Sotorasib for Lung Cancers with KRAS p.G12C Mutation
Open accessAbstract
BACKGROUND: p.G12C-mutated advanced solid tumors in a phase 1 study, and particularly promising anticancer activity was observed in a subgroup of patients with non-small-cell lung cancer (NSCLC). METHODS: p.G12C-mutated advanced NSCLC previously treated with standard therapies. The primary end point was objective response (complete or partial response) according to independent central review. Key secondary end points included duration of response, disease control (defined as complete response, partial response, or stable disease), progression-free survival, overall survival, and safety. Exploratory biomarkers were evaluated for their association with response to sotorasib therapy. RESULTS: . CONCLUSIONS: p.G12C-mutated NSCLC. (Funded by Amgen and the National Institutes of Health; CodeBreaK100 ClinicalTrials.gov number, NCT03600883.).
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The sotorasib response rate in colorectal cancer is lower than that in NSCLC.
“The sotorasib response rate in colorectal cancer is lower than that in NSCLC (7).”
From Cetuximab Enhances the Efficacy of MRTX1133, a Novel KRAS<sup>G12D</sup>Inhibitor, in Colorectal Cancer Treatment (2023) · cites this paper as [7]
The Results > Efficacy section reports a 37.1% objective response rate to sotorasib in patients with NSCLC. Our copy does not report a colorectal cancer response rate or compare the two cancers, so it does not support the claimed difference. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn a preliminary analysis, the response rate of MRTX849 in NSCLC patients harboring mutations in both KRAS G12C and KEAP1 was reduced compared to the response rate in KRAS G12C, KEAP1 WT patients.
“Of note, in a preliminary analysis, the response rate of MRTX849 in NSCLC patients harboring mutations in both KRAS G12C and KEAP1 was reduced compared to the response rate in KRAS G12C , KEAP1 WT patients [13, 14].”
From Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor (2022) · cites this paper as [14]
The Discussion (page not provided) reports a lower response percentage in KEAP1-mutated than KEAP1-wild-type tumors, but this exploratory finding concerns sotorasib, not MRTX849. The paper therefore does not support the claim about response to MRTX849. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe clinical response data indicate rapid development of acquired resistance to KRAS G12C inhibitors.
“These results indicate the rapid development of acquired resistance to KRAS G12C inhibitors [18, 26, 27, 49].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [26]
The Results (Efficacy; page not provided) report a median progression-free survival of 6.8 months and a median response duration of 11.1 months with sotorasib. The Discussion suggests tumors may adapt quickly, but treats this as a possible explanation and says mechanisms of adaptation or resistance require further investigation. The paper does not establish that the observed progression was rapid acquired resistance, or extend that finding to KRAS G12C inhibitors generally. (LLM, conf=0.84)
Experimental — accuracy not yet measuredKRAS G12C inhibition produces substantially different outcomes in NSCLC and CRC, largely due to lineage-specific feedback regulation.
“For example, KRAS G12C inhibition produces substantially different outcomes in NSCLC and CRC, largely due to lineage-specific feedback regulation [23,26,27,28,32].”
From Precision Targeting of KRAS-Mutant Cancers: Beyond G12C Toward G12D and Pan-RAS Therapeutic Strategies (2026) · cites this paper as [23]
The Results (Efficacy; page unavailable) report an objective response to sotorasib in 37.1% of patients with KRAS p.G12C–mutated NSCLC. The Discussion (page unavailable) raises possible tumor adaptation, but the paper does not compare outcomes with CRC or attribute a difference to lineage-specific feedback regulation. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSotorasib and adagrasib were effective at halting the growth of G12C-mutant cancer cells in 2-dimensional, 3-dimensional, and xenograft models.
“Sotorasib and adagrasib, two prominent members of this class, were effective at halting the growth of G12C-mutant cancer cells in 2-dimensional, 3-dimensional, and xenograft models, clearing the path for clinical trials [48,49,50,51].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [49]
The Discussion reports tumor shrinkage and disease control with sotorasib in patients with KRAS p.G12C–mutated lung cancer. It does not report results for adagrasib or for either drug in 2-dimensional, 3-dimensional, or xenograft models; the evidence here is from a clinical trial, not the preclinical models claimed. (LLM, conf=0.81)
Experimental — accuracy not yet measured
Inactive-state KRASG12C inhibitors adagrasib and sotorasib achieve anti-tumor response rates of 37-43% in NSCLC patients, with most patients experiencing disease progression 6-12 months after starting therapy.
“In clinical trials, the inactive-state KRASG12C mutant-specific inhibitors adagrasib (MRTX849) and sotorasib (AMG510) achieved 37–43% anti-tumor response rates in NSCLC patients with most experiencing disease progression 6–12 months after initiation of therapy7–9.”
From Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer (2024) · cites this paper as [7]
The Results > Efficacy and Discussion passages (page numbers unavailable) report a 37.1% objective response rate and 6.8-month median progression-free survival for sotorasib in previously treated KRAS p.G12C–mutated NSCLC. The paper also describes sotorasib as targeting inactive KRASG12C, but it does not establish the claimed 43% response rate or progression timing for adagrasib. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSTK11/LKB1 loss and KEAP1 mutations may contribute to lack of response to different therapies including anti-PD-(L)1 immune checkpoint inhibitors and KRASG12C inhibitors.
“STK11/LKB1 loss and KEAP1 mutations may contribute to lack of response to different therapies including anti-PD-(L)1 immune checkpoint inhibitors9,10 and KRASG12C inhibitors3,4.”
From LKB1 regulates JNK-dependent stress signaling and apoptotic dependency of KRAS-mutant lung cancers (2025) · cites this paper as [4]
The citation is attached to the claim about KRAS G12C inhibitors. In Results > Exploratory Biomarkers and the Discussion, patients with KEAP1-mutated tumors had a lower response percentage to sotorasib than those with wild-type KEAP1, which is consistent with a possible contribution to lack of response. The paper does not show the same pattern for STK11: responses occurred in that subgroup, and the STK11-mutated, KEAP1-wild-type subgroup had a numerically higher response rate. The authors caution that these exploratory comparisons were not statistically powered. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAll patients with KRASG12C-driven NSCLC eventually developed therapeutic resistance to AMG510, limiting long-term survival.
“but all patients eventually developed therapeutic resistance, limiting long-term survival.19”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [19]
Results > Patients (page not available) reports disease progression in 83 of 126 patients, not all patients. Results > Efficacy reports that 16 responders remained on treatment without progression at the data cutoff and gives a median overall survival of 12.5 months. The paper does not establish that every patient eventually developed resistance or that resistance caused the survival outcome. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMany patients with KRAS G12C cancers did not respond to sotorasib and adagrasib.
“Clinical studies have shown that many patients with KRAS G12C cancers did not respond to sotorasib and adagrasib.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [26]
The Results > Efficacy section (page not provided) reports an objective response to sotorasib in 46 of 124 patients (37.1%), so many did not have an objective response. The trial studied previously treated patients with KRAS p.G12C–mutated NSCLC, not all KRAS G12C cancers, and the cited passages provide no finding about adagrasib. Lack of an objective response also does not necessarily mean lack of disease control. (LLM, conf=0.90)
Experimental — accuracy not yet measuredEven in NSCLC patients, the response to KRAS G12C inhibitors was often short-lived, with a DOR of 10.9-11.1 months and PFS of 6.3-6.8 months for sotorasib, and a DOR of 8.5 months and PFS of 6.5 months for adagrasib.
“Even in NSCLC patients, the response to KRAS G12C inhibitors was often short-lived, with a DOR of 10.9–11.1 months and PFS of 6.3–6.8 months for sotorasib, and a DOR of 8.5 months and PFS of 6.5 months for adagrasib (Table 1).”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [26]
The Results > Efficacy section reports a median duration of response of 11.1 months and median progression-free survival of 6.8 months for sotorasib in previously treated NSCLC. It does not provide the other ends of the sotorasib ranges (10.9 and 6.3 months) or the adagrasib figures; the Discussion describes the sotorasib benefit as durable rather than short-lived. No page numbers are available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredColorectal cancer has a markedly lower response rate to KRAS G12C inhibitors compared to non-small cell lung cancer.
“Colorectal cancer, in particular, has a markedly lower response rate to KRAS G12C inhibitors compared to non-small cell lung cancer.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [26]
The Results > Efficacy section reports a 37.1% objective response rate to sotorasib in patients with non-small-cell lung cancer. Our copy does not report a colorectal cancer response rate or compare the two cancers (searched: colorectal cancer, colorectal), so it does not support the claimed difference. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe therapeutic response to KRAS G12C inhibition was short-lived, with quick emergence of acquired resistance.
