Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma
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The advent of genomics has led to the identification of specific "driver" mutations in oncogenic kinases, and the development of targeted small molecule inhibitors to block their tumor-driving functions. These specific inhibitors have been a clinical success, and often significantly prolong the lives of individuals with cancer. Inevitably, however, the treated tumors recur as resistance to these targeted therapies develops. Here, we review the major mechanisms by which a cancer cell can evade targeted therapy, focusing on mechanisms of resistance to kinase inhibitors in lung cancer. We discuss the promising concept of rational upfront polytherapy in lung cancer, which involves concurrently targeting multiple proteins in critical signaling pathways in a cancer cell to prevent or delay resistance.
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In the clinic, the persister state most closely corresponds to minimal residual disease from which relapse can occur if treatment is discontinued or if acquired drug resistance develops in response to continuous therapy.
“In the clinic, the persister state most closely corresponds to minimal residual disease from which relapse can occur if treatment is discontinued or if acquired drug resistance develops in response to continuous therapy.”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [27]
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- Authors
- Neel, D. S., & Bivona, T. G.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Bivona, Trever G.
- Venue
- npj Precision Oncology
- Published
- 2017-03-20
- Volume
- 1
- Issue
- 1
- ISSN
- 2397-768X (ISSN-L)
- PMC
- PMC5687582
- OpenAlex
- W2592643813
- Cited by
- 98
- References
- 76
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 6 · 2023: 8 · 2022: 11 · 2021: 14 · 2020: 23 · 2019: 16 · 2018: 9
- FWCI
- 10.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- npj Precision Oncology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Pew Charitable Trusts
- National Institutes of Health
- National Cancer Institute (R01CA169338, DP2CA174497, R01CA211052, R01CA204302)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- lung adenocarcinoma, targeted therapy resistance, kinase inhibitors, driver mutations, oncogenic kinase, polypharmacy, combination therapy, tumor recurrence, signaling pathways
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.
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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