The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index; none of the 22 sources its claims cite is checked for support yet.
Rociletinib in EGFR-Mutated Non–Small-Cell Lung Cancer
Open accessAbstract
BACKGROUND: Non-small-cell lung cancer (NSCLC) with a mutation in the gene encoding epidermal growth factor receptor (EGFR) is sensitive to approved EGFR inhibitors, but resistance develops, mediated by the T790M EGFR mutation in most cases. Rociletinib (CO-1686) is an EGFR inhibitor active in preclinical models of EGFR-mutated NSCLC with or without T790M. METHODS: In this phase 1-2 study, we administered rociletinib to patients with EGFR-mutated NSCLC who had disease progression during previous treatment with an existing EGFR inhibitor. In the expansion (phase 2) part of the study, patients with T790M-positive disease received rociletinib at a dose of 500 mg twice daily, 625 mg twice daily, or 750 mg twice daily. Key objectives were assessment of safety, side-effect profile, pharmacokinetics, and preliminary antitumor activity of rociletinib. Tumor biopsies to identify T790M were performed during screening. Treatment was administered in continuous 21-day cycles. RESULTS: A total of 130 patients were enrolled. The first 57 patients to be enrolled received the free-base form of rociletinib (150 mg once daily to 900 mg twice daily). The remaining patients received the hydrogen bromide salt (HBr) form (500 mg twice daily to 1000 mg twice daily). A maximum tolerated dose (the highest dose associated with a rate of dose-limiting toxic effects of less than 33%) was not identified. The only common dose-limiting adverse event was hyperglycemia. In an efficacy analysis that included patients who received free-base rociletinib at a dose of 900 mg twice daily or the HBr form at any dose, the objective response rate among the 46 patients with T790M-positive disease who could be evaluated was 59% (95% confidence interval [CI], 45 to 73), and the rate among the 17 patients with T790M-negative disease who could be evaluated was 29% (95% CI, 8 to 51). CONCLUSIONS: Rociletinib was active in patients with EGFR-mutated NSCLC associated with the T790M resistance mutation. (Funded by Clovis Oncology; ClinicalTrials.gov number, NCT01526928.).
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Among 20 patients whose tumors were not assessable for T790M at the central laboratory, the response rate was 15% (3 of 20 patients).”
§ Rociletinib was > Efficacy
Strength:plain· not yet calibratedn = 20Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the objective response rate among the 46 patients with T790M-positive disease who could be evaluated was 59% (95% confidence interval [CI], 45 to 73)”
- Also stated in: § Efficacy · plain
“The response rate among 46 patients with centrally confirmed T790M-positive tumors was 59% (95% confidence interval [CI], 45 to 73)”
§ Rociletinib was > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Efficacy · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the disease-control rate was 59% (10 of 17 patients)”
§ Rociletinib was > Efficacy
Strength:plain· not yet calibratedn = 17Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the rate among the 17 patients with T790Mnegative disease who could be evaluated was 29% (95% CI, 8 to 51)”
- Also stated in: § Efficacy · plain
“Among 17 patients whose tumors were T790Mnegative by central testing, the response rate was 29% (95% CI, 8 to 51)”
§ Rociletinib was > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Efficacy · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the disease-control rate (the proportion of patients with a complete or partial response or stable disease) was 93% (43 of 46 patients)”
§ Rociletinib was > Efficacy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this group, the median progression-free survival was 5.6 months (95% CI, 1.3 to not reached).”
§ Rociletinib was > Efficacy
Strength:plain· not yet calibratedn = 17Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Treatment-related adverse events were generally infrequent and mild”
§ Rociletinib was > Safety
Strength:plain· not yet calibratedn = 92Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the best responses were observed among those with T790M-positive cancers, rociletinib showed some antitumor activity in patients without a documented T790M mutation.”
§ Rociletinib was > Discussion
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The most common grade 3 toxic effect associated with rociletinib was hyperglycemia.”