“Furthermore, the therapeutic response to KRAS G12C inhibition was short-lived, with quick emergence of acquired resistance.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [26]
The Results > Efficacy section reports a median progression-free survival of 6.8 months, but a median response duration of 11.1 months among responders. The Discussion suggests tumors may adapt quickly to KRAS G12C inhibition, while saying that mechanisms of adaptation or resistance require further investigation. The paper therefore supports limited durability and possible adaptation, but not the claim that acquired resistance was shown to emerge quickly. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSotorasib demonstrates satisfactory efficacy in patients with non-small cell lung cancer, with a satisfactory response rate.
“Clinical studies have revealed that sotorasib demonstrates satisfactory efficacy in patients with non–small cell lung cancer, with a satisfactory response rate [12, 13].”
From Feedback activation of EGFR/wild-type RAS signaling axis limits KRASG12D inhibitor efficacy in KRASG12D-mutated colorectal cancer (2023) · cites this paper as [12]
The Results (Efficacy) report a 37.1% objective response rate, and the Discussion describes clinical efficacy. However, the trial studied previously treated patients with advanced, KRAS p.G12C–mutated NSCLC; the claim does not state those limits and could imply efficacy across NSCLC generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPatients with KRASG12C-mutated non-small cell lung cancer achieved a durable clinical benefit from sotorasib, whereas patients with CRC bearing the same mutation responded less to the same treatment.
“For example, patients with KRASG12C-mutated non–small cell lung cancer achieved a durable clinical benefit from sotorasib, the first approved KRASG12C mutant-selective inhibitor, whereas patients with CRC bearing the same mutation responded less to the same treatment [12].”
From Feedback activation of EGFR/wild-type RAS signaling axis limits KRASG12D inhibitor efficacy in KRASG12D-mutated colorectal cancer (2023) · cites this paper as [12]
The Discussion (page not available) states that sotorasib produced rapid and durable clinical benefit in patients with KRAS p.G12C–mutated NSCLC. This paper reports the NSCLC phase 2 trial, but our copy does not report a colorectal cancer response rate or compare it with the NSCLC response (searched: colorectal, CRC). It also does not establish that sotorasib was the first approved KRASG12C-selective inhibitor. (LLM, conf=0.89)
Experimental — accuracy not yet measuredSotorasib produced an objective response rate of 37.1% and median progression-free survival of 6.8 months in NSCLC and a response rate of 7.1% in colorectal cancer.
“Sotorasib was associated with an objective response rate of 37.1% and a median progression-free survival of 6.8 months among patients with NSCLC14 and a response rate of 7.1% among those with colorectal cancer.10”
From Acquired Resistance to KRAS <sup>G12C</sup> Inhibition in Cancer (2021) · cites this paper as [14]
The overall response rate of inactive-state KRASG12C inhibitors sotorasib and adagrasib in patients with KRASG12C mutant NSCLC is 37-43%.
“The overall response rate of inactive-state KRASG12C inhibitors sotorasib and adagrasib in patients with KRASG12C mutant NSCLC is 37-43%, a major advance albeit with significant room for improvement7,8.”
From Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer (2024) · cites this paper as [7]
AMG510 treatment in patients with KRASG12C-driven NSCLC achieved a response rate of over 30%.
“For instance, AMG510 treatment in patients with KRASG12C-driven NSCLC achieved a response rate of over 30%,18,19”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [19]
In patients with non-small cell lung cancer, divarasib had a numerically higher ORR (56.4%) than sotorasib (37% in a phase 2 trial and 28% in a phase 3 trial) and adagrasib (43% in a phase 2 trial).
“This is further supported by a numerically higher ORR seen with divarasib in patients with non-small cell lung cancer (56.4%) compared with sotorasib (37% in a phase 2 trial and 28% in a phase 3 trial) and adagrasib (43% in a phase 2 trial)11,23–25.”
From Divarasib plus cetuximab in KRAS G12C-positive colorectal cancer: a phase 1b trial (2024) · cites this paper as [25]
For sotorasib, an overall response rate of 7.1-9.7% was observed in patients with advanced CRC, compared to 32.2-37.1% in those with advanced NSCLC.
“For sotorasib, an overall response rate (ORR) of 7.1–9.7% was observed in patients with advanced CRC, compared to 32.2–37.1% in those with advanced NSCLC (Table 1) [26, 46, 47].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [26]
Sotorasib, adagrasib, and divarasib monotherapies have demonstrated objective response rates ranging from 7.1% to 53.4% and median progression-free survival of 4.0-13.1 months.
“For example, sotorasib, adagrasib, and divarasib monotherapies have demonstrated objective response rates ranging from 7.1% to 53.4% and median progression-free survival of 4.0-13.1 months, 13-20”
From Anti-tumor efficacy of HRS-4642 and its potential combination with proteasome inhibition in KRAS G12D-mutant cancer (2024) · cites this paper as [13]
Some patients selected for these trials may have preexisting multidrug resistance, which could contribute to treatment failure.
“In addition, some patients selected for these trials may have preexisting multidrug resistance (9, 37, 74), which could contribute to treatment failure.”
From SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition (2024) · cites this paper as [9]
The Abstract Results say that most enrolled patients had previously received both platinum-based chemotherapy and PD-1 or PD-L1 inhibitors, but do not establish preexisting multidrug resistance. The Discussion considers tumor adaptation or resistance as a possible explanation for lower response; it does not say that resistance to multiple treatments was present before enrollment or contributed to treatment failure. Searches for preexisting multidrug resistance and resistance before sotorasib found no passage making that link. (LLM, conf=0.73)
Experimental — accuracy not yet measuredSotorasib strongly inhibits phosphorylation of ERK protein in KRASG12C cells, thereby suppressing cell proliferation.
“In addition, sotorasib has been shown to strongly inhibit phosphorylation of ERK protein in KRASG12C cells, thereby suppressing cell proliferation.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [53]
Sotorasib specifically and irreversibly inhibits KRASG12C by binding to GDP and locking KRAS in an inactive state.
“Sotorasib specifically and irreversibly inhibits KRASG12C by binding to GDP and locking KRAS in an inactive state.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [53]
The approval of Lumakras, an Amgen-developed drug, in May 2021 for treating NSCLC patients with KRASG12C mutations marks a significant milestone in KRAS-targeting drug discovery.
“The approval of Lumakras, an Amgen-developed drug, in May 2021 for treating NSCLC patients with KRASG12C mutations marks a significant milestone in KRAS-targeting drug discovery.53”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [53]
Some preclinical and clinical studies have reported that drugs such as sotorasib, dasatinib and metformin could reverse resistance induced by RAS.
“Some preclinical and clinical studies have reported that some drugs could reverse resistance induced by RAS, such as sotorasib, dasatinib and metformin [155,156,157].”
From Drug Resistance in Colorectal Cancer: From Mechanism to Clinic (2022) · cites this paper as [157]
The incidence of gastrointestinal adverse effects was generally lower in garsorasib (diarrhea 11.5%, nausea 7.7%, no vomiting) compared with other KRAS G12C inhibitors (diarrhea 31.7-69%, nausea 19-78%, vomiting 7.9-58%).
“In terms of gastrointestinal adverse effects frequently observed in other KRAS G12C inhibitors, 11,12,28 the incidence was generally lower in garsorasib (diarrhea at 11.5%, nausea at 7.7%, and no vomiting reported), compared to those reported of other KRAS G12C inhibitors (diarrhea at 31.7-69%, nausea at 19-78%, and vomiting at 7.9-58%).”
Sotorasib and adagrasib showed antitumor activity against KRASG12C-mutated tumors in early-phase clinical trials, leading to accelerated approval of sotorasib by the FDA in May 2021 and conditional marketing authorization by the European Commission in January 2022.
“Both also showed antitumor activity against KRASG12C-mutated tumors in early-phase clinical trials (20), leading to the accelerated approval of sotorasib by the FDA in May 2021 and conditional marketing authorization by the European Commission in January 2022.”
Single-agent JDQ443 demonstrated antitumor activity in both NSCLC and colorectal cancer PDX panels, with deeper responses in NSCLC than colorectal cancer.
“Single-agent JDQ443 demonstrated antitumor activity in both panels, with deeper responses in NSCLC than colorectal cancer (Fig. 4A vs. 4E; Supplementary Table S7), consistent with reported clinical findings for other single-agent KRASG12C inhibitors in these indications (20, 21, 25, 33).”
Some KRAS inhibitors have demonstrated efficacy in patients with KRASG12C-mutant cancers and have changed clinical practice.
“Some of these inhibitors have proven efficacy in patients with KRASG12C-mutant cancers and have become practice changing.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
Improved drug design has produced inhibitors selective for mutant KRAS in either its active or inactive state.
