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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Janne, P. A., Shaw, A. T., Camidge, D. R., Giaccone, G., Shreeve, S. M., Tang, Y., Goldberg, Z., Martini, J., Xu, H., James, L. P., et al. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.01.022 · Cited by 57
Self-citationTargeted Therapy in Brain Metastases: Ready for Primetime?
Venur, V. A., & Ahluwalia, M. S. (2016) · American Society of Clinical Oncology Educational Book · doi:10.1200/edbk_100006 · Cited by 57
Yang, M., Xu, X., Cai, J., Ning, J., Wery, J. P., & Li, Q. (2016) · International Journal of Cancer · doi:10.1002/ijc.30047 · Cited by 55
Inhibition of osimertinib-resistant epidermal growth factor receptor EGFR-T790M/C797S
Lategahn, J., Keul, M., Klövekorn, P., Tumbrink, H. L., Niggenaber, J., Müller, M. P., Hodson, L. E., Flaßhoff, M., Hardick, J., Grabe, T., et al. (2019) · Chemical Science · doi:10.1039/c9sc03445e · Cited by 56
Tang, Z.-H., Jiang, X., Guo, X., Fong, C. M. V., Chen, X., & Lu, J. (2016) · Oncotarget · doi:10.18632/oncotarget.13150 · Cited by 56
Indazole-Based Covalent Inhibitors To Target Drug-Resistant Epidermal Growth Factor Receptor
Tomassi, S., Lategahn, J., Engel, J., Keul, M., Tumbrink, H. L., Ketzer, J., Mühlenberg, T., Baumann, M., Schultz‐Fademrecht, C., Bauer, S., et al. (2017) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.6b01626 · Cited by 56
Re-Evaluating Clonal Dominance in Cancer Evolution
Burrell, R. A., & Swanton, C. (2016) · Trends in cancer · doi:10.1016/j.trecan.2016.04.002 · Cited by 54
Wang, X., Goldstein, D., Crowe, P. J., & Yang, J. (2016) · OncoTargets and Therapy · doi:10.2147/ott.s94745 · Cited by 55
Advances of small molecule targeting of kinases
Berndt, N., Karim, R. M., & Schönbrunn, E. (2017) · Current Opinion in Chemical Biology · doi:10.1016/j.cbpa.2017.06.015 · Cited by 56
Biomaterials and Culture Systems for Development of Organoid and Organ-on-a-Chip Models
D’Costa, K. A., Kosic, M., Lam, A., Moradipour, A., Zhao, Y., & Radisic, M. (2020) · Annals of Biomedical Engineering · doi:10.1007/s10439-020-02498-w · Cited by 54
Receptor tyrosine kinases in PI3K signaling: The therapeutic targets in cancer
Jiang, W., & Ji, M. (2019) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2019.03.006 · Cited by 55
Tripathi, S. K., Pandey, K., Rengasamy, K. R. R., & Biswal, B. K. (2020) · Medicinal Research Reviews · doi:10.1002/med.21700 · Cited by 54
Targeting Cell Signaling Pathways in Lung Cancer by Bioactive Phytocompounds
Choudhary, N., Bawari, S., Burcher, J. T., Sinha, D., Tewari, D., & Bishayee, A. (2023) · Cancers · doi:10.3390/cancers15153980 · Cited by 56
Associations between Diabetes Mellitus and Selected Cancers
Pliszka, M., & Szablewski, L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25137476 · Cited by 53
Steen, N. V. D., Caparello, C., Rolfo, C. D., Pauwels, P., Peters, G. J., & Giovannetti, E. (2016) · OncoTargets and Therapy · doi:10.2147/ott.s97644 · Cited by 55
Discovery of a potent dual ALK and EGFR T790M inhibitor
Jang, J., Son, J. B., To, C., Bahcall, M., Kim, S. Y., Kang, S. Y., Mushajiang, M., Lee, Y., Janne, P. A., Choi, H. G., et al. (2017) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2017.04.079 · Cited by 51