§ Rociletinib was > Discussion
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rociletinib did not cause the syndrome of rash, stomatitis, and paronychia that is associated with inhibition of nonmutant EGFR”
§ Rociletinib was > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The rash, stomatitis, and paronychia syndrome is caused by inhibition of nonmutant EGFR.
- The quote only partly states this claim. 1
- It may state two separate claims as one. 19
- Probably not a substantial claim. 11
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“QTc prolongation 11 (12) 3 (3) 3 (3) 5 (5)”
§ Rociletinib was > Discussion
Strength:plain· not yet calibratedn = 11Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The antitumor activity of rociletinib was observed regardless of initial activating mutation and in a trial population of heavily pretreated patients (median number of previous therapies, 4).”
§ Rociletinib was > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“in this study 72% of patients overall and 70% of T790M-positive patients who had a response were also taking an EGFR inhibitor immediately before study therapy”
§ Rociletinib was > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, rociletinib was associated with tumor responses and sustained disease control among patients with heavily pretreated EGFR-mutated NSCLC from the United States, Europe, and Australia in whom the T790M resistance mutation has developed.”
§ Rociletinib was > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Objective responses were consistently observed at a dose of 900 mg twice daily of the free-base form and all doses of the HBr form (hereafter referred to as therapeutic doses).”
§ Rociletinib was > Efficacy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“though a single patient had a grade 1 maculopapular rash.”
§ Rociletinib was > Safety
Strength:plain· not yet calibratedSingle caseTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“A maximum tolerated dose was not defined in the phase 1 portion.”
§ Rociletinib was > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One patient had a treatment-related grade 4 event (hypokalemia), and there were no treatment-related grade 5 events.”
§ Rociletinib was > Discussion
Strength:plain· not yet calibratedSingle caseTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rociletinib was absorbed rapidly, with an elimination half-life of 2 to 4 hours”
§ Rociletinib was > Pharmacokinetics
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“12 of the 17 T790M-negative patients, and 80% of the T790Mnegative patients who had a response, had been taking an EGFR inhibitor immediately before rociletinib.”
§ Rociletinib was > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The study included some patients with preexisting diabetes, who were treated uneventfully”
§ Rociletinib was > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The response rate of 59% and prolonged disease control among some T790M-positive patients are encouraging”
- Also stated in: § Discussion · plain
“A response rate of 59% with prolonged disease control was noted.”
§ Rociletinib was > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Discussion · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A maximum tolerated dose (the highest dose associated with a rate of dose-limiting toxic effects of less than 33%) was not identified.”
- Also stated in: § Patient Characteristics · plain
“The maximum tolerated dose was not reached according to the protocol definition, because all doses studied had a cycle 1 rate of doselimiting toxic effects of less than 33%.”
§ Rociletinib was > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Patient Characteristics · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Nevertheless, in our study, those who were T790M-negative on the central assay had a response rate of 29% (5 of the 17 patients) and a median progression-free survival of 5.6 months.”
§ Rociletinib was > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The central genotyping assay accurately identifies T790M mutation status in tumor biopsies.
In the paper
“In xenograft models with EGFR-activating mutations alone or combined with T790M resistance mutations, rociletinib resulted in durable tumor shrinkage, 7 which was most marked when plasma concentrations were maintained at more than 200 ng per milliliter across the dosing interval.”
§ Rociletinib was > Abstract
What the sources say
- Not checked yetcites [7] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Rociletinib (CO-1686; Clovis Oncology) is a small-molecule, orally available, mutant-selective covalent inhibitor of commonly mutated forms of EGFR, including exon 19 deletions, L858R, and T790M, but not exon 20 insertions.”
§ Rociletinib was > Abstract
What the sources say
- Not checked yetcites [7] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Rociletinib (CO-1686) is an EGFR inhibitor active in preclinical models of EGFR-mutated NSCLC with or without T790M.”
§ Rociletinib was > Abstract
What the sources say
- Not checked yetcites [7] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This study was conducted in accordance with the principles of the Declaration of Helsinki and the Good Clinical Practice guidelines of the International Conference on Harmonisation.”
§ Rociletinib was > Study Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The study was designed by study investigators together with the sponsor (Clovis Oncology).”
