The DOI matches its Crossref record; 41 of the 42 references it cites were found in a registry or an index, and 1 are not checked yet; 1 of the 16 sources its claims cite were checked for support.
The Allelic Context of the C797S Mutation Acquired upon Treatment with Third-Generation EGFR Inhibitors Impacts Sensitivity to Subsequent Treatment Strategies
Open accessPublished version of a preprint
Abstract
Purpose: A secondary EGFR mutation, T790M, is the most common resistance mechanism in EGFR-mutant adenocarcinomas that have progressed on erlotinib. Third-generation EGFR inhibitors capable of inhibiting mutant EGFR with T790M produce responses in nearly two thirds of patients. However, acquired resistance mechanisms in patients treated with these drugs are yet to be described. Experimental Design: To study acquired resistance to third-generation EGFR inhibitors, T790M-positive cells derived from an erlotinib-resistant cancer were made resistant to a third-generation TKI and then characterized using cell and molecular analyses. Results: Cells resistant to a third-generation TKI acquired an additional EGFR mutation, C797S, which prevented suppression of EGFR. Our results demonstrate that the allelic context in which C797S was acquired may predict responsiveness to alternative treatments. If the C797S and T790M mutations are in trans, cells will be resistant to third-generation EGFR TKIs, but will be sensitive to a combination of first- and third-generation TKIs. If the mutations are in cis, no EGFR TKIs alone or in combination can suppress activity. If C797S develops in cells wild-type for T790 (when third-generation TKIs are administered in the first-line setting), the cells are resistant to third-generation TKIs, but retain sensitivity to first-generation TKIs. Conclusions: Mutation of C797S in EGFR is a novel mechanism of acquired resistance to third-generation TKIs. The context in which the C797S develops with respect to the other EGFR alleles affects the efficacy of subsequent treatments. Clin Cancer Res; 21(17); 3924–33. ©2015 AACR. See related commentary by Ayeni et al., p. 3818
Verified 2026-10-06 · 1 reference not checked yet
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24 Own result · 18 Own interpretation · 8 Not checked yet · 3 Own method · 1 Partly supported · accuracy not yet measured
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In the paper
“Sequencing of the kinase domain of EGFR revealed a single point mutation resulting in a cysteine to serine change at position 797 (C797S). This mutation was present in the MGH121 Res # 1 cells, but not the MGH121 parental cells (Figure 1D).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“expression of mutant EGFR with C797S in PC9 cells results in a significant increase in the IC50 of afatinib compared to parental PC9 cells.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Of note, the concentration of afatinib required to suppress the growth of cells expressing the Exon 19 Del/C797S construct was markedly higher than the PC9 parental cells (Figure 4B)”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, none of the EGFR TKIs suppressed EGFR signaling in MGH121 Res # 1 cells.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plainSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“Our data reveal that at a concentration of 1μM, afatinib can inhibit mutant EGFR with C797S in the absence of T790M.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The sensitivity of the MGH121 parental and Res # 1 cells to different EGFR TKIs correlate with the ability of the inhibitors to block EGFR signaling.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Finally, EGFR in the triple mutant (cis scenario) was resistant to all three generations of TKI as well as the combination of gefitinib and WZ4002 (Figure 3B, lanes 14-18).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Of note, the second generation inhibitor, afatinib, suppressed EGFR when C797S and T790M were in trans.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Conversely, EGFR with the Exon 19 del/C797S double mutant was inhibited by gefitinib and afatinib, but not WZ4002 (Fig 3B, lanes 5-8).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“By comparison, PC9 triple mutant cells were resistant to all EGFR inhibitors that were tested.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plain- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 21
- The quote only partly states this claim. 2
- Probably not a substantial claim. 6
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“C797 is located opposite T790 in the ATP binding pocket and forms a covalent bond with all third-generation TKIs and is necessary for the inhibitor to suppress EGFR (21).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
What the sources say
- Partly supportedcites [21] Zhou, 2009, Novel mutant-selective EGFR kinase inhibitors against EGFR T790M, Nature sourceExperimental — accuracy not yet measured
The crystal-structure passage (section labeled Abstract; page unavailable) places WZ4002 in the ATP-binding cleft and reports a covalent bond with Cys797. Another passage in the same section says the WZ compounds rely on that bond for potent cellular inhibition. The paper does not establish that C797 lies opposite T790 or that all third-generation EGFR TKIs bond with C797 and require it to suppress EGFR. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
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
“This cell line, MGH121, was resistant to the first generation EGFR TKI gefitinib, consistent with the presence of the T790M resistance mutation, but was highly sensitive to the third generation TKI WZ4002 (Figure 1A).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaincorrelationalSingle case- Asserted: passes — The authors put it forward as true.