Nakatani, K., Yamaoka, T., Ohba, M., Fujita, K., Arata, S., Kusumoto, S., Taki-Takemoto, I., Kamei, D., Iwai, S., Tsurutani, J., et al. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-18-0591 · Cited by 55
Mancini, M., Gal, H., Gaborit, N., Mazzeo, L., Romaniello, D., Salame, T. M., Lindzen, M., Mahlknecht, G., Enuka, Y., Burton, D. G. A., et al. (2017) · EMBO Molecular Medicine · doi:10.15252/emmm.201708076 · Cited by 52
Liao, B.-C., Lin, C., Lee, J., & Yang, J. C. (2016) · Journal of Biomedical Science · doi:10.1186/s12929-016-0305-9 · Cited by 52
Danesi, R., Fogli, S., Indraccolo, S., Re, M. D., Tos, A. P. D., Leoncini, L., Antonuzzo, L., Bonanno, L., Guarneri, V., Pierini, A., et al. (2021) · ESMO Open · doi:10.1016/j.esmoop.2020.100040 · Cited by 52
Novel irreversible covalent BTK inhibitors discovered using DNA-encoded chemistry
Guilinger, J. P., Archna, A., Augustin, M., Bergmann, A., Centrella, P. A., Clark, M. A., Cuozzo, J. W., Däther, M., Guié, M.-A., Habeshian, S., et al. (2021) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2021.116223 · Cited by 49
Biological therapies in nonsmall cell lung cancer
Zugazagoitia, J., Molina‐Pinelo, S., López‐Ríos, F., & Paz-Ares, L. G. (2017) · European Respiratory Journal · doi:10.1183/13993003.01520-2016 · Cited by 49
Srivastava, S., Jayaswal, N., Kumar, S., Sharma, P. K., Behl, T., Khalid, A., Mohan, S., Najmi, A., Zoghebi, K. A., & Alhazmi, H. A. (2023) · Cellular Signalling · doi:10.1016/j.cellsig.2023.110932 · Cited by 48
Tsakonas, G., Petris, L. D., & Ekman, S. (2017) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2017.02.004 · Cited by 48
Liao, B.-C., Lin, C., Lee, J., & Yang, J. C. (2017) · Lung Cancer · doi:10.1016/j.lungcan.2017.05.009 · Cited by 48
Xu, J., Wang, J., & Zhang, S. (2017) · Oncotarget · doi:10.18632/oncotarget.21164 · Cited by 52
Distinct Afatinib Resistance Mechanisms Identified in Lung Adenocarcinoma Harboring an EGFR Mutation
Yamaoka, T., Ohmori, T., Ohba, M., Arata, S., Murata, Y., Kusumoto, S., Andō, K., Ishida, H., Ohnishi, T., & Sasaki, Y. (2017) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-16-0482 · Cited by 49
Mayo‐de‐las‐Casas, C., Garzón‐Ibáñez, M., Jordana‐Ariza, N., García‐Peláez, B., Balada‐Bel, A., Villatoro, S., Malapelle, U., Karachaliou, N., Troncone, G., Rosell, R., et al. (2017) · Expert Review of Molecular Diagnostics · doi:10.1080/14737159.2018.1407243 · Cited by 47
Costa, D. B., & Kobayashi, S. S. (2015) · PubMed Central · doi:10.3978/j.issn.2218-6751.2015.05.05 · Cited by 46
Pirazzoli, V., Ayeni, D. O., Meador, C. B., Sanganahalli, B. G., Hyder, F., de Stanchina, E., Goldberg, S. B., Pao, W. J., & Politi, K. A. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-0620 · Cited by 46
Epidermal Growth Factor Receptor–Mutant Lung Cancer
Piotrowska, Z., & Sequist, L. V. D. (2015) · The Cancer Journal · doi:10.1097/ppo.0000000000000147 · Cited by 45
Self-citationStructural pharmacological studies on EGFR T790M/C797S
Kong, L., Ma, R., Yao, M.-Y., Yan, X.-E., Zhu, S., Zhao, P., & Yun, C. (2017) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2017.04.138 · Cited by 45
Cell-Free DNA in Oncology: Gearing up for Clinic