§ Rociletinib was > Study Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Written informed consent was obtained from all patients.”
§ Rociletinib was > Study Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, studies of afatinib monotherapy showed a response rate of less than 10% among patients with acquired resistance to erlotinib or gefitinib, with a progression-free survival of approximately 4 months.13,15”
§ Rociletinib was > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All the authors made the decision to submit the manuscript for publication and vouch for the accuracy and completeness of the data and analyses reported and for the fidelity of the study to the protocol.”
§ Rociletinib was > Study Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“although several other molecules are in development.11”
§ Rociletinib was > Discussion
What the sources say
- Not checked yetcites [11] source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The most successful therapy to date for acquired resistance has been a combination of daily afatinib and the EGFR monoclonal antibody cetuximab every other week, with a response rate of 30% and a median progression-free survival of 4.7 months.16”
§ Rociletinib was > Discussion
What the sources say
- Not checked yetcites [16] source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The sponsor collected the data and analyzed them in conjunction with the authors.”
§ Rociletinib was > Study Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“However, this combination is associated with substantial skin and gastrointestinal toxic effects, which may limit its use.”
§ Rociletinib was > Discussion
What the sources say
- Not checked yetcites [16] source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The protocol was approved by the local human investigations committee at each site.”
§ Rociletinib was > Study Oversight
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Activation of the IGF-IR pathway is a proposed resistance mechanism for EGFR inhibition, 21,22”
§ Rociletinib was > Discussion
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
No approved therapy specifically targets T790M.
“There are no approved therapies that specifically target T790M”
The paper relies on this without support.
Cytotoxic chemotherapy is the usual treatment for T790M-positive patients.
“so cytotoxic chemotherapy is typically used.”
The paper relies on this without support.
Approved EGFR inhibitors strongly inhibit wild-type EGFR, leading to rash and diarrhea as common dose-limiting toxicities.
“currently approved EGFR tyrosine kinase inhibitors result in substantial inhibition of nonmutant EGFR, leading to rash and diarrhea as their two most common and dose-limiting side effects.”
The paper relies on this without support.
The central genotyping assay accurately identifies T790M mutation status in tumor biopsies.
“those who were T790M-negative on the central assay”
The paper relies on this without support.
The rash, stomatitis, and paronychia syndrome is caused by inhibition of nonmutant EGFR.
“the syndrome of rash, stomatitis, and paronychia that is associated with inhibition of nonmutant EGFR”
The paper relies on this without support.
There are no approved therapies that specifically target T790M.
“there are no approved therapies that specifically target T790M”
The paper relies on this without support.
Rociletinib has a short half-life.
“Because of the short half-life of rociletinib”
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?
In the citing paper
“Third generation EGFR inhibitors capable of inhibiting mutant EGFR with T790M produce responses in nearly two thirds of patients.”
In the citing paper
“In addition, both agents are associated with substantially less skin toxicity than typically observed for EGFR TKIs (17, 18).”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [18]
In the citing paper
“In phase I studies to date, treatment with either CO-1686 or AZD9291, has resulted in a RR > 50% in EGFR mutant EGFR T790M NSCLC patients that have developed resistance to gefitinib or erlotinib (17, 18).”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [18]
In the citing paper
“These include the development of mutant selective EGFR kinase inhibitors, including WZ4002, CO-1686 and AZD9291, which to date have demonstrated encouraging efficacy in both preclinical models and in EGFR mutant NSCLC patients with EGFR T790M mediated drug resistance (14–18).”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [18]
In the citing paper
“Recently, Sequist and coll. reported the preliminary results of the ongoing phase I/II study TIGER X in patients with NSCLC harboring EGFR mutations and T790M-positive that previously received an EGFR TKI. The results, albeit preliminary, are quite impressive with a 59% ORR and a median PFS not yet reached, but exceeding 12 months. The safety profile of this agent is also interesting with the most”
From A decade of EGFR inhibition in EGFR-mutated non small cell lung cancer (NSCLC): Old successes and future perspectives (2015) · cites this paper as [86]
In the citing paper
“Similarly, the response rate of rociletinib for EGFR T790M positive patients was 59% [39].”
