Cited by 291Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCancer Genomics and Diagnostics

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Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer

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Shah, Khyati N., Bhatt, Roma, Rotow, Julia, Rohrberg, Julia, Olivas, Victor, Wang, Victoria E., Hemmati, Golzar, Martins, Maria M., Maynard, Ashley, Kuhn, Jonathan, Galeas, Jacqueline, Donnella, Hayley J., Kaushik, Swati, Ku, Angel, Dumont, Sophie, Krings, Gregor, Haringsma, Henry J., Robillard, Liliane, Simmons, Andrew D., Harding, Thomas C., McCormick, Frank, Goga, Andrei, Blakely, Collin M., Bivona, Trever G., Bandyopadhyay, Sourav·2019·Nature Medicine

DOI 10.1038/s41591-018-0264-7PMC PMC6324945

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Abstract

Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance. How tumors transition between drug responsiveness, tolerance and resistance, especially in the absence of preexisting subclones, remains unclear. In epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual disease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity. Nongenetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chronic EGFR inhibition where it mitigates drug-induced apoptosis. Aurora kinase inhibitors suppress this adaptive survival program, increasing the magnitude and duration of EGFR inhibitor response in preclinical models. Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individuals with EGFR-mutant lung adenocarcinoma. These findings delineate a molecular path whereby drug resistance emerges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance.

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Authors: Shah, K. N., Bhatt, R., Rotow, J., Rohrberg, J., Olivas, V., Wang, V. E., Hemmati, G., Martins, M. M., Maynard, A., Kuhn, J., Galeas, J., Donnella, H. J., Kaushik, S., Ku, A., Dumont, S., Krings, G., Haringsma, H. J., Robillard, L., Simmons, A. D., Harding, T. C., McCormick, F., Goga, A., Blakely, C. M., Bivona, T. G., & Bandyopadhyay, S.
Affiliations: University of California, San Francisco (US)
Clovis Oncology (United States) (US)
Corresponding author: Bandyopadhyay, Sourav
ORCID: Shah, Khyati N.
Rotow, Julia
Rohrberg, Julia
Wang, Victoria E.
Hemmati, Golzar
Maynard, Ashley
Kuhn, Jonathan
Galeas, Jacqueline
Donnella, Hayley J.
Kaushik, Swati
Ku, Angel
Dumont, Sophie
Krings, Gregor
Simmons, Andrew D.
McCormick, Frank
Goga, Andrei
Blakely, Collin M.
Bivona, Trever G.
Bandyopadhyay, Sourav
Venue: Nature Medicine
Publisher: Springer Science and Business Media LLC
Published: 2018-11-26
Volume: 25
Issue: 1
Pages: 111-118
ISSN: 1078-8956 (ISSN-L)
1546-170X
DOI: 10.1038/s41591-018-0264-7
PMC: PMC6324945
OpenAlex: W2901591386
Cited by: 286
References: 43
Citations by year: 2026: 19 · 2025: 43 · 2024: 33 · 2023: 37 · 2022: 44 · 2021: 54 · 2020: 37 · 2019: 18 · 2018: 1
FWCI: 20.70
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Medicine (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: Doris Duke Charitable Foundation (2018110)
National Cancer Institute (R01CA169338, U01CA217882, U01CA168370, U54CA224081)
National Institute of General Medical Sciences (R01GM107671)
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: AURKA, TPX2, EGFR inhibitors, acquired drug resistance, EGFR-mutant lung adenocarcinoma, drug tolerance, residual disease, apoptosis, synthetic lethality, Aurora kinase inhibitors
MeSH terms: Animals, Cell Count, Humans, Lung Neoplasms, Microtubule-Associated Proteins, Mutation, Nuclear Proteins, Phosphorylation, Apoptosis, Neoplasm, Residual, Cell Cycle Proteins, Drug Resistance, Neoplasm, Cell Line, Tumor, Protein Kinase Inhibitors, Mice, Aurora Kinase A, ErbB Receptors

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Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer

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