Ulrich, B. C., & Paweletz, C. P. (2017) · Annals of Laboratory Medicine · doi:10.3343/alm.2018.38.1.1 · Cited by 47
Frontiers of ctDNA, targeted therapies, and immunotherapy in non-small-cell lung cancer
Zhu, C., Zhuang, W., Chen, L., Yang, W., & Ou, W. (2020) · Translational Lung Cancer Research · doi:10.21037/tlcr.2020.01.09 · Cited by 46
Emerging Agents and New Mutations in EGFR-Mutant Lung Cancer
Ayeni, D. O., Politi, K. A., & Goldberg, S. B. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1211 · Cited by 44
Sesumi, Y., Suda, K., Mizuuchi, H., Kobayashi, Y., Sato, K., Chiba, M., Shimoji, M., Tomizawa, K., Takemoto, T., & Mitsudomi, T. (2016) · Lung Cancer · doi:10.1016/j.lungcan.2016.12.012 · Cited by 44
Hidaka, N., Iwama, E., Kubo, N., Harada, T., Miyawaki, K., Tanaka, K., Okamoto, I., Baba, E., Akashi, K., Sasaki, H., et al. (2017) · Lung Cancer · doi:10.1016/j.lungcan.2017.02.019 · Cited by 44
Structural basis of mutant-selectivity and drug-resistance related to CO-1686
Yan, X.-E., Zhu, S.-J., Liang, L., Zhao, P., Choi, H. G., & Yun, C.-H. (2017) · Oncotarget · doi:10.18632/oncotarget.18588 · Cited by 43
Managing Resistance to EFGR- and ALK-Targeted Therapies
Lovly, C. M., Iyengar, P., & Gainor, J. F. (2017) · American Society of Clinical Oncology Educational Book · doi:10.1200/edbk_176251 · Cited by 43
EGFR-TKI rechallenge with bevacizumab in EGFR-mutant non-small cell lung cancer
Otsuka, K., Hata, A., Takeshita, J., Okuda, C., Kaji, R., Masago, K., Fujita, S., & Katakami, N. (2015) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-015-2867-8 · Cited by 44
Li, X., & Zhou, C. (2017) · Oncotarget · doi:10.18632/oncotarget.19007 · Cited by 43
Spira, A. E., Halmos, B., & Powell, C. A. (2015) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201504-0756up · Cited by 44
Drug Resistance and its Clinical Circumvention
Moscow, J. A., Cowan, K. H., & Sikic, B. I. (2017) · Wiley eBooks · doi:10.1002/9781119000822.hfcm063 · Cited by 43
Husain, H., Scur, M. D., Murtuza, A., Bui, N. Q., Woodward, B. D., & Kurzrock, R. (2017) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-16-0105 · Cited by 44
Zhao, J. Y., Guerrero, A., Kelnar, K., Peltier, H. J., & Bader, A. G. (2017) · Lung Cancer · doi:10.1016/j.lungcan.2017.02.020 · Cited by 41
Zhang, H., Wu, W., Feng, C., Liu, Z., Bai, E., Wang, X., Lei, M., Cheng, H., Feng, H., Shi, J., et al. (2017) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2017.04.036 · Cited by 41
Murillo, M. M., Rana, S., Spencer‐Dene, B., Nye, E. L., Stamp, G., & Downward, J. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.12.003 · Cited by 41
Mapping the Pathways of Resistance to Targeted Therapies
Wood, K. C. (2015) · Cancer Research · doi:10.1158/0008-5472.can-15-1248 · Cited by 41
Socinski, M. A., Villaruz, L. C., & Ross, J. S. (2016) · The Oncologist · doi:10.1634/theoncologist.2016-0285 · Cited by 40
Park, M.-Y., Jung, M. H., Eo, E. Y., Kim, S., Lee, S. H., Lee, Y. J., Park, J. S., Cho, Y., Chung, J. H., Kim, C. H., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.16752 · Cited by 40
You, W., Liu, M., Miao, J., Liao, Y., Song, Y.-B., Cai, D.-K., Gao, Y., & Peng, H. (2018) · Journal of Cancer · doi:10.7150/jca.22361 · Cited by 40