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In the paper
“WZ4002 treatment failed to suppress EGFR phosphorylation and downstream signaling in these cells (Figure 1C).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plainSingle case- Asserted: passes — The authors put it forward as true.
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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
“The resulting resistant model, MGH121 Res # 1, was highly resistant to WZ4002 (Figure 1A, B)”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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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
“In the MGH121 parental cells, gefitinib failed to suppress EGFR phosphorylation and downstream pathway components ERK and S6, whereas afatinib, WZ4002, CO-1686 and AZD-9291 were all able to do so (Figure 2B).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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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
“Indeed, MGH121 parental cells are also sensitive to the second generation inhibitor afatinib and other third generation inhibitors CO-1686 and AZD-9291 (Figure 2A left). These inhibitors similarly bind covalently to C797 of EGFR (22, 23, 35) and are ineffective at suppressing the growth of MGH121 Res # 1 cells (Figure 2A right)”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plainSingle case- Asserted: passes — The authors put it forward as true.
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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
“We observed results consistent with those from the previous over-expression experiment: The trans setting induced resistance to third generation TKI, but the combination of gefitinib and WZ4002 inhibited EGFR signaling (Figure 3C) and cell growth (Figure 3D). However, this combination was not effective when all the mutations were in cis.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“When Exon 19 del/T790M and Exon 19 del/C797S were co-expressed in the same cells to model the trans scenario, treatment with either gefitinib or WZ4002 alone each partially suppressed EGFR phosphorylation, consistent with each drug suppressing a fraction of the EGFR protein expressed in the cells. The combination of gefitinib and WZ4002, however, completely inhibited EGFR phosphorylation (Figure 3”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“In this system, EGFR Exon 19 del/T790M phosphorylation was effectively inhibited by second and third generation TKIs, while phosphorylation of EGFR Exon 19 Del/T790M/C797S was not suppressed by any of the inhibitors tested (Figure 2C).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“As expected for Exon 19 del/T790M, the first generation TKI gefitinib did not inhibit EGFR phosphorylation while afatinib and WZ4002 suppressed it (Figure 3B, lanes 1-4).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“Neither afatinib nor WZ4002 were able to block EGFR phosphorylation or the downstream signaling in these cells (Figure 2D). Accordingly, the growth of these cells was resistant to all generations of EGFR TKIs (Figure 2E).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“PC9 Exon 19 Del/C797S cells were indeed resistant to WZ4002, but sensitive to gefitinib and afatinib (Figure 4 A, B).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“MGH121 Res # 1 have over 9 fold more EGFR gDNA compared to normal control DNA, equal to roughly 18 copies of EGFR and consistent with amplification versus the MGH121 parental cells.”
- Also stated in: § Results · plain
“variant allele frequency analysis revealed that the C797S mutant allele was specifically amplified in the MGH121 Res # 1, as the majority of EGFR alleles harbor this mutation (Supplemental Figure 1B).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaincorrelationalSingle case- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · 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
“This analysis revealed that the T790M and C797S were in cis in MGH121 Res # 1 cells, as the C797S mutation coexisted with T790M on 85% of alleles (n = 101). The other 15% of alleles had no mutations in exon 20. Thus, there were no exon 20 alleles harboring only T790M or C797S (n = 18, Figure 3A).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
plaincorrelationalSingle case- Asserted: passes — The authors put it forward as true.
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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
“Cells resistant to a third generation TKI acquired an additional EGFR mutation, C797S, which prevented suppression of EGFR.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Abstract > Results
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“A secondary epidermal growth factor receptor (EGFR) mutation, T790M, is the most common resistance mechanism in EGFR mutant adenocarcinomas that have progressed on erlotinib.”
- Also stated in: § Introduction · plain
“T790M is the most common resistance mechanism in these cancers and is observed in over 50% of resistant biopsies (12, 14).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Abstract > Purpose
What the sources say
- Not checked yetcites [12] Yu, 2013, Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers, Clin Cancer Res source
- Not checked yetcites [14] Sequist, 2011, Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors, Sci Transl Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Also stated in: § Introduction · plain
None of the sources cited for this claim have been checked yet.
In the paper
“The covalent interaction with C797 has also been demonstrated to be important to the activity of the pan-HER inhibitor CI-1033 (38, 39) and exogenous expression of a C797A mutant can confer resistance to another second generation inhibitor, HKI-272 (36).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Discussion
What the sources say
- Not checked yetcites [38] Godin-Heymann, 2008, The T790M “gatekeeper” mutation in EGFR mediates resistance to low concentrations of an irreversible EGFR inhibitor, Mol Cancer Ther source
- Not checked yetcites [39] Lee, 2013, Noncovalent wild-type-sparing inhibitors of EGFR T790M, Cancer Discov source
- Not checked yetcites [36] Lovly, 2014, Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer, Nat Med source
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These experiments demonstrate an important difference in drug response if the T790M and C797S mutations occur on the same or on different alleles, a result that has clinical implications.”