“improvements in drug design have culminated in the development of inhibitors that are selective for mutant KRAS in its active or inactive state.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
In the phase II portion of CodeBreaK 100, 124 evaluable patients with previously treated advanced KRASG12C-mutant NSCLC had an ORR of 37.1%, median DoR of 11.1 months, median PFS of 6.8 months and median OS of 12.5 months; these results led to the 2021 FDA accelerated approval of sotorasib.
“The phase II portion of CodeBreaK 100, which involved 124 evaluable patients with previously treated advanced-stage KRASG12C-mutant NSCLC, demonstrated an ORR of 37.1%, a median duration of response (DoR) of 11.1 months, median PFS of 6.8 months and median OS of 12.5 months67. These impressive results led to the 2021 FDA accelerated approval of sotorasib for this indication.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
Data on KRASG12C inhibitors show that these agents are far from curative.
“However, the data on KRASG12C inhibitors, which have advanced the furthest in development and are entering clinical practice, emphasize that these agents are far from curative67.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
Disease progression occurs in many patients treated with KRASG12Ci, and resistance is recapitulated in preclinical studies.
“Despite this success, disease progression occurs in many patients4,5,7, with development of resistance to KRASG12Ci recapitulated in preclinical studies9–11.”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [7]
Cancers lose sensitivity to KRASG12Ci and re-establish RAS-MAPK signaling through multiple mechanisms, including increased activation of mutant or WT RAS and/or gain of upstream/downstream bypass events.
“Preclinical and clinical studies, however, have demonstrated that cancers lose sensitivity to KRASG12Ci and re-establish RAS-MAPK signaling through multiple mechanisms, including increased activation of mutant or wild-type (WT) RAS and/or gain of upstream/downstream bypass events1,7,9,10,13,14.”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [7]
In advanced KRASG12C-mutant NSCLC, sotorasib and adagrasib have objective response rates of 37% and 45%, and disease control rates of 81% and 96%, respectively.
“sotorasib (AMG 510) and adagrasib (MRTX849) have demonstrated robust efficacy with objective response rates of 37% and 45%, and disease control rates of 81% and 96%, respectively (20, 23–25).”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [24]
Exploratory analyses from KRYSTAL-1 and CodeBreaK 100 suggest higher response rates for adagrasib (64% vs 45%) and sotorasib (50% vs 39%) in patients with STK11 co-mutation versus entire cohort.
“Exploratory correlative analyses from the KRYSTAL-1 and CodeBreaK 100 trials in this context suggest higher response rates for single agent adagrasib (64% vs 45%) and sotorasib (50% vs 39%) among patients whose tumors harbored an STK11 co-mutation, versus the entire treatment cohort (24, 25).”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [24]
All patients who achieved an objective response to sotorasib in a Phase II study ultimately progressed on treatment.
“While KRASG12C inhibitors deliver clinical benefit, all patients who achieved an objective response ultimately progressed on treatment with sotorasib in a Phase II study (24).”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [24]
The median overall survival of 12.5 months compares favorably to the historical benchmark of 10.5 months for docetaxel combined with ramucirumab in the REVEL study.
“The median overall survival was estimated at 12.5 months, which compares favorably to historical benchmarks in this disease setting (i.e. docetaxel combined with ramucirumab had 10.5 months overall survival in the REVEL study)32.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the updated analysis of the 126-patient Phase II NSCLC cohort, the overall response rate remained at 37.1% although one of the partial responses converted to a complete response.
“In the updated analysis, the overall response rate remained at 37.1% although one of the partial responses converted to a complete response.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
The updated analysis provided the first report of overall survival for NSCLC patients treated with a selective KRAS G12C inhibitor.
“The updated analysis provided the first report of overall survival for NSCLC patients treated with a selective KRAS G12C inhibitor.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
The median overall survival was estimated at 12.5 months.
“The median overall survival was estimated at 12.5 months, which compares favorably to historical benchmarks in this disease setting (i.e. docetaxel combined with ramucirumab had 10.5 months overall survival in the REVEL study)32.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the Phase II NSCLC cohort from CodeBreaK 100, patients appear to derive benefit after PD1/PD-L1 checkpoint inhibition, including when the checkpoint inhibitor was applied within 3 months of sotorasib initiation.
“Per recent subgroup analyses of the Phase II NSCLC cohort from CodeBreaK 100, patients appear to derive benefit after PD1/PD-L1 checkpoint inhibition, including the application of the checkpoint inhibitor within 3 months of sotorasib initiation31.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In CodeBreaK 100, 115 of 126 patients received prior PD-1/PD-L1 checkpoint inhibition.
“The vast majority of patients (115 of 126) received prior PD-1/PD-L1 checkpoint inhibition and the response rate was 36.3% (vs. 37.1% in the overall population) and median overall survival was 12.0 months (versus 12.5 months in the overall population).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In CodeBreaK 100, patients with checkpoint therapy within 3 months had an ORR of 34.4% and median OS of 11.7 months, compared to an ORR of 39.7% and not evaluable OS in patients with more than 3 months between checkpoint inhibition and sotorasib.
“Patients whom have had checkpoint therapy within 3 months had overall response of 34.4% and median overall survival of 11.7 months, compared to 39.7% and not evaluable in patients that had more than 3 months between checkpoint inhibition and sotorasib.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In CodeBreaK 100, the response rate was 36.3% in the prior checkpoint subgroup versus 37.1% in the overall population.
“The vast majority of patients (115 of 126) received prior PD-1/PD-L1 checkpoint inhibition and the response rate was 36.3% (vs. 37.1% in the overall population) and median overall survival was 12.0 months (versus 12.5 months in the overall population).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
Prior immune therapy does not meaningfully negatively impact the activity of sotorasib.
“These data may indicate that prior immune therapy does not meaningfully negatively impact the activity of sotorasib, suggesting a possible combination approach may be further explored given non-overlapping mechanisms of action.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In CodeBreaK 100, median overall survival was 12.0 months in the prior checkpoint subgroup versus 12.5 months in the overall population.
“The vast majority of patients (115 of 126) received prior PD-1/PD-L1 checkpoint inhibition and the response rate was 36.3% (vs. 37.1% in the overall population) and median overall survival was 12.0 months (versus 12.5 months in the overall population).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
Recent overall survival data for sotorasib is favorable, with an overall survival of 12.5 months including second and third line and beyond patients receiving benefit.
“Recent overall survival data has been favorable with an overall survival of 12.5 months including second and third line and beyond patients receiving benefit.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
Multiple intrinsic and acquired resistance mechanisms to G12C inhibitors are known, and drug combinations will likely be required to maximize their clinical efficacy in NSCLC and other diseases.
“Multiple mechanisms of intrinsic and acquired resistance (10,12,13), have been identified; hence, drug combinations will likely be needed to maximize the clinical efficacy of G12Cis (and probably other, emerging KRAS inhibitors) in NSCLC and other diseases.”
From Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy (2023) · cites this paper as [12]
In CodeBreaK100 phase II, median PFS was 6.8 months and median survival was 12.5 months.
“Median PFS was 6.8 months and median survival was 12.5 months (Table 2).”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [94]
In CodeBreaK100 phase II, sotorasib 960 mg once daily in KRAS G12C NSCLC cohort of 126 patients produced response rate 37.1% and disease control 80.6% with median follow-up 15.3 months.
“The NSCLC cohort included 126 patients, 81% of whom had received prior platinum-based chemotherapy and PD(L)1 inhibitor therapy. With a median follow-up of 15.3 months, the response rate was 37.1%; 80.6% of patients achieved disease control.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [94]
In CodeBreak100 phase II, ORR to sotorasib was 50% in STK11-mutated/KEAP1-wild-type, 23% when both KEAP1 and STK11 were mutated, and 14% when KEAP1 was mutated with wild-type STK11.
“While ORR was 50% in those with mutated STK11 and wild-type KEAP1, it was only 23% when both KEAP1 and STK11 were mutated and 14% when KEAP1 was mutated with wild-type STK11 (Table 3).”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [94]
Drugs against KRAS mutations in codons 12, 13 and 61 remain to be developed.
“Nevertheless, drugs again other KRAS mutations in codons 12, 13 and 61 still remain to be developed [87].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [87]
Sotorasib was the first selective KRAS(G12C) inhibitor to enter clinical trials in 2018 and was FDA-approved in May 2021 for KRASG12C-mutated NSCLC.
“Sotorasib (AMG-510) (Table 1) was the first selective KRAS(G12C) inhibitor to enter clinical trials in 2018 and was developed by Amgen, building on discoveries from a partnership with Carmot Therapeutics in which a custom library of small molecules that covalently bind cysteine were screened against KRAS(G12C)93.”