In the citing paper
“In human clinical trials, osimertinib and rociletinib showed promising safety and efficacy, even though some hyperglycemia was observed in patients treated with rociletinib [38, 39].”
In the citing paper
“The number of patients with Del19 + T790M tumors who enrolled in phase I/II trials for osimertinib38 and rociletinib39 was approximately twice as large as the number of patients with L858R+T790M.”
From Not all epidermal growth factor receptor mutations in lung cancer are created equal: Perspectives for individualized treatment strategy (2016) · cites this paper as [39]
In the citing paper
“At least five third-generation EGFR-TKIs are in clinical development (rociletinib, osimertinib, HM61713/BI1482694, ASP8273, and EGF816) and all have reported objective response rates (ORRs) that exceed 45% in patients with EGFR-mutant NSCLC and T790M-positive resistance.12-16”
From Association Between Plasma Genotyping and Outcomes of Treatment With Osimertinib (AZD9291) in Advanced Non–Small-Cell Lung Cancer (2016) · cites this paper as [13]
In the citing paper
“Another third-generation EGFR TKI, rociletinib, was initially reported as having similarly high responses in the T790M-positive group (RR 59%).85”
In the citing paper
“Patients with cancer who are members of racial or ethnic minorities may disproportionately experience comorbidities, experience more substantial obstacles to receiving care, be more likely lack insurance, and face a greater risk of receiving poor-quality care than other Americans.140,141,146,147”
From Systemic Therapy for Stage IV Non–Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update (2015) · cites this paper as [146]
Citations
Cites
Lynch, T. J., Bell, D. W., Sordella, R., Gurubhagavatula, S., Okimoto, R. A., Brannigan, B. W., Harris, P. L., Haserlat, S. M., Supko, J. G., Haluska, F. G., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040938 · Cited by 11,486
Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Mok, T. S., Wu, Y.-L., Thongprasert, S., Yang, C.-H., Chu, D.-T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0810699 · Cited by 8,261
Dermatology Life Quality Index (DLQI)-a simple practical measure for routine clinical use
Finlay, A. Y., & KHAN, G. K. (1994) · Clinical and Experimental Dermatology · doi:10.1111/j.1365-2230.1994.tb01167.x · Cited by 5,610
Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., et al. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70393-x · Cited by 5,489
Anaplastic Lymphoma Kinase Inhibition in Non–Small-Cell Lung Cancer
Kwak, E. L., Bang, Y., Camidge, D. R., Shaw, A. T., Solomon, B., Maki, R. G., Ou, S. I., Dezube, B. J., Janne, P. A., Costa, D. B., et al. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa1006448 · Cited by 4,477
Self-citationGenotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Sequist, L. V., Waltman, B. A., Dias-Santagata, D., Digumarthy, S., Turke, A. B., Fidias, P., Bergethon, K., Shaw, A. T., Gettinger, S., Cosper, A. K., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002003 · Cited by 3,499
Self-citationSequist, L. V., Yang, J. C.-H., Yamamoto, N., O'Byrne, K., Hirsh, V., Mok, T., Geater, S. L., Orlov, S., Tsai, C.-M., Boyer, M., et al. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2012.44.2806 · Cited by 3,228
Self-citationEpidermal growth factor receptor mutations in lung cancer
Sharma, S. V., Bell, D. W., Settleman, J., & Haber, D. A. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2088 · Cited by 3,170
Yu, H. A., Arcila, M. E., Rekhtman, N., Sima, C. S., Zakowski, M. F., Pao, W., Kris, M. G., Miller, V. A., Ladanyi, M., & Riely, G. J. (2013) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-12-2246 · Cited by 2,454
AZD9291 in EGFR Inhibitor–Resistant Non–Small-Cell Lung Cancer
