Erratum to EGFR exon 20 insertion mutations and ERBB2 mutations in lung cancer: a narrative review on approved targeted therapies from oral kinase inhibitors to antibody-drug conjugates
Erratum

Erratum to EGFR exon 20 insertion mutations and ERBB2 mutations in lung cancer: a narrative review on approved targeted therapies from oral kinase inhibitors to antibody-drug conjugates

Editorial Office

Translational Lung Cancer Research

Correspondence to: Editorial Office. Translational Lung Cancer Research. Email: editor@tlcr.org.

Submitted Aug 30, 2024. Accepted for publication Sep 13, 2024. Published online Oct 12, 2024.

doi: 10.21037/tlcr-2024-1


Erratum to: Transl Lung Cancer Res 2023;12:1590-610.

In the July 2023 issue of Translational Lung Cancer Research, the article “EGFR exon 20 insertion mutations and ERBB2 mutations in lung cancer: a narrative review on approved targeted therapies from oral kinase inhibitors to antibody-drug conjugates” authored by Dr. Sentana-Lledo et al. (1) was published with some minor errors in Figure 2 and its figure legend. The data “0.5%” under “G719X” should be corrected as “5%”. In the figure legend, the sentence “EGFR-S768I is placed out of position for better representation” should be added.

The whole Figure 2 should be corrected as:

Figure 2 Subtypes of EGFR mutations with a focus on preclinical patterns of response/resistance to EGFR TKIs. (A) Representation of the EGFR protein by key gene numbers, overlaid with clinically-relevant types of mutations mostly centered within the kinase domain. The prevalence of these mutation subtypes are indicated by exon location. The frequency of EGFR mutations was obtained from (17-22,49-56). EGFR-S768I is placed out of position for better representation. (B) Summary of preclinical models driven by selected EGFR mutations paired with the in vitro sensitivity and also in vitro selectivity pattern against EGFR WT of the diversity of approved EGFR TKIs. Data was extrapolated from (23,50,57-62) and unpublished data from the authors’ translational thoracic oncology laboratory. The degree of sensitivity and resistance is indicated by number of + (sensitive/selective) or − (resistant/non-selective) signs as extrapolated from preclinical studies. Please, refer to aforementioned references for each individual half maximal inhibitory concentration (IC50) for preclinical proliferation assays. EGFR, epidermal growth factor receptor; ERBB2, erb-b2 receptor tyrosine kinase 2 (also known as HER2, human epidermal growth factor receptor-2); WT, wild-type; TKIs, tyrosine kinase inhibitors.

The authors regret for the errors and confirm that they would not change the results or conclusion of the article.

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Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.


References

  1. Sentana-Lledo D, Academia E, Viray H, et al. EGFR exon 20 insertion mutations and ERBB2 mutations in lung cancer: a narrative review on approved targeted therapies from oral kinase inhibitors to antibody-drug conjugates. Transl Lung Cancer Res 2023;12:1590-610. [Crossref] [PubMed]
Cite this article as: Editorial Office. Erratum to EGFR exon 20 insertion mutations and ERBB2 mutations in lung cancer: a narrative review on approved targeted therapies from oral kinase inhibitors to antibody-drug conjugates. Transl Lung Cancer Res 2024;13(10):2861-2863. doi: 10.21037/tlcr-2024-1

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