From Advances in covalent drug discovery (2022) · cites this paper as [95]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
PD-1 and PD-L1 Immune Checkpoint Blockade to Treat Breast Cancer
Hartkopf, A. D., Taran, F., Wallwiener, M., Walter, C. B., Krämer, B., Grischke, E., & Brucker, S. Y. (2016) · Breast Care · doi:10.1159/000453569 · Cited by 30,989 · see citing works
Siegel, R. L., Miller, K. D., Fuchs, H. E., & Jemal, A. (2021) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.21654 · Cited by 16,522 · see citing works
Adverse Renal Effects of Immune Checkpoint Inhibitors: A Narrative Review
Wanchoo, R., Karam, S., Uppal, N. N., Barta, V. S., Deray, G., Devoe, C., Launay‐Vacher, V., Jhaveri, K. D., & on behalf of Cancer and Kidney International Network Workgroup on Immune Checkpoint Inhibitors (2017) · American Journal of Nephrology · doi:10.1159/000455014 · Cited by 15,314 · see citing works
Nivolumab versus docetaxel in advanced nonsquamous non-small-cell lung cancer
Borghaei, H., Paz-Ares, L., Horn, L., Spigel, D. R., Steins, M., Ready, N. E., Chow, L. Q., Vokes, E. E., Felip, E., Holgado, E., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1507643 · Cited by 9,335 · see citing works
Self-citationPembrolizumab plus chemotherapy in metastatic non–small-cell lung cancer
Gandhi, L., Rodríguez-Abreu, D., Gadgeel, S., Esteban, E., Felip, E., De Angelis, F., Domine, M., Clingan, P., Hochmair, M. J., Powell, S. F., et al. (2018) · New England Journal of Medicine · doi:10.1056/nejmoa1801005 · Cited by 6,607 · see citing works
Herbst, R. S., Baas, P., Kim, D.-W., Felip, E., Pérez-Gracia, J. L., Han, J.-Y., Molina, J., Kim, J.-H., Arvis, C. D., Ahn, M.-J., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(15)01281-7 · Cited by 6,449 · see citing works
Rittmeyer, A., Barlési, F., Waterkamp, D., Park, K., Ciardiello, F., von Pawel, J., Gadgeel, S. M., Hida, T., Kowalski, D. M., Cobo, M., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(16)32517-x · Cited by 4,684 · see citing works
Mok, T. S. K., Wu, Y.-L. L. C., Kudaba, I., Kowalski, D. M., Cho, B. C., Turna, H. Z., de Castro, G., Srimuninnimit, V., Лактионов, К. К., Bondarenko, I., et al. (2019) · The Lancet · doi:10.1016/s0140-6736(18)32409-7 · Cited by 3,319 · see citing works
K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
Ostrem, J. M., Peters, U., Sos, M. L., Wells, J. A., & Shokat, K. M. (2013) · Nature · doi:10.1038/nature12796 · Cited by 2,557 · see citing works
First-Line Nivolumab in Stage IV or Recurrent Non–Small-Cell Lung Cancer
Carbone, D. P., Reck, M., Paz-Ares, L., Creelan, B., Horn, L., Steins, M., Felip, E., van den Heuvel, M. M., Ciuleanu, T.-E., Badin, F., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1613493 · Cited by 2,503 · see citing works
Self-citationHanna, N., Shepherd, F. A., Fossella, F. V., Pereira, J. R., De Marinis, F., von Pawel, J., Gatzemeier, U., Tsao, T. C. Y., Pless, M., Muller, T., et al. (2004) · Journal of Clinical Oncology · doi:10.1200/jco.2004.08.163 · Cited by 2,426 · see citing works
The Clinical KRAS(G12C) Inhibitor AMG 510 Drives Anti-Tumour Immunity
Canon, J., Rex, K., Saiki, A. Y., Mohr, C., Cooke, K., Bagal, D., Gaida, K., Holt, T., Knutson, C. G., Koppada, N., et al. (2019) · Nature · doi:10.1038/s41586-019-1694-1 · Cited by 2,277 · see citing works
Self-citationShepherd, F. A., Dancey, J. E., Ramlau, R., Mattson, K. V., Gralla, R. J., O’Rourke, M. A., Levitan, N. I., Gressot, L., Vincent, M. D., Burkes, R. L., et al. (2000) · Journal of Clinical Oncology · doi:10.1200/jco.2000.18.10.2095 · Cited by 2,178 · see citing works
Drugging the undruggable RAS: Mission Possible?
Cox, A. D., Fesik, S. W., Kimmelman, A. C., Luo, J., & Der, C. J. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4389 · Cited by 1,997 · see citing works
KRAS <sup>G12C</sup> Inhibition with Sotorasib in Advanced Solid Tumors
Hong, D. S., Fakih, M. G., Strickler, J. H., Desai, J., Durm, G. A., Shapiro, G. I., Falchook, G. S., Price, T. J., Sacher, A., Denlinger, C. S., et al. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa1917239 · Cited by 1,733 · see citing works
Self-citationThe Effect of Advances in Lung-Cancer Treatment on Population Mortality
Howlader, N., Forjaz, G., Mooradian, M. J., Meza, R., Kong, C. Y., Cronin, K. A., Mariotto, A. B., Lowy, D. R., & Feuer, E. J. (2020) · New England Journal of Medicine · doi:10.1056/nejmoa1916623 · Cited by 1,720 · see citing works
<i>STK11/LKB1</i> Mutations and PD-1 Inhibitor Resistance in <i>KRAS</i> -Mutant Lung Adenocarcinoma
Skoulidis, F., Goldberg, M. E., Greenawalt, D. M., Hellmann, M. D., Awad, M. M., Gainor, J. F., Schrock, A. B., Hartmaier, R. J., Trabucco, S. E., Gay, L., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-18-0099 · Cited by 1,641 · see citing works
Self-citationGaron, E. B., Ciuleanu, T.-E., Arrieta, O., Prabhash, K., Syrigos, K. N., Goksel, T., Park, K., Gorbunova, V., Kowalyszyn, R. D., Pikiel, J., et al. (2014) · The Lancet · doi:10.1016/s0140-6736(14)60845-x · Cited by 1,309 · see citing works
Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy
Skoulidis, F., & Heymach, J. V. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0179-8 · Cited by 1,019 · see citing works
Self-citationReck, M., Kaiser, R., Mellemgaard, A., Douillard, J.-Y., Orlov, S., Krzakowski, M., von Pawel, J., Gottfried, M., Bondarenko, I., Liao, M., et al. (2014) · The Lancet Oncology · doi:10.1016/s1470-2045(13)70586-2 · Cited by 951 · see citing works
Skoulidis, F., Byers, L. A., Diao, L., Papadimitrakopoulou, V. A., Tong, P., Izzo, J., Behrens, C., Kadara, H., Parra, E. R., Canales, J. R., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-14-1236 · Cited by 936 · see citing works
Self-citationSelective inhibition of oncogenic KRAS output with small molecules targeting the inactive state
Patricelli, M. P., Janes, M. R., Li, L.-S., Hansen, R., Peters, U., Kessler, L. V., Chen, Y., Kucharski, J. M., Feng, J., Ely, T., et al. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-1105 · Cited by 759 · see citing works
Allele-specific inhibitors inactivate mutant KRAS G12C by a trapping mechanism
Lito, P., Solomon, M., Li, L.-S., Hansen, R., & Rosen, N. (2016) · Science · doi:10.1126/science.aad6204 · Cited by 691 · see citing works
Direct small-molecule inhibitors of KRAS: from structural insights to mechanism-based design
Ostrem, J. M. L., & Shokat, K. M. (2016) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2016.139 · Cited by 641 · see citing works
Dogan, S., Shen, R., Ang, D. C., Johnson, M. L., D'Angelo, S. P., Paik, P. K., Brzostowski, E. B., Riely, G. J., Kris, M. G., Zakowski, M. F., et al. (2012) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-11-3265 · Cited by 639 · see citing works
Riely, G. J., Kris, M. G., Rosenbaum, D., Marks, J., Li, A., Chitale, D. A., Nafa, K., Riedel, E. R., Hsu, M., Pao, W., et al. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-0646 · Cited by 578 · see citing works
Rapid non-uniform adaptation to conformation-specific KRAS(G12C) inhibition
Xue, J. Y., Zhao, Y., Aronowitz, J., Mai, T. T., Vides, A., Qeriqi, B., Kim, D., Li, C., de Stanchina, E., Mazutis, L., et al. (2020) · Nature · doi:10.1038/s41586-019-1884-x · Cited by 543 · see citing works