Jänne, P. A., Yang, J. C.-H., Kim, D.-W., Planchard, D., Ohe, Y., Ramalingam, S. S., Ahn, M.-J., Kim, S.-W., Su, W.-C., Horn, L., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1411817 · Cited by 2,116
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Zhang, Q., & Wu, Y.-L. L. C. (2015) · Expert Review of Clinical Pharmacology · doi:10.1586/17512433.2016.1101340 · Cited by 1
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Galazi, M., Weitsman, G. E., Monypenny, J., Coban, O., Milewicz, H., Gómez, V., Ciccarelli, F. D., & Ng, T. (2017) · Springer eBooks · doi:10.1007/978-3-319-53661-3_15 · Cited by 1
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Durrett, S., Bowling, M., & Oliver, A. L. (2018) · Clinical Pulmonary Medicine · doi:10.1097/cpm.0000000000000249 · Cited by 1
Noor, Z. S., & Goldman, J. W. (2019) · Current cancer research · doi:10.1007/978-3-030-17832-1_1 · Cited by 1
Self-citationPatel, J. N., & Villadolid, J. J. (2016) · IGI Global eBooks · doi:10.4018/978-1-5225-1762-7.ch008 · Cited by 1
Zalcman, G., Brosseau, S., & Gounant, V. (2015) · Journal of Clinical Oncology · doi:10.1200/jco.2015.64.7529 · Cited by 1
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Ganey, P. E., & Misek, S. A. (2019) · Wiley eBooks · doi:10.1002/9781119060208.ch4 · Cited by 1
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Gold, K. A., & Erasmus, J. J. (2015) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000599
Kim, E. S. (2015) · American Journal of Hematology / Oncology®
Lung cancer diagnostics and treatments 2015: a renaissance of patient care.
Kim, E. S. (2015) · PubMed Central · doi:10.3978/j.issn.2218-6751.2015.10.04
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Cappuzzo, F. (2015) · Springer eBooks · doi:10.1007/978-3-319-20741-4_4
Moro‐Sibilot, D., Duruisseaux, M., Levra, M. G., Sakhri, L., & Toffart, A. (2015) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(16)30033-7
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Raimbourg, J., & Douillard, J. (2015) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(16)30032-5
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Mohindra, N. A., & Patel, J. D. (2015) · Lung Cancer Management · doi:10.2217/lmt.15.30
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Tomasini, P., Fina, F., Greillier, L., & Barlési, F. (2016) · Current Pulmonology Reports · doi:10.1007/s13665-016-0137-9
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Fink, M. (2015) · Info Onkologie · doi:10.1007/s15004-015-0885-7
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Yano, S. (2016) · Haigan · doi:10.2482/haigan.56.55
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Artal, A., Pelegrín, J. G., & Alejandro, M. Á. (2016) · Medicina Clínica · doi:10.1016/s0025-7753(16)30259-7
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Li, L. (2016) · International Journal of Cancer and Oncology · doi:10.15436/2377-0902.16.027
Zabernigg, A. F. (2016) · memo - Magazine of European Medical Oncology · doi:10.1007/s12254-016-0288-y
Targeting epidermal growth factor receptor: An important strategy in oncology
Kharatmol, M. G., & Jagdale, D. M. (2017) · International Journal of Pharma and Bio Sciences · doi:10.22376/ijpbs.2017.8.1.p174-182
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Svatoň, M. (2016) · Onkologie · doi:10.36290/xon.2016.005
Nandhabalan, M. (2017) · Neuro-Oncology · doi:10.1093/neuonc/now293.000
Reichegger, H., Jochum, W., Förbs, D., Hader, C., & Früh, M. (2017) · Kompass Pneumologie · doi:10.1159/000455111
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Yonesaka, K. (2015) · Haigan · doi:10.2482/haigan.55.948
Kardas, J., Buraczewska, A., Chrom, P., Waśko-Grabowska, A., Młot, B., & Szczylik, C. A. (2017) · Oncoreview · doi:10.24292/01.or.300617.7
Clay, T. D. (2017) · Minerva Access (University of Melbourne)
Les rebiopsies : pourquoi ? Comment ?
