Evidence map›Paper›PMID 40110764›Full record

ArticleThe oncologist2025

Overcoming amplification-mediated resistance to sotorasib by dose re-escalation in KRAS G12C mutant NSCLC: a case report.

Antonio Vitale, Emanuele Vita, Alessio Stefani, Alessandra Cancellieri, Filippo Lococo, Giampaolo Tortora, Emilio Bria

Abstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in The oncologist, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Review
  2. Article
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

7 authors.

Antonio VitaleComprehensive Cancer Center, Medical Oncology Department, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.ORCID 0000-0003-1582-8006
Emanuele VitaComprehensive Cancer Center, Medical Oncology Department, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Alessio StefaniComprehensive Cancer Center, Medical Oncology Department, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Alessandra CancellieriPathology Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Filippo LococoFaculty of Medicine and Surgery, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Giampaolo TortoraComprehensive Cancer Center, Medical Oncology Department, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Emilio BriaComprehensive Cancer Center, Medical Oncology Department, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.ORCID 0000-0002-2333-704X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Precision oncology has transformed non-small cell lung cancer (NSCLC) treatment by tailoring therapies to the genomic profile of the disease, significantly improving clinical outcomes. However, acquired resistance to molecularly targeted therapies remains a major challenge. This report details a 69-year-old woman with KRAS G12C-mutant metastatic NSCLC who developed resistance to sotorasib, a KRAS G12C inhibitor. Initially responding to the standard dose of 960 mg, the patient required a dose reduction to 480 mg due to liver toxicity. After 20 months, oligoprogression occurred, managed through surgical resection. Molecular analysis of the resected tissue identified KRAS amplification as a resistance mechanism. Following disease progression, re-escalation of sotorasib to 960 mg led to renewed tumor response without additional toxicity. This case highlights dose re-escalation as a potential strategy to address resistance in selected patients and underscores the critical role of molecular profiling and personalized approaches in optimizing targeted NSCLC treatments.

Indexed as

Carcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmLung NeoplasmsProto-Oncogene Proteins p21(ras)PyridinesPyrimidinesAgedFemaleHumansMutationPiperazinesKRAS protein, humanPiperazinesProto-Oncogene Proteins p21(ras)PyridinesPyrimidinessotorasibacquired resistancecase reportKRAS G12Csotorasib

Identifiers

PMID40110764
PMCPMC11923590

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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.