Arbour, K. C., Jordan, E., Kim, H. R., Dienstag, J., Yu, H. A., Sanchez-Vega, F., Lito, P., Berger, M., Solit, D. B., Hellmann, M., et al. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-1841 · Cited by 466 · see citing works
Jänne, P. A., van den Heuvel, M. M., Barlesi, F., Cobo, M., Mazieres, J., Crinò, L., Orlov, S., Blackhall, F., Wolf, J., Garrido, P., et al. (2017) · JAMA · doi:10.1001/jama.2017.3438 · Cited by 335 · see citing works
Self-citationK-ras Mutation Subtypes in NSCLC and Associated Co-occuring Mutations in Other Oncogenic Pathways
Scheffler, M., Ihle, M. A., Hein, R., Merkelbach-Bruse, S., Scheel, A. H., Siemanowski, J., Brägelmann, J., Kron, A., Abedpour, N., Ueckeroth, F., et al. (2019) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2018.12.013 · Cited by 264 · see citing works
Self-citationFleur, L. L., Falk-Sörqvist, E., Smeds, P., Berglund, A., Sundström, M., Mattsson, J. S., Brandén, E., Koyi, H., Isaksson, J., Brunnström, H., et al. (2019) · Lung Cancer · doi:10.1016/j.lungcan.2019.01.003 · Cited by 202 · see citing works
NRF2 Activation Promotes Aggressive Lung Cancer and Associates with Poor Clinical Outcomes
Singh, A., Daemen, A., Nickles, D., Jeon, S., Foreman, O., Sudini, K. R., Gnad, F., Lajoie, S., Gour, N., Mitzner, W., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-1985 · Cited by 169 · see citing works
Boch, C., Kollmeier, J., Roth, A. J., Stephan-Falkenau, S., Misch, D., Grüning, W., Bauer, T. T., & Mairinger, T. (2013) · BMJ Open · doi:10.1136/bmjopen-2013-002560 · Cited by 151 · see citing works
Jeong, Y., Hellyer, J. A., Stehr, H., Hoang, N. T., Niu, X., Das, M. S., Padda, S. K., Ramchandran, K. J., Neal, J. W., Wakelee, H. A., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-1237 · Cited by 125 · see citing works
Biernacka, A., Tsongalis, P., Peterson, J. D., Abreu, F. B. D., Black, C. C., Gutmann, E. J., Liu, X., Tafe, L. J., Amos, C. I., & Tsongalis, G. J. (2016) · Cancer Genetics · doi:10.1016/j.cancergen.2016.03.001 · Cited by 121 · see citing works
Negrao, M. V., Lam, V. K. L., Reuben, A., Rubin, M. L., Landry, L. L., Roarty, E. B., Rinsurongkawong, W., Lewis, J., Roth, J. A., Swisher, S. G., et al. (2019) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2019.02.008 · Cited by 112 · see citing works
Pan-cancer analysis of KEAP1 mutations as biomarkers for immunotherapy outcomes
Chen, X., Su, C., Ren, S., Zhou, C., & Jiang, T. (2020) · Annals of Translational Medicine · doi:10.21037/atm.2019.11.52 · Cited by 65 · see citing works
NSCLC: An Update of Driver Mutations, Their Role in Pathogenesis and Clinical Significance.
Black, R. C., & Khurshid, H. (2015) · PubMed · Cited by 52 · see citing works
Pallis, A. G., Agelaki, S., Agelidou, A., Varthalitis, I., Syrigos, K., Kentepozidis, N., Pavlakou, G., Kotsakis, A., Kontopodis, E., & Georgoulias, V. (2010) · BMC Cancer · doi:10.1186/1471-2407-10-633 · Cited by 36 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Non–Small Cell Lung Cancer, Version 3.2022, NCCN Clinical Practice Guidelines in Oncology
Ettinger, D. S., Wood, D. E., Aisner, D. L., Akerley, W., Bauman, J. R., Bharat, A., Bruno, D. S., Chang, J. Y., Chirieac, L. R., D’Amico, T. A., et al. (2022) · Journal of the National Comprehensive Cancer Network · doi:10.6004/jnccn.2022.0025 · Cited by 1,405 · see citing works
Acquired Resistance to KRAS <sup>G12C</sup> Inhibition in Cancer
Awad, M. M., Liu, S., Rybkin, I. I., Arbour, K. C., Dilly, J., Zhu, V. W., Johnson, M. L., Heist, R. S., Patil, T., Riely, G. J., et al. (2021) · New England Journal of Medicine · doi:10.1056/nejmoa2105281 · Cited by 1,247 · see citing works
Exploring treatment options in cancer: tumor treatment strategies
Liu, B., Zhou, H., Tan, L., Siu, K. T. H., & Guan, X.-Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01856-7 · Cited by 1,201 · see citing works
Toward personalized treatment approaches for non-small-cell lung cancer
Wang, M., Herbst, R. S., & Boshoff, C. (2021) · Nature Medicine · doi:10.1038/s41591-021-01450-2 · Cited by 1,113 · see citing works
Adagrasib in Non–Small-Cell Lung Cancer Harboring a <i> KRAS <sup>G12C</sup> </i> Mutation
Jänne, P. A., Riely, G. J., Gadgeel, S. M., Heist, R. S., Ou, S.-H. I., Pacheco, J. M., Johnson, M. L., Sabari, J. K., Leventakos, K., Yau, E., et al. (2022) · New England Journal of Medicine · doi:10.1056/nejmoa2204619 · Cited by 1,061 · see citing works
Self-citationTargeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies
Bahar, M. E., Kim, H. J., & Kim, D. R. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01705-z · Cited by 888 · see citing works
Non–Small Cell Lung Cancer, Version 4.2024
Riely, G. J., Wood, D. E., Ettinger, D. S., Aisner, D. L., Akerley, W., Bauman, J. R., Bharat, A., Bruno, D. S., Chang, J. Y., Chirieac, L. R., et al. (2024) · Journal of the National Comprehensive Cancer Network · doi:10.6004/jnccn.2204.0023 · Cited by 897 · see citing works
Advances in covalent drug discovery
Boike, L., Henning, N. J., & Nomura, D. K. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00542-z · Cited by 823 · see citing works
Targeted Therapies for Lung Cancer Patients With Oncogenic Driver Molecular Alterations
Tan, A. C., & Tan, D. S. W. (2022) · Journal of Clinical Oncology · doi:10.1200/jco.21.01626 · Cited by 782 · see citing works
Pascual, J., Attard, G., Bidard, F.-C., Curigliano, G., De Mattos-Arruda, L., Diehn, M., Italiano, A., Lindberg, J., Merker, J. D., Montagut, C., et al. (2022) · Annals of Oncology · doi:10.1016/j.annonc.2022.05.520 · Cited by 783 · see citing works
Self-citationRingel, M. D., Sosa, J. A., Baloch, Z. W., Bischoff, L. A., Bloom, G., Brent, G. A., Brock, P. L., Chou, R., Flavell, R. R., Goldner, W. S., et al. (2025) · Thyroid · doi:10.1177/10507256251363120 · Cited by 833 · see citing works
Tumor biomarkers for diagnosis, prognosis and targeted therapy
Zhou, Y., Tao, L., Qiu, J., Xu, J., Yang, X., Zhang, Y., Tian, X., Guan, X., Cen, X., & Zhao, Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01823-2 · Cited by 772 · see citing works
Non‐small cell lung cancer in China
Chen, P., Liu, Y., Wen, Y., & Zhou, C. (2022) · 癌症：英文版 · doi:10.1002/cac2.12359 · Cited by 673 · see citing works
de Langen, A. J., Johnson, M. L., Mazieres, J., Dingemans, A.-M. C., Mountzios, G., Pless, M., Wolf, J., Schuler, M., Lena, H., Skoulidis, F., et al. (2023) · The Lancet · doi:10.1016/s0140-6736(23)00221-0 · Cited by 619 · see citing works
Self-citationHendriks, L. E. L., Remón, J., Finn, C. F., Garassino, M. C., Heymach, J. V., Kerr, K. M., Tan, D. S. W., Veronesi, G., & Reck, M. (2024) · Nature Reviews Disease Primers · doi:10.1038/s41572-024-00551-9 · Cited by 672 · see citing works
The current state of the art and future trends in RAS-targeted cancer therapies
Punekar, S. R., Velcheti, V., Neel, B. G., & Wong, K.-K. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00671-9 · Cited by 549 · see citing works
Self-citationPan-KRAS Inhibitor Disables Oncogenic Signalling and Tumour Growth
