Evidence map›Paper›PMID 41167084›Full record

Trial reportESMO open2025

Negative hyperselection of patients with stage III colon cancer receiving anti-EGFR-based adjuvant treatment.

M Ambrosini, H Blons, S Garinet, C Mulot, D Le Corre, S Mouillet-Richard, F Pietrantonio, M Sroussi, C Lepage, P Laurent-Puig and 1 more

Abstract readRandomized Controlled TrialClinical Trial, Phase III
PubMed Full text at PMC Publisher
In one paragraph

Trial report in ESMO open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

M AmbrosiniInstitut du Cancer Paris Carpem, Assistance Publique-Hôpitaux de Paris, Université Paris Cité, Department of Gastroenterology and Gastrointestinal Oncology, Georges-Pompidou European Hospital, Paris, France; Centre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France; Department of Medical Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
H BlonsCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France; Assistance Publique-Hôpitaux de Paris, Department of Biochemistry, Pharmacogenetics and Molecular Oncology, European Georges-Pompidou Hospital, Paris Cancer Institute CARPEM, Paris, France; Institut du Cancer Paris Carpem, Assistance Publique-Hôpitaux de Paris, Université Paris Cité, Genomic Medicine of Tumors and Cancers Department, Georges-Pompidou European Hospital, Paris, France.
S GarinetCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France; Assistance Publique-Hôpitaux de Paris, Department of Biochemistry, Pharmacogenetics and Molecular Oncology, European Georges-Pompidou Hospital, Paris Cancer Institute CARPEM, Paris, France; Institut du Cancer Paris Carpem, Assistance Publique-Hôpitaux de Paris, Université Paris Cité, Genomic Medicine of Tumors and Cancers Department, Georges-Pompidou European Hospital, Paris, France.
C MulotCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France.
D Le CorreCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France.
S Mouillet-RichardCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France.
F PietrantonioDepartment of Medical Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
M SroussiCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France.
C LepageUniversité de Bourgogne, CHU Dijon-Bourgogne, INSERM U1231, Dijon, France.
P Laurent-PuigCentre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France.
J TaiebInstitut du Cancer Paris Carpem, Assistance Publique-Hôpitaux de Paris, Université Paris Cité, Department of Gastroenterology and Gastrointestinal Oncology, Georges-Pompidou European Hospital, Paris, France; Centre de Recherche des Cordeliers, INSERM, CNRS, Université Paris Cité, Sorbonne Université, USPC, Equipe labellisée Ligue Nationale Contre le Cancer, Paris, France. Electronic address: jtaieb75@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe paradigm of molecular negative hyperselection, beyond RAS and BRAF, identifies metastatic colorectal cancer (mCRC) patients with the greatest benefit from anti-epidermal growth factor receptor (anti-EGFR) agents. We hypothesize that applying this model to stage III colon cancer (CC) might identify a subgroup deriving benefit from anti-EGFRs in the adjuvant setting. PATIENTS AND

methodsWe used a 'simplified PRESSING panel' grouping genomic alterations related to anti-EGFR primary resistance in mCRC, to select the proficient mismatch repair or microsatellite stable (pMMR/MSS) population of the randomized phase III PETACC-8 clinical trial, testing adjuvant FOLFOX ± cetuximab in resectable stage III CC. Patients without any tumor alterations in RAS/BRAF, or the simplified PRESSING panel were defined as 'hyperselected' (HS), whereas those with at least one such alteration were considered 'gene altered' (GA).

resultsOf 1421 eligible patients, 536 (37.7%) were HS and 885 (62.2%) GA. HS patients were more frequently male, with distal tumor of lower stage and grade. HS patients showed improved 5-year relapse-free survival (RFS) (81% versus 68%) and overall survival (OS) (89% versus 77%) as compared with GA patients. A statistically significant interaction was observed for RFS between molecular profile and treatment (P = 0.05). Among HS patients, adding cetuximab to FOLFOX yielded a 5-year RFS of 83% versus 78% with FOLFOX alone [hazard ratio (HR) 0.81, 95% confidence interval (CI) 0.55-1.19, P = 0.28]. Adding distal tumor location further improved the HR to 0.72 (P for interaction = 0.03). No significant interaction for OS was observed. In GA patients, the addition of cetuximab to FOLFOX was detrimental for RFS and OS.

conclusionsHS was prognostic for RFS and OS in patients with resected stage III pMMR/MSS CