term outcomes and molecular correlates of sotorasib efficacy in patients with pretreated kras g12c-mutated non–small-cell lung cancer: 2-year analysis of codebreak 100. Journal of Clinical Oncology, 41:3311-3317, Jun 2023. URL: https://doi.org/10.1200/jco.22.02524, doi:10.1200/jco.22.02524. This article has 175 citations and is from a highest quality peer-reviewed journal.

  23. (langen2023sotorasibversusdocetaxel pages 37-39): Adrianus Johannes de Langen, Melissa L Johnson, Julien Mazieres, Anne-Marie C Dingemans, Giannis Mountzios, Miklos Pless, Jürgen Wolf, Martin Schuler, Hervé Lena, Ferdinandos Skoulidis, Yasuto Yoneshima, Sang-We Kim, Helena Linardou, Silvia Novello, Anthonie J van der Wekken, Yuanbin Chen, Solange Peters, Enriqueta Felip, Benjamin J Solomon, Suresh S. Ramalingam, Christophe Dooms, Colin R Lindsay, Carlos Gil Ferreira, Normand Blais, Cynthia C Obiozor, Yang Wang, Bhakti Mehta, Tracy Varrieur, Gataree Ngarmchamnanrith, Björn Stollenwerk, David Waterhouse, and Luis Paz-Ares. Sotorasib versus docetaxel for previously treated non-small-cell lung cancer with krasg12c mutation: a randomised, open-label, phase 3 trial. The Lancet, 401:733-746, Mar 2023. URL: https://doi.org/10.1016/s0140-6736(23)00221-0, doi:10.1016/s0140-6736(23)00221-0. This article has 650 citations and is from a highest quality peer-reviewed journal.

  24. (langen2023sotorasibversusdocetaxel media 3169850c): Adrianus Johannes de Langen, Melissa L Johnson, Julien Mazieres, Anne-Marie C Dingemans, Giannis Mountzios, Miklos Pless, Jürgen Wolf, Martin Schuler, Hervé Lena, Ferdinandos Skoulidis, Yasuto Yoneshima, Sang-We Kim, Helena Linardou, Silvia Novello, Anthonie J van der Wekken, Yuanbin Chen, Solange Peters, Enriqueta Felip, Benjamin J Solomon, Suresh S. Ramalingam, Christophe Dooms, Colin R Lindsay, Carlos Gil Ferreira, Normand Blais, Cynthia C Obiozor, Yang Wang, Bhakti Mehta, Tracy Varrieur, Gataree Ngarmchamnanrith, Björn Stollenwerk, David Waterhouse, and Luis Paz-Ares. Sotorasib versus docetaxel for previously treated non-small-cell lung cancer with krasg12c mutation: a randomised, open-label, phase 3 trial. The Lancet, 401:733-746, Mar 2023. URL: https://doi.org/10.1016/s0140-6736(23)00221-0, doi:10.1016/s0140-6736(23)00221-0. This article has 650 citations and is from a highest quality peer-reviewed journal.

  25. (langen2023sotorasibversusdocetaxel media 9b269017): Adrianus Johannes de Langen, Melissa L Johnson, Julien Mazieres, Anne-Marie C Dingemans, Giannis Mountzios, Miklos Pless, Jürgen Wolf, Martin Schuler, Hervé Lena, Ferdinandos Skoulidis, Yasuto Yoneshima, Sang-We Kim, Helena Linardou, Silvia Novello, Anthonie J van der Wekken, Yuanbin Chen, Solange Peters, Enriqueta Felip, Benjamin J Solomon, Suresh S. Ramalingam, Christophe Dooms, Colin R Lindsay, Carlos Gil Ferreira, Normand Blais, Cynthia C Obiozor, Yang Wang, Bhakti Mehta, Tracy Varrieur, Gataree Ngarmchamnanrith, Björn Stollenwerk, David Waterhouse, and Luis Paz-Ares. Sotorasib versus docetaxel for previously treated non-small-cell lung cancer with krasg12c mutation: a randomised, open-label, phase 3 trial. The Lancet, 401:733-746, Mar 2023. URL: https://doi.org/10.1016/s0140-6736(23)00221-0, doi:10.1016/s0140-6736(23)00221-0. This article has 650 citations and is from a highest quality peer-reviewed journal.

  26. (langen2023sotorasibversusdocetaxel media f94b5c79): Adrianus Johannes de Langen, Melissa L Johnson, Julien Mazieres, Anne-Marie C Dingemans, Giannis Mountzios, Miklos Pless, Jürgen Wolf, Martin Schuler, Hervé Lena, Ferdinandos Skoulidis, Yasuto Yoneshima, Sang-We Kim, Helena Linardou, Silvia Novello, Anthonie J van der Wekken, Yuanbin Chen, Solange Peters, Enriqueta Felip, Benjamin J Solomon, Suresh S. Ramalingam, Christophe Dooms, Colin R Lindsay, Carlos Gil Ferreira, Normand Blais, Cynthia C Obiozor, Yang Wang, Bhakti Mehta, Tracy Varrieur, Gataree Ngarmchamnanrith, Björn Stollenwerk, David Waterhouse, and Luis Paz-Ares. Sotorasib versus docetaxel for previously treated non-small-cell lung cancer with krasg12c mutation: a randomised, open-label, phase 3 trial. The Lancet, 401:733-746, Mar 2023. URL: https://doi.org/10.1016/s0140-6736(23)00221-0, doi:10.1016/s0140-6736(23)00221-0. This article has 650 citations and is from a highest quality peer-reviewed journal.