Kim, D., Herdeis, L., Rudolph, D., Zhao, Y., Böttcher, J., Vides, A., Ayala-Santos, C. I., Pourfarjam, Y., Cuevas-Navarro, A., Xue, J. Y., et al. (2023) · Nature · doi:10.1038/s41586-023-06123-3 · Cited by 534 · see citing works
Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor
Hallin, J., Bowcut, V., Calinisan, A., Briere, D. M., Hargis, L., Engstrom, L. D., Laguer, J., Medwid, J., Vanderpool, D., Lifset, E., et al. (2022) · Nature Medicine · doi:10.1038/s41591-022-02007-7 · Cited by 533 · see citing works
Sotorasib in <i>KRAS</i> p.G12C–Mutated Advanced Pancreatic Cancer
Strickler, J. H., Satake, H., George, T. J., Yaeger, R., Hollebecque, A., Garrido-Laguna, I., Schuler, M., Burns, T. F., Coveler, A. L., Falchook, G. S., et al. (2023) · New England Journal of Medicine · doi:10.1056/nejmoa2208470 · Cited by 527 · see citing works
Self-citationRational combinations of targeted cancer therapies: background, advances and challenges
Jin, H., Wang, L., & Bernards, R. (2023) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00615-z · Cited by 503 · see citing works
Advances and challenges in the treatment of lung cancer
Li, Y., Yan, B., & He, S. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115891 · Cited by 492 · see citing works
Sotorasib plus Panitumumab in Refractory Colorectal Cancer with Mutated <i>KRAS</i> G12C
Fakih, M. G., Salvatore, L., Esaki, T., Modest, D. P., Lopez-Bravo, D. P., Taieb, J., Karamouzis, M. V., Ruiz-Garcia, E., Kim, T.-W., Kuboki, Y., et al. (2023) · New England Journal of Medicine · doi:10.1056/nejmoa2308795 · Cited by 398 · see citing works
Self-citationRecent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials
Xie, X., Yu, T., Li, X., Zhang, N., Foster, L. J., Peng, C., Huang, W., & He, G. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01589-z · Cited by 396 · see citing works
Ricciuti, B., Arbour, K. C., Lin, J. J., Vajdi, A., Vokes, N., Hong, L., Zhang, J., Tolstorukov, M. Y., Li, Y. Y., Spurr, L. F., et al. (2022) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2021.10.013 · Cited by 394 · see citing works
Self-citationEfficacy of a small-molecule inhibitor of KrasG12D in immunocompetent models of pancreatic cancer
Kemp, S. B., Cheng, N., Markosyan, N., Sor, R., Kim, I.-K., Hallin, J., Shoush, J., Quinones, L., Brown, N. V., Bassett, J. B., et al. (2023) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-1066 · Cited by 370 · see citing works
Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy
Holderfield, M., Lee, B. J., Jiang, J., Tomlinson, A., Seamon, K. J., Mira, A., Patrucco, E., Goodhart, G., Dilly, J., Gindin, Y., et al. (2024) · Nature · doi:10.1038/s41586-024-07205-6 · Cited by 369 · see citing works
Singhal, A., Li, B. T., & O'Reilly, E. M. (2024) · Nature Medicine · doi:10.1038/s41591-024-02903-0 · Cited by 358 · see citing works
Self-citationTranslational and therapeutic evaluation of RAS-GTP inhibition by RMC-6236 in RAS-driven cancers
Jiang, J., Jiang, L., Maldonato, B. J., Wang, Y., Holderfield, M., Aronchik, I., Winters, I. P., Salman, Z., Blaj, C., Menard, M., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-24-0027 · Cited by 343 · see citing works
Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants
Hofmann, M. H., Gerlach, D., Misale, S., Petronczki, M., & Kraut, N. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-1331 · Cited by 336 · see citing works
Recent advances in non-small cell lung cancer targeted therapy; an update review
Araghi, M., Mannani, R., Maleki, A. H., Hamidi, A., Rostami, S. M., Safa, S. H., Faramarzi, F., Khorasani, S., Alimohammadi, M., Tahmasebi, S., et al. (2023) · Cancer Cell International · doi:10.1186/s12935-023-02990-y · Cited by 352 · see citing works
Single-Agent Divarasib (GDC-6036) in Solid Tumors with a <i>KRAS</i> G12C Mutation
Sacher, A., LoRusso, P., Patel, M. R., Miller, W. H., Garralda, E., Forster, M. D., Santoro, A., Falcon, A., Kim, T. W., Paz-Ares, L., et al. (2023) · New England Journal of Medicine · doi:10.1056/nejmoa2303810 · Cited by 328 · see citing works
Self-citationFakih, M. G., Kopetz, S., Kuboki, Y., Kim, T. W., Munster, P. N., Krauss, J. C., Falchook, G. S., Han, S.-W., Heinemann, V., Muro, K., et al. (2022) · The Lancet Oncology · doi:10.1016/s1470-2045(21)00605-7 · Cited by 320 · see citing works
Self-citationAdagrasib in Advanced Solid Tumors Harboring a <i>KRAS</i> <sup> <i>G12C</i> </sup> Mutation
Bekaii-Saab, T. S., Yaeger, R., Spira, A. I., Pelster, M. S., Sabari, J. K., Hafez, N., Barve, M., Velastegui, K., Yan, X., Shetty, A., et al. (2023) · Journal of Clinical Oncology · doi:10.1200/jco.23.00434 · Cited by 313 · see citing works
Self-citationThe Drug-Dosing Conundrum in Oncology — When Less Is More
Shah, M., Rahman, A., Theoret, M. R., & Pazdur, R. (2021) · New England Journal of Medicine · doi:10.1056/nejmp2109826 · Cited by 298 · see citing works
The Promise of Nanotechnology in Personalized Medicine
Alghamdi, M. A., Fallica, A. N., Virzì, N. F., Kesharwani, P., Pittalà, V., & Greish, K. F. (2022) · Journal of Personalized Medicine · doi:10.3390/jpm12050673 · Cited by 291 · see citing works
Targeted therapy in advanced non-small cell lung cancer: current advances and future trends
Majeed, U., Manochakian, R., Zhao, Y., & Lou, Y. (2021) · Journal of Hematology & Oncology · doi:10.1186/s13045-021-01121-2 · Cited by 269 · see citing works
Chemical remodeling of a cellular chaperone to target the active state of mutant KRAS
Schulze, C. J., Seamon, K. J., Zhao, Y., Yang, Y. C., Cregg, J., Kim, D., Tomlinson, A., Choy, T. J., Wang, Z., Sang, B., et al. (2023) · Science · doi:10.1126/science.adg9652 · Cited by 264 · see citing works
Translational advances in pancreatic ductal adenocarcinoma therapy
Hosein, A. N., Dougan, S. K., Aguirre, A. J., & Maitra, A. (2022) · Nature Cancer · doi:10.1038/s43018-022-00349-2 · Cited by 249 · see citing works
Mapping the energetic and allosteric landscapes of protein binding domains
Faure, A. J., Domingo, J., Schmiedel, J. M., Hidalgo-Carcedo, C., Diss, G., & Lehner, B. (2022) · Nature · doi:10.1038/s41586-022-04586-4 · Cited by 246 · see citing works
RETRACTED ARTICLE: Antibodies against endogenous retroviruses promote lung cancer immunotherapy
Ng, K. W., Boumelha, J., Enfield, K. S. S., Almagro, J., Cha, H., Pich, O., Karasaki, T., Moore, D. A., Salgado, R., Sivakumar, M., et al. (2023) · Nature · doi:10.1038/s41586-023-05771-9 · Cited by 250 · see citing works
RetractedZhou, J., Ji, Q., & Li, Q. (2021) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-021-02130-2 · Cited by 246 · see citing works
Emerging strategies to target RAS signaling in human cancer therapy
Chen, K., Zhang, Y., Qian, L. M., & Wang, P. (2021) · Journal of Hematology & Oncology · doi:10.1186/s13045-021-01127-w · Cited by 231 · see citing works
The KRAS-G12C inhibitor: activity and resistance
Liu, J., Kang, R., & Tang, D. (2021) · Cancer Gene Therapy · doi:10.1038/s41417-021-00383-9 · Cited by 222 · see citing works
NCCN Guidelines® Insights: Biliary Tract Cancers, Version 2.2023
Benson, A. B., D'Angelica, M. I., Abrams, T. A., Abbott, D. E., Ahmed, A., Anaya, D. A., Anders, R. A., Are, C., Bachini, M., Binder, D. C., et al. (2023) · Journal of the National Comprehensive Cancer Network · doi:10.6004/jnccn.2023.0035 · Cited by 220 · see citing works