Eldehna, W. M., Maklad, R. M., Almahli, H., Al-Warhi, T. I., Elkaeed, E. B., Abourehab, M. A. S., Abdel‐Aziz, H. A., & Kerdawy, A. M. E. (2022) · Journal of Enzyme Inhibition and Medicinal Chemistry · doi:10.1080/14756366.2022.2062337 · Cited by 40
Tao, G., & Chityala, P. K. (2021) · Toxicology Research · doi:10.1093/toxres/tfab026 · Cited by 39
Overcoming Resistance to Targeted Therapies in Cancer
Redmond, K. L., Papafili, A., Lawler, M., & Schaeybroeck, S. V. (2015) · Seminars in Oncology · doi:10.1053/j.seminoncol.2015.09.028 · Cited by 39
Han, J., Lee, K. H., Kim, S., Min, Y. J., Cho, E., Lee, Y., Lee, S.-H., Kim, H. Y., Lee, G. K., Nam, B., et al. (2016) · Cancer Research and Treatment · doi:10.4143/crt.2016.058 · Cited by 39
Cappuzzo, F., Morabito, A., Normanno, N., Bidoli, P., Conte, A. D., Giannetta, L. G., Montanino, A., Mazzoni, F., Buosi, R., Burgio, M. A., et al. (2016) · Lung Cancer · doi:10.1016/j.lungcan.2016.06.008 · Cited by 39
Ricciuti, B., Baglivo, S., Paglialunga, L., Giglio, A. D., Bellezza, G., Chiari, R., Crinò, L., & Metro, G. (2017) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758834017702820 · Cited by 39
Russo, G. L., Imbimbo, M., Corrao, G., Proto, C., Signorelli, D., Vitali, M., Ganzinelli, M., Botta, L., Zilembo, N., de Braud, F., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.17431 · Cited by 40
THERAPY OF ENDOCRINE DISEASE: Endocrine-metabolic effects of treatment with multikinase inhibitors
Fallahi, P., Ferrari, S. M., Elia, G., Ragusa, F., Paparo, S. R., Camastra, S., Mazzi, V., Miccoli, M., Benvenga, S., & Antonelli, A. (2020) · European Journal of Endocrinology · doi:10.1530/eje-20-0683 · Cited by 39
Schrock, A. B., Frampton, G. M., Herndon, D., Greenbowe, J. R., Wang, K., Lipson, D., Yelensky, R., Chalmers, Z. R., Chmielecki, J., Elvin, J. A., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1668 · Cited by 39
Piotrowska, Z., & Sequist, L. V. D. (2016) · JAMA Oncology · doi:10.1001/jamaoncol.2016.0333 · Cited by 39
Self-citationWu, D.-W., Chen, T.-C., Huang, H., & Lee, H. (2016) · Cell Death and Disease · doi:10.1038/cddis.2016.192 · Cited by 39
Dalurzo, M. L., Avilés‐Salas, A., Soares, F. A., Hou, Y., Li, Y., Строганова, А. М., Öz, B., Abdillah, A., Wan, H., & Choi, Y. (2021) · OncoTargets and Therapy · doi:10.2147/ott.s313669 · Cited by 39
Emerging roles of RAC1 in treating lung cancer patients
Zou, T., Mao, X., Yin, J., Li, X., Chen, J., Zhu, T., Li, Q., Zhou, H., & Liu, Z. (2016) · Clinical Genetics · doi:10.1111/cge.12908 · Cited by 38
Hu, W., Liu, Y., & Chen, J. (2017) · Oncotarget · doi:10.18632/oncotarget.15337 · Cited by 38
Chiba, M., Togashi, Y., Bannno, E., Kobayashi, Y., Nakamura, Y., Hayashi, H., Terashima, M., Velasco, M. A. D., Sakai, K., Fujita, Y., et al. (2017) · BMC Cancer · doi:10.1186/s12885-017-3263-z · Cited by 38
Programmed death-ligand 1 expression and T790M status in EGFR -mutant non-small cell lung cancer
Hata, A., Katakami, N., Nanjo, S., Okuda, C., Kaji, R., Masago, K., Fujita, S., Yoshida, H., Zama, K., Imai, Y., et al. (2017) · Lung Cancer · doi:10.1016/j.lungcan.2017.07.022 · Cited by 38
Endocrine-related adverse conditions induced by tyrosine kinase inhibitors
Leo, S. D., Trevisan, M., Moneta, C., & Colombo, C. (2023) · Annales d Endocrinologie · doi:10.1016/j.ando.2023.03.009 · Cited by 40
