Evidence map›Paper›PMID 36765799›Full record

ReviewCancers2023

Osimertinib Resistance: Molecular Mechanisms and Emerging Treatment Options.

Georgia Gomatou, Nikolaos Syrigos, Elias Kotteas

Abstract readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

83 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. The microRNA Expression Signature of Lung Adenocarcinoma HarboringInternational journal of molecular sciences · 2026
    Article
  7. Article
  8. Review
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  18. Article
  19. Article
  20. PTPN9 dephosphorylates IGF1RJournal of experimental & clinical cancer research : CR · 2025
    Article

23 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Georgia GomatouOncology Unit, Third Department of Medicine, "Sotiria" General Hospital for Diseases of the Chest, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0002-1031-8261
Nikolaos SyrigosOncology Unit, Third Department of Medicine, "Sotiria" General Hospital for Diseases of the Chest, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0001-8082-594X
Elias KotteasOncology Unit, Third Department of Medicine, "Sotiria" General Hospital for Diseases of the Chest, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0003-2563-0968

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of tyrosine kinase inhibitors (TKIs) targeting the mutant epidermal growth factor receptor (EGFR) protein initiated the success story of targeted therapies in non-small-cell lung cancer (NSCLC). Osimertinib, a third-generation EGFR-TKI, is currently indicated as first-line therapy in patients with NSCLC with sensitizing EGFR mutations, as second-line therapy in patients who present the resistance-associated mutation T790M after treatment with previous EGFR-TKIs, and as adjuvant therapy for patients with early stage resected NSCLC, harboring EGFR mutations. Despite durable responses in patients with advanced NSCLC, resistance to osimertinib, similar to other targeted therapies, inevitably develops. Understanding the mechanisms of resistance, including both EGFR-dependent and -independent molecular pathways, as well as their therapeutic potential, represents an unmet need in thoracic oncology. Interestingly, differential resistance mechanisms develop when osimertinib is administered in a first-line versus second-line setting, indicating the importance of selection pressure and clonal evolution of tumor cells. Standard therapeutic approaches after progression to osimertinib include other targeted therapies, when a targetable genetic alteration is detected, and cytotoxic chemotherapy with or without antiangiogenic and immunotherapeutic agents. Deciphering the when and how to use immunotherapeutic agents in EGFR-positive NSCLC is a current challenge in clinical lung cancer research. Emerging treatment options after progression to osimertinib involve combinations of different therapeutic approaches and novel EGFR-TKI inhibitors. Research should also be focused on the standardization of liquid biopsies in order to facilitate the monitoring of molecular alterations after progression to osimertinib.

Indexed as

EGFRNSCLCosimertinibresistancetargeted therapy

Identifiers

PMID36765799
PMCPMC9913144

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.