Hagenbeek, T. J., Zbieg, J. R., Hafner, M., Mroue, R., Lacap, J. A., Sodir, N. M., Noland, C. L., Afghani, S., Kishore, A., Bhat, K. P., et al. (2023) · Nature Cancer · doi:10.1038/s43018-023-00577-0 · Cited by 215 · see citing works
The Ascension of Targeted Covalent Inhibitors
Singh, J. (2022) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.1c02134 · Cited by 210 · see citing works
Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer
Wasko, U. N., Jiang, J., Dalton, T. C., Curiel-Garcia, A., Edwards, A. C., Wang, Y., Lee, B., Orlen, M., Tian, S., Stalnecker, C. A., et al. (2024) · Nature · doi:10.1038/s41586-024-07379-z · Cited by 209 · see citing works
Non-Small Cell Lung Cancer Targeted Therapy: Drugs and Mechanisms of Drug Resistance
Wu, J., & Lin, Z. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232315056 · Cited by 211 · see citing works
Wu, Q., Qian, W., Sun, X., & Jiang, S. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01362-9 · Cited by 202 · see citing works
Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araujo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M., Minuti, G., et al. (2023) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-1420 · Cited by 203 · see citing works
Self-citationKRAS inhibitors: resistance drivers and combinatorial strategies
Isermann, T., Sers, C., Der, C. J., & Papke, B. (2024) · Trends in cancer · doi:10.1016/j.trecan.2024.11.009 · Cited by 207 · see citing works
Targeting cancer with small-molecule pan-KRAS degraders
Popow, J., Farnaby, W., Gollner, A., Kofink, C., Fischer, G., Wurm, M., Zollman, D., Wijaya, A., Mischerikow, N., Hasenoehrl, C., et al. (2024) · Science · doi:10.1126/science.adm8684 · Cited by 198 · see citing works
Advances in molecular pathology and therapy of non-small cell lung cancer
Huang, Q., Li, Y., Huang, Y., Wu, J., Bao, W., Xue, C., Li, X., Dong, S., Dong, Z., & Hu, S. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02243-6 · Cited by 197 · see citing works
The path to the clinic: a comprehensive review on direct KRASG12C inhibitors
Kwan, A. K., Piazza, G. A., Keeton, A. B., & Leite, C. A. (2022) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-021-02225-w · Cited by 192 · see citing works
Small molecule inhibitors targeting the cancers
Liu, G., Chen, T., Zhang, X., Ma, X., & Shi, H. (2022) · MedComm · doi:10.1002/mco2.181 · Cited by 198 · see citing works
NRF2: KEAPing Tumors Protected
Pillai, R., Hayashi, M., Zavitsanou, A.-M., & Papagiannakopoulos, T. Y. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-0922 · Cited by 187 · see citing works
Ashrafi, A., Akter, Z., Modareszadeh, P., Modareszadeh, P., Berisha, E., Alemi, P. S., Castro, M. D. C. C., Deese, A. R., & Li, Z. (2022) · Cancers · doi:10.3390/cancers14194562 · Cited by 193 · see citing works
Lee, J. K., Sivakumar, S., Schrock, A. B., Madison, R., Fabrizio, D., Gjoerup, O., Ross, J. S., Frampton, G. M., Napalkov, P., Montesion, M., et al. (2022) · npj Precision Oncology · doi:10.1038/s41698-022-00334-z · Cited by 187 · see citing works
Drugging KRAS: Current perspectives and state-of-art review
Parikh, K., Banna, G., Liu, S. V., Friedlaender, A., Desai, A., Subbiah, V., & Addeo, A. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01375-4 · Cited by 164 · see citing works
Dy, G. K., Govindan, R., Velcheti, V., Falchook, G. S., Italiano, A., Wolf, J., Sacher, A. G., Takahashi, T., Ramalingam, S. S., Dooms, C., et al. (2023) · Journal of Clinical Oncology · doi:10.1200/jco.22.02524 · Cited by 163 · see citing works
Self-citationDrug Resistance in Colorectal Cancer: From Mechanism to Clinic
Wang, Q., Shen, X., Chen, G., & Du, J. (2022) · Cancers · doi:10.3390/cancers14122928 · Cited by 160 · see citing works
At the crossroads of immunotherapy for oncogene-addicted subsets of NSCLC
Otano, I., Ucero, A. C., Zugazagoitia, J., & Paz-Ares, L. G. (2023) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00718-x · Cited by 161 · see citing works
Rappaport, A., Kyi, C., Lane, M., Hart, M. G., Johnson, M. L., Henick, B. S., Liao, C., Mahipal, A., Shergill, A. P., Spira, A. I., et al. (2024) · Nature Medicine · doi:10.1038/s41591-024-02851-9 · Cited by 161 · see citing works
Self-citationThe energetic and allosteric landscape for KRAS inhibition
Weng, C., Faure, A. J., Escobedo, A., & Lehner, B. (2023) · Nature · doi:10.1038/s41586-023-06954-0 · Cited by 157 · see citing works
KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance
Zavitsanou, A., Pillai, R., Yuan, H., Wu, W., Bartnicki, E., Karakousi, T. R., Rajalingam, S., Herrera, A. M., Karatza, A., Rashidfarrokhi, A., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113295 · Cited by 153 · see citing works
Exploiting the therapeutic implications of KRAS inhibition on tumor immunity
Molina-Arcas, M., & Downward, J. (2024) · Cancer Cell · doi:10.1016/j.ccell.2024.02.012 · Cited by 152 · see citing works
A Small Molecule with Big Impact: MRTX1133 Targets the KRASG12D Mutation in Pancreatic Cancer
Wei, D., Wang, L., Zuo, X., Maitra, A., & Bresalier, R. S. (2023) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-23-2098 · Cited by 163 · see citing works
Weiss, A., Lorthiois, E., Barys, L., Beyer, K. S., Bomio-Confaglia, C., Burks, H., Chen, X., Cui, X., de Kanter, R., Dharmarajan, L., et al. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-0158 · Cited by 150 · see citing works
Recent advances in therapeutic strategies for non-small cell lung cancer
Su, P., Furuya, N., Asrar, A., Rolfo, C. D., Li, Z., Carbone, D. P., & He, K. (2025) · Journal of Hematology & Oncology · doi:10.1186/s13045-025-01679-1 · Cited by 156 · see citing works
Mugarza, E., van Maldegem, F., Boumelha, J., Moore, C., Rana, S., Llorian, M., East, P., Ambler, R., Anastasiou, P., Romero-Clavijo, P., et al. (2022) · Science Advances · doi:10.1126/sciadv.abm8780 · Cited by 144 · see citing works
Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer
Yaeger, R., Mezzadra, R., Sinopoli, J., Bian, Y., Marasco, M., Kaplun, E., Gao, Y., Zhao, H., Paula, A. D. C., Zhu, Y., et al. (2023) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-0405 · Cited by 144 · see citing works
Self-citationAdeno-to-squamous transition drives resistance to KRAS inhibition in LKB1 mutant lung cancer
Tong, X., Patel, A. S., Kim, E., Li, H., Chen, Y., Li, S., Liu, S., Dilly, J., Kapner, K. S., Zhang, N., et al. (2024) · Cancer Cell · doi:10.1016/j.ccell.2024.01.012 · Cited by 142 · see citing works
Self-citationXiang, Y., Liu, X., Wang, Y., Zheng, D., Meng, Q., Jiang, L., Yang, S., Zhang, S., Zhang, X., Liu, Y., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1366260 · Cited by 146 · see citing works
Divarasib plus cetuximab in KRAS G12C-positive colorectal cancer: a phase 1b trial
Desai, J., Alonso, G., Kim, S. H., Cervantes, A., Karasic, T., Medina, L., Shacham-Shmueli, E., Cosman, R., Falcon, A., Gort, E., et al. (2024) · Nature Medicine · doi:10.1038/s41591-023-02696-8 · Cited by 132 · see citing works
“%) compared with sotorasib (37% in a phase 2 trial and 28% in a phase 3 trial) and adagrasib (43% in a phase 2 trial) 11,23–25 .”
