ArticlePloS one2026
Higher frequency of subclonal anti-EGFR resistance mutations in post-treatment samples from patients with colorectal cancer liver metastases following anti-EGFR-based conversion chemotherapy.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsInitially unresectable colorectal liver metastases may become resectable after chemotherapy. The acquisition of somatic mutations has been demonstrated to indicate evolving tumor subclones resistant to therapy and hinder R0 resection. However, the added value of mutational profiling in a real-world setting remains to be elucidated. The objective of the present study was to identify recurrent molecular profiles in colorectal cancer liver metastases that had been pre-treated with anti-EGFR monoclonal antibodies plus chemotherapy.
methodsA retrospective, single-centre analysis of colorectal cancer liver metastases samples from 30 patients (9 pre-therapy/21 post-therapy) who received chemotherapy and anti-EGFR agents between January 2008 and February 2014 was conducted. Targeted next-generation resequencing (NGS) was performed. Subsequently, the results were compared to publicly available genomic datasets of primary colorectal cancer and colorectal cancer liver metastasis.
results145 mutations were identified (mean, 5.2 ± 1.3 mutations per sample; range 0-28, median 2, IQR 3.75). Neither mutation count nor RAS status did correlate with the achievement of resectability. NGS confirmed prior identified KRAS mutations in 4/29 patients (14.8%) and revealed further somatic RAS alterations in 5 cases. In addition to the classical colorectal cancer driver mutations, tumors exhibited recurrent mutations in genes implicated in anti-EGFR resistance such as HNF1A (34.4%, 10/29), FGFR2 (31%, 9/29), VHL (27.5%, 8/29) and PDGFR (27.5%, 8/29), ERBB2 (24.1%, 7/29), ABL1 (24.1%, 7/29), SMO (24.1%, 7/29), GNA11 (20.6%, 6/29), RET (20.6%, 6/29), STK11 (20.6%, 6/29), HRAS (20.6%, 6/29) and NRAS (17.2%, 5/29).
conclusionIn the current study, we describe a higher frequency of potential anti-EGFR treatment resistance mutations in patients who respond well to the combination of chemotherapy and anti-EGFR monoclonal antibody treatment. Nevertheless, subclonal mutations associated with resistance to anti-EGFR therapy did not affect the secondary resectability of colorectal liver metastases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.