Saint-Paul, A., Ballouhey, J., & Vergnenégre, A. (2017) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(17)30044-7
Gillis, N. (2019) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/3ttj-j094
Topham, M. K., Kim, M., & Iravani, A. (2020) · Cancer translational medicine · doi:10.4103/ctm.ctm_7_20
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Hu, M. S., & Wang, Z. (2021) · Springer eBooks · doi:10.1007/978-981-16-1037-0_30
Kobayashi, K., & Kagamu, H. (2017) · Springer eBooks · doi:10.1007/978-981-10-2002-5_10
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Subramaniam, D. S., Hartley, M. L., Pishvaian, M. J., He, R., & Marshall, J. L. (2015) · Springer eBooks · doi:10.1007/978-3-642-27841-9_1931-3
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Subramaniam, D. S., Hartley, M. L., Pishvaian, M. J., He, R., & Marshall, J. L. (2015) · Springer eBooks · doi:10.1007/978-3-662-46875-3_1931
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Martinelli, C. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-821789-4.00012-6
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Fujii, H., & Okuma, Y. (2022) · Translational Lung Cancer Research · doi:10.21037/tlcr-22-478
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Neuwelt, A. J., & Camidge, D. R. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-822833-3.00007-3
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Yadav, T., Mehta, V., Bhusare, N., Chintamaneni, M., & Mayur, Y. C. (2023) · Springer eBooks · doi:10.1007/978-981-19-5399-6_7
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Kasherman, L., Lau, S. C. M., Karakasis, K., Leighl, N. B., & Oza, A. M. (2023) · Medical radiology · doi:10.1007/174_2023_383
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Krishnamoorthy, S., Periyasamy, L., Gnanagurusamy, J., Sabanayagam, R., Elango, H., Vishwanathan, M., & Muthusami, S. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-95699-4.00018-9
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Hoe, H. J., Balasubramanian, A., & John, T. (2023) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2023.07.007
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Sarkate, A. P., Bhandari, S. V., Inamdar, P. R., Kuthe, P. V., & Padvi, K. S. (2023) · Springer eBooks · doi:10.1007/978-981-99-5281-6_7
Qi, R., Fu, X., Liang, J., Yu, Y., Xu, H., Shen, M., He, S., & Lv, D. (2023) · Research Square · doi:10.21203/rs.3.rs-3337468/v1
Cao, B., Huang, L., Liu, M., Lin, H. Y., Ma, T., Zhao, Y., Geng, Y., Yang, Y., Guo, H., & Li, J. (2023) · Expert Opinion on Drug Metabolism & Toxicology · doi:10.1080/17425255.2023.2260738
Rajendran, R., & Mathaiyan, J. (2024) · Current Cancer Therapy Reviews · doi:10.2174/0115733947276538240129053601
Yang, X., Zhong, J., Yu, Z., Zhuo, M., Zhang, M., Chen, R., Xia, X., & Zhao, J. (2021) · Figshare · doi:10.6084/m9.figshare.16821698
AI-driven design of Novel EGFR Inhibitors with Enhanced Potency and Drug-Like PropertiesPreprint
Yata, V. K., Asma, S., Das, O. P., Mattaparthi, V. S. K., Thalluri, C., Gladys, T. M., Ezeonwumelu, J. O. C., & Bukke, S. P. N. (2025) · Research Square · doi:10.21203/rs.3.rs-6888580/v1
Palanisamy, M., Sugan, S., Venugopal, T., & Rajagopal, K. (2025) · Research Square · doi:10.21203/rs.3.rs-7289669/v1
Zhao, Y., He, J. Y., Cui, J. Z., Meng, Z.-Q., Zou, Y. L., Guo, X. S., Chen, X., Wang, X., Yan, L.-T., Han, W. X., et al. (2020) · Figshare · doi:10.6084/m9.figshare.12719930
Medicinal Chemistry of Fourth-generation Tyrosine Kinase Inhibitors
Zayed, M. F. (2026) · Mini-Reviews in Medicinal Chemistry · doi:10.2174/0113895575451047260306044852
Chen, J., Lin, L., Wang, Y., Lin, Y., Li, Y., Zhang, W., Fu, Y., Xie, J., Zhu, J., Sun, C., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.04.22.719826
Seo, J., & Kim, J.-H. (2026) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2026.112117
From single to dual targeting: Recent advances in EGFR-based dual inhibitors for cancer therapy
YALCIN, Z. S., Alagöz, M. A., & Algül, Ö. (2026) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2026.119400
BindingDB Entry 50016732: The Ascension of Targeted Covalent Inhibitors.