BackgroundSelf-citationClassification of KRAS -Activating Mutations and the Implications for Therapeutic Intervention
Johnson, C. W., Burkhart, D. L., & Haigis, K. M. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-0035 · Cited by 130 · see citing works
Coleman, N., Hong, L., Zhang, J., Heymach, J. V., Hong, D. S., & Le, X. (2021) · ESMO Open · doi:10.1016/j.esmoop.2021.100319 · Cited by 132 · see citing works
Next batter up! Targeting cancers with KRAS-G12D mutations
Zeissig, M. N., Ashwood, L. M., Kondrashova, O., & Sutherland, K. D. (2023) · Trends in Cancer · doi:10.1016/j.trecan.2023.07.010 · Cited by 128 · see citing works
Prospects of targeting PI3K/AKT/mTOR pathway in pancreatic cancer
Mortazavi, M., Moosavi, F., Martini, M., Giovannetti, E., & Firuzi, O. (2022) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2022.103749 · Cited by 126 · see citing works
Defining the KRAS- and ERK-dependent transcriptome in KRAS-mutant cancers
Klomp, J. A., Klomp, J. E., Stalnecker, C. A., Bryant, K. L., Edwards, A. C., Drizyte‐Miller, K., Hibshman, P. S., Diehl, J. N., Lee, Y. S., Morales, A. J., et al. (2024) · Science · doi:10.1126/science.adk0775 · Cited by 133 · see citing works
Modulation of the proteostasis network promotes tumor resistance to oncogenic KRAS inhibitors
Lv, X., Lu, X., Cao, J., Luo, Q., Ding, Y., Peng, F., Pataer, A., Lu, D., Han, D., Malmberg, E., et al. (2023) · Science · doi:10.1126/science.abn4180 · Cited by 123 · see citing works
Cheng, Y., Zhang, T., & Xu, Q. (2021) · MedComm · doi:10.1002/mco2.105 · Cited by 125 · see citing works
Multiple myeloma with high-risk cytogenetics and its treatment approach
Hanamura, I. (2022) · International Journal of Hematology · doi:10.1007/s12185-022-03353-5 · Cited by 122 · see citing works
KRAS G12C in advanced NSCLC: Prevalence, co-mutations, and testing
Lim, T. K. H., Skoulidis, F., Kerr, K. M., Ahn, M., Kapp, J. R., Soares, F. A., & Yatabe, Y. (2023) · Lung Cancer · doi:10.1016/j.lungcan.2023.107293 · Cited by 126 · see citing works
Self-citationCregg, J., Edwards, A. V., Chang, S., Lee, B. J., Knox, J. E., Tomlinson, A. C. A., Marquez, A., Liu, Y., Freilich, R., Aay, N., et al. (2025) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.4c02314 · Cited by 124 · see citing works
Biomarker-Targeted Therapies in Non–Small Cell Lung Cancer: Current Status and Perspectives
Guo, H., Zhang, J., Qin, C., Yan, H., Liu, T., Hu, H., Tang, S., Tang, S., & Zhou, H. (2022) · Cells · doi:10.3390/cells11203200 · Cited by 118 · see citing works
RAS signaling in carcinogenesis, cancer therapy and resistance mechanisms
Yang, X., & Wu, H. K. (2024) · Journal of Hematology & Oncology · doi:10.1186/s13045-024-01631-9 · Cited by 122 · see citing works
García-Pardo, M., Makarem, M., Li, J. J. N., Kelly, D., & Leighl, N. B. (2022) · British Journal of Cancer · doi:10.1038/s41416-022-01776-9 · Cited by 118 · see citing works
Targeting the Estrogen Receptor for the Treatment of Breast Cancer: Recent Advances and Challenges
Rej, R. K., Thomas, J. E., Acharyya, R. K., Rae, J. M., & Wang, S. (2023) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.3c00136 · Cited by 115 · see citing works
Ricciuti, B., Alessi, J. V., Elkrief, A., Wang, X., Cortellini, A., Li, Y. Y., Vaz, V. R., Gupta, H., Pecci, F., Barrichello, A., et al. (2022) · Annals of Oncology · doi:10.1016/j.annonc.2022.07.005 · Cited by 112 · see citing works
Self-citationKetcham, J. M., Haling, J. R., Khare, S., Bowcut, V., Briere, D. M., Burns, A. C., Gunn, R. J., Ivetac, A., Kuehler, J. E., Kulyk, S., et al. (2022) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.2c00741 · Cited by 111 · see citing works
Lorthiois, E., Gerspacher, M., Beyer, K. S., Vaupel, A., Leblanc, C., Stringer, R., Weiss, A., Wilcken, R., Guthy, D. A., Lingel, A., et al. (2022) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.2c01438 · Cited by 110 · see citing works
The translational challenges of precision oncology
Pich, O., Bailey, C., Watkins, T. B. K., Zaccaria, S., Jamal‐Hanjani, M., & Swanton, C. (2022) · Cancer Cell · doi:10.1016/j.ccell.2022.04.002 · Cited by 111 · see citing works
AACR Project GENIE: 100,000 Cases and Beyond
Pugh, T. J., Bell, J. L., Bruce, J. P., Doherty, G. J., Galvin, M., Green, M. F., Hunter-Zinck, H., Kumari, P., Lenoue-Newton, M. L., Li, M. M., et al. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-1547 · Cited by 103 · see citing works
Using cfDNA and ctDNA as Oncologic Markers: A Path to Clinical Validation
Dao, J., Conway, P., Subramani, B., Meyyappan, D., Russell, S., & Mahadevan, D. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241713219 · Cited by 107 · see citing works
Mukhopadhyay, S., Huang, H.-Y., Lin, Z., Ranieri, M., Li, S., Sahu, S., Liu, Y., Ban, Y., Guidry, K., Hu, H., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-23-2729 · Cited by 105 · see citing works
Self-citationTargeting KRAS in pancreatic cancer: new drugs on the horizon
Bannoura, S. F., Uddin, M. H., Nagasaka, M., Fazili, F., Hallak, M. N. A., Philip, P. A., El‐Rayes, B. F., & Azmi, A. S. (2021) · Cancer and Metastasis Reviews · doi:10.1007/s10555-021-09990-2 · Cited by 105 · see citing works
Zhou, C., Li, C., Luo, L., Li, X., Jia, K., He, N., Mao, S., Wang, W., Shao, C., Liu, X., et al. (2024) · Cancer Cell · doi:10.1016/j.ccell.2024.06.001 · Cited by 102 · see citing works
Combinatorial strategies to target RAS-driven cancers
Perurena, N., Situ, L., & Cichowski, K. M. (2024) · Nature reviews. Cancer · doi:10.1038/s41568-024-00679-6 · Cited by 104 · see citing works
Zhu, Z., McGray, A. R., Jiang, W., Lu, B., Kaliński, P., & Guo, Z. S. (2022) · Molecular Cancer · doi:10.1186/s12943-022-01664-z · Cited by 102 · see citing works
Targeting KRAS in pancreatic cancer
Stickler, S., RATH, B., & Hamilton, G. (2024) · Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics · doi:10.32604/or.2024.045356 · Cited by 99 · see citing works
- Authors
- Skoulidis, F., Li, B. T., Dy, G. K., Price, T. J., Falchook, G. S., Wolf, J., Italiano, A., Schuler, M., Borghaei, H., Barlesi, F., Kato, T., Curioni-Fontecedro, A., Sacher, A., Spira, A., Ramalingam, S. S., Takahashi, T., Besse, B., Anderson, A., Ang, A., Tran, Q., Mather, O., Henary, H., Ngarmchamnanrith, G., Friberg, G., Velcheti, V., & Govindan, R.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- From the University of Texas M.D. Anderson Cancer Center, Houston (F.S.), and U.S. Oncology Research, the Woodlands (A. Spira) — both in Texas; Memorial Sloan Kettering Cancer Center and Weill Cornell Medicine (B.T.L.) and Thoracic Medical Oncology, Perlmutter Cancer Center, New York University (V.V.), New York, and Roswell Park Cancer Institute, Buffalo (G.K.D.) — all in New York; the Queen Elizabeth Hospital and University of Adelaide, Woodville, SA, Australia (T.J.P.); Sarah Cannon Research Institute at HealthONE, Denver (G.S.F.); Department I of Internal Medicine, Center for Integrated Oncology, University Hospital Cologne, Cologne (J.W.), the West German Cancer Center, University Hospital Essen, University Duisburg–Essen, Essen (M.S.), and the German Cancer Consortium, Heidelberg (M.S.) — all in Germany; the Early Phase Trials and Sarcoma Units, Bergonie Cancer Institute, Bordeaux (A.I.), and Gustave Roussy Institute, Villejuif (F.B., B.B.) — both in France; Fox Chase Cancer Center, Philadelphia (H.B....
- Fox Chase Cancer Center (US)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2021-06-24
- Volume
- 384
- Issue
- 25
- Pages
- 2371-2381
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC9116274
- OpenAlex
- W3172081492
- Semantic Scholar
- 3c89f24ad219bec52684f03b8df3c5d8feb81a72
- Cited by
- 1,849
- References
- 39
- Citations by year
- 2026: 317 · 2025: 348 · 2024: 398 · 2023: 382 · 2022: 319 · 2021: 84
- FWCI
- 192.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Universitätsbibliographie, Universität Duisburg-Essen (submittedVersion)
- Funders
- Amgen
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- sotorasib, non-small cell lung cancer, KRAS inhibitors, advanced solid tumors, objective response, progression-free survival, biomarkers, drug safety
- MeSH terms
- Progression-Free Survival, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Piperazines, Pyridines, Pyrimidines, Biomarkers, Proto-Oncogene Proteins p21(ras), B7-H1 Antigen
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