Villadolid, J. J., Ersek, J. L., Fong, M. K., Sirianno, L., & Story, E. S. (2015) · PubMed Central · doi:10.3978/j.issn.2218-6751.2015.10.01 · Cited by 37
Suda, K., Murakami, I., Sakai, K., Tomizawa, K., Mizuuchi, H., Sato, K., Nishio, K., & Mitsudomi, T. (2015) · Lung Cancer · doi:10.1016/j.lungcan.2015.11.016 · Cited by 37
Targeted therapies and immunotherapy in non-small-cell lung cancer
Cortinovis, D. L., Abbate, M. I., Bidoli, P., Capici, S., & Canova, S. (2016) · ecancermedicalscience · doi:10.3332/ecancer.2016.648 · Cited by 37
Proto, C., Imbimbo, M., Gallucci, R., Brissa, A., Signorelli, D., Vitali, M., Macerelli, M., Corrao, G., Ganzinelli, M., Greco, F. G., et al. (2016) · Translational Lung Cancer Research · doi:10.21037/tlcr.2016.10.16 · Cited by 37
Lee, J. Y., Sun, J.-M., Lim, S. H., Kim, H. S., Yoo, K. H., Jung, K. S., Song, H.-N., Ku, B. M., Koh, J., Bae, Y.-H., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1653 · Cited by 36
“Recently, third-generation EGFR TKI, AZD9291 and rociletinib demonstrated robust and durable response in both T790M-positive and -negative patients (43, 44).”
BackgroundLi, J., An, B., Song, X., Zhang, Q., Chen, C., Wei, S., Fan, R., Li, X., & Zou, Y. (2020) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2020.113019 · Cited by 36
Michels, S. Y. F., Heydt, C., van Veggel, B. A. M. H., Deschler-Baier, B., Pardo, N., Monkhorst, K., Rüsseler, V., Stratmann, J., Griesinger, F., Steinhauser, S., et al. (2019) · JCO Precision Oncology · doi:10.1200/po.18.00210 · Cited by 36
Mao, X., Chen, Z., Zhao, Y., Yu, Y., Guan, S., Woodfield, S. E., Vasudevan, S. A., Tao, L., Pang, J. C., Lu, J., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.13657 · Cited by 35
Targeting the EGFR T790M mutation in non-small-cell lung cancer
Normanno, N., Maiello, M. R., Chicchinelli, N., Iannaccone, A., Esposito, C., Cecio, R. D., D’Alessio, A., & Luca, A. D. (2016) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2017.1272582 · Cited by 37
Ding, C., Guo, X., Wang, G.-L., Wang, H.-T., Xu, G., Liu, Y.-Y., Wu, Z., Chen, Y., Wang, J., & Wang, W. (2018) · Bioscience Reports · doi:10.1042/bsr20171014 · Cited by 36
Targeting MERTK and AXL in EGFR Mutant Non-Small Cell Lung Cancer
Yan, D., Earp, H. S., DeRyckere, D., & Graham, D. K. (2021) · Cancers · doi:10.3390/cancers13225639 · Cited by 35
Advances in the diagnosis, evaluation, and management of leptomeningeal disease
Sener, U. T., Kumthekar, P., & Boire, A. A. (2021) · Neuro-Oncology Advances · doi:10.1093/noajnl/vdab108 · Cited by 35
AZD9291 in EGFR -Mutant Advanced Non-Small-Cell Lung Cancer Patients
Remon, J., & Planchard, D. (2015) · Future Oncology · doi:10.2217/fon.15.250 · Cited by 33
Treatment Algorithms for Patients with Metastatic Non-Small Cell, Non-Squamous Lung Cancer
Melosky, B. L. (2014) · Frontiers in Oncology · doi:10.3389/fonc.2014.00256 · Cited by 33
Kim, D., Lee, K. H., Han, J., Lee, J.-S., Cho, B. C., Kang, J. H., Lee, K. H., Cho, E. K., Kim, J.-S., Min, Y. J., et al. (2019) · Lung Cancer · doi:10.1016/j.lungcan.2019.07.007 · Cited by 33
Yamaoka, T., Ohmori, T., Ohba, M., Arata, S., Kishino, Y., Murata, Y., Kusumoto, S., Ishida, H., Shirai, T., Hirose, T., et al. (2016) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-16-0313 · Cited by 32