- Also stated in: § Discussion · hedged
“For T790M positive, erlotinib-resistant NSCLCs that develop a C797S mutation following treatment with a third generation TKI, the configuration of the T790M and C797S mutations affect how the cells could respond to therapy.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Results
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Discussion · hedged
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
“Experiments involving the 293FT cells were completed within 6 months of purchasing from Invitrogen and did not undergo any further testing.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Materials and methods > Reagents and cell culture
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If the C797S and T790M mutations are in trans, cells will be resistant to third generation EGFR TKIs, but will be sensitive to a combination of first and third generation TKIs.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Abstract > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“PC9 cells were verified by STR analysis within 6 months to 1 year of experimentation.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Materials and methods > Reagents and cell culture
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If C797S develops in cells wild type for T790 (when third generation TKIs are administered in the first line setting), the cells are resistant to third generation TKIs, but retain sensitivity to first generation TKIs.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Abstract > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: PC9 cells are sensitive to all classes of EGFR inhibitors.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Importantly, these results suggest that combining first and third generation TKIs in the first line setting may be particularly powerful since neither a T790M nor a C797S mutation alone would be sufficient to drive resistance to this combination.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Of note, a similar reduction in activity of second generation inhibitors towards EGFR is caused by T790M (36, 40).”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Discussion
What the sources say
- Not checked yetcites [36] Lovly, 2014, Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer, Nat Med source
- Not checked yetcites [40] Avizienyte, 2008, Comparison of the EGFR resistance mutation profiles generated by EGFR-targeted tyrosine kinase inhibitors and the impact of drug combinations, Biochem J source
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably 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
“Once completed the cell line was sequenced to confirm that it matched the patient effusion sample.”
§ The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies > Materials and methods > Reagents and cell culture
plainSingle case- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Acquired resistance mechanisms in patients treated with third-generation EGFR inhibitors have not yet been described.
“However, acquired resistance mechanisms in patients treated with these drugs are yet to be described.”
The paper relies on this without support.
PC9 cells are sensitive to all classes of EGFR inhibitors.
“PC9, which is sensitive to all classes of EGFR inhibitors.”
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
“In a study analysing cell-free DNA of 15 patients with resistance to AZD9291 by next-generation sequencing (NGS), distinct EGFR genotypes before and after AZD9291 treatment were defined: acquired C797S together with a T790M mutation (40%), T790M mutation without a C797S mutation (33%) and loss of the T790M mutation without a C797S mutation (27%).33”
From Mechanisms of resistance to EGFR-targeted drugs: lung cancer (2016) · cites this paper as [33]
In the citing paper
“In these models, the tumour growth is still dependent on EGFR signalling and under the strong selective pressure of EGFR-TKIs, the tumour developed secondary and tertiary mutations in the EGFR gene (T790M and C797S, respectively).33”
From Mechanisms of resistance to EGFR-targeted drugs: lung cancer (2016) · cites this paper as [33]
In the citing paper
“Furthermore, C797S mutation appeared to be sensitive to 1G‐TKI, and even C797S+T790M in trans can be treated with a combination of 1G and 3G‐TKI.41”
From Not all epidermal growth factor receptor mutations in lung cancer are created equal: Perspectives for individualized treatment strategy (2016) · cites this paper as [41]
Citations
Cites
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Gefitinib or Chemotherapy for Non–Small-Cell Lung Cancer with Mutated EGFR
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Metadata
- Authors
- Niederst, M. J., Hu, H., Mulvey, H. E., Lockerman, E. L., Garcia, A. R., Piotrowska, Z., Sequist, L. V., & Engelman, J. A.
- Affiliations
- Harvard University (US)
- Corresponding author
- Engelman, Jeffrey A.
- ORCID
- Venue
- Clinical Cancer Research
- Published
- 2015-08-31
- Volume
- 21
- Issue
- 17
- Pages
- 3924-3933
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC4587765
- OpenAlex
- W1908940658
- Cited by
- 583
- References
- 42
- Citations by year
- 2026: 33 · 2025: 47 · 2024: 47 · 2023: 50 · 2022: 49 · 2021: 57 · 2020: 66 · 2019: 53 · 2018: 65 · 2017: 57 · 2016: 49 · 2015: 10
- FWCI
- 48.25
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA137008)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- C797S mutation, T790M mutation, acquired drug resistance, third-generation EGFR tyrosine kinase inhibitors, erlotinib resistance, EGFR-mutant lung adenocarcinoma, predictive biomarkers
- MeSH terms
- Alleles, Antineoplastic Agents, Cell Survival, Codon, Humans, Mutation, Gene Expression, Drug Resistance, Neoplasm, Amino Acid Substitution, Cell Line, Tumor, 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.
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