BindingDB (2023) · UC San Diego · doi:10.7270/q23f4tpf
BindingDB (2018) · UC San Diego · doi:10.7270/q2rf5x00
BindingDB Entry 50047333: Recent progress on third generation covalent EGFR inhibitors.
BindingDB (2017) · UC San Diego · doi:10.7270/q2c24z9v
BindingDB Entry 50014256: A sulfonyl fluoride derivative inhibits EGFR
BindingDB (2022) · UC San Diego · doi:10.7270/q2sq946r
BindingDB (2022) · UC San Diego · doi:10.7270/q2m04964
BindingDB Entry 50008580: Discovery of a potent dual ALK and EGFR T790M inhibitor.
BindingDB (2021) · UC San Diego · doi:10.7270/q2wh2tcg
Metadata
- Authors
- Sequist, L. V., Soria, J.-C., Goldman, J. W., Wakelee, H. A., Gadgeel, S. M., Varga, A., Papadimitrakopoulou, V., Solomon, B. J., Oxnard, G. R., Dziadziuszko, R., Aisner, D. L., Doebele, R. C., Galasso, C., Garon, E. B., Heist, R. S., Logan, J., Neal, J. W., Mendenhall, M. A., Nichols, S., Piotrowska, Z., Wozniak, A. J., Raponi, M., Karlovich, C. A., Jaw-Tsai, S., Isaacson, J., Despain, D., Matheny, S. L., Rolfe, L., Allen, A. R., & Camidge, D. R.
- Affiliations
- Université Paris-Sud (FR)
- University of California, Los Angeles (US)
- Stanford Cancer Institute (US)
- Wayne State University (US)
- Institut Gustave Roussy (FR)
- The University of Texas MD Anderson Cancer Center (US)
- Peter MacCallum Cancer Centre (AU)
- Harvard University (US)
- University of Colorado Cancer Center (US)
- Massachusetts General Hospital (US)
- Clovis Oncology (United States) (US)
- ORCID
- Sequist, Lecia V.
- Soria, Jean-Charles
- Goldman, Jonathan W.
- Wakelee, Heather A.
- Gadgeel, Shirish M.
- Papadimitrakopoulou, Vassiliki
- Solomon, Benjamin J.
- Oxnard, Geoffrey R.
- Aisner, Dara L.
- Doebele, Robert C.
- Garon, Edward B.
- Heist, Rebecca S.
- Neal, Joel W.
- Piotrowska, Zofia
- Raponi, Mitch
- Karlovich, Chris A.
- Despain, Darrin
- Camidge, D. Ross
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2015-04-30
- Volume
- 372
- Issue
- 18
- Pages
- 1700-1709
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2126177831
- Cited by
- 665
- References
- 25
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 13 · 2023: 30 · 2022: 20 · 2021: 29 · 2020: 39 · 2019: 39 · 2018: 60 · 2017: 133 · 2016: 190 · 2015: 90
- FWCI
- 125.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Diagnosis and Treatment
- Keywords
- rociletinib, EGFR-mutant non-small cell lung cancer, T790M mutation, EGFR inhibitors, acquired drug resistance, tyrosine kinase inhibitors, maximum tolerated dose, hyperglycemia, objective response rate, pharmacokinetics, anticancer activity, safety and tolerability, dose-limiting toxicity
- MeSH terms
- Acrylamides, Aged, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Dose-Response Relationship, Drug, Female, Humans, Hyperglycemia, Lung Neoplasms, Male, Middle Aged, Mutation, Pyrimidines, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, ErbB Receptors
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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.
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