Diverse Targeted Approaches to Battle Multidrug Resistance in Cancer
Shankaraiah, N., Nekkanti, S., Ommi, O., & Soukya, P. S. L. (2018) · Current Medicinal Chemistry · doi:10.2174/0929867325666180410110729 · Cited by 32
Nile Tilapia Derived TP4 Shows Broad Cytotoxicity toward to Non-Small-Cell Lung Cancer Cells
Ting, C.-H., & Chen, J. (2018) · Marine Drugs · doi:10.3390/md16120506 · Cited by 32
Patel, H., Ansari, A., Pawara, R. H., Ansari, I., Jadhav, H., & Surana, S. J. (2018) · Journal of Receptors and Signal Transduction · doi:10.1080/10799893.2018.1557207 · Cited by 32
Bronchoscopic Re-biopsy for Mutational Analysis of Non-small Cell Lung Cancer
Kirita, K., Izumo, T., Matsumoto, Y., Hiraishi, Y., & Tsuchida, T. (2016) · Lung · doi:10.1007/s00408-016-9864-5 · Cited by 32
Engel, J., Smith, S. P., Lategahn, J., Tumbrink, H. L., Goebel, L., Becker, C., Hennes, E., Keul, M., Unger, A., Müller, H., et al. (2017) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.7b00515 · Cited by 32
Gene mutation‐based and specific therapies in precision medicine
Wang, X. (2016) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12722 · Cited by 32
Singh, S., Yeat, N. Y., Wang, Y., Lin, S., Kuo, I., Wu, K., Wang, W., Wang, W., Su, W., Wang, Y., et al. (2023) · Cell Death and Disease · doi:10.1038/s41419-023-06201-4 · Cited by 31
Uchida, J., Imamura, F., Kukita, Y., Oba, S., Kumagai, T., Nishino, K., Inoue, T., Kimura, M., & Kato, K. (2015) · Cancer Science · doi:10.1111/cas.12860 · Cited by 31
Mizuuchi, H., Suda, K., Murakami, I., Sakai, K., Sato, K., Kobayashi, Y., Shimoji, M., Chiba, M., Sesumi, Y., Tomizawa, K., et al. (2016) · Cancer Science · doi:10.1111/cas.12905 · Cited by 31
Romanidou, O., Landi, L. M., Cappuzzo, F., & Califano, R. (2016) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758834016631531 · Cited by 31
Labbé, C., Leung, Y. W., Lemes, J. G. S., Stewart, E., Brown, C., Cosio, A. P., Doherty, M. K., O'Kane, G. M., Patel, D., Cheng, N., et al. (2016) · Clinical Lung Cancer · doi:10.1016/j.cllc.2016.12.015 · Cited by 33
Sands, J. M., Li, Q., & Hornberger, J. C. (2017) · Lung Cancer · doi:10.1016/j.lungcan.2017.05.014 · Cited by 31
Song, Z., Zheng, Y., Wang, X., Su, H., Zhang, Y., & Song, Y. (2017) · Journal of Thoracic Disease · doi:10.21037/jtd.2017.09.79 · Cited by 31
Aryal, S., Park, S., Park, H., Park, C., Kim, W. C., Thakur, D., Won, Y., & Key, J. (2023) · International Journal of Nanomedicine · doi:10.2147/ijn.s432839 · Cited by 30
Recent Advances in Targetable Therapeutics in Metastatic Non-Squamous NSCLC
Bansal, P., Osman, D. I., Gan, G. N., Simon, G. R., & Boumber, Y. (2016) · Frontiers in Oncology · doi:10.3389/fonc.2016.00112 · Cited by 31
Nam, B., Rho, J. K., Shin, D., & Son, J. (2016) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2016.08.083 · Cited by 30
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
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.
A language model drew the claims from the paper on 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-06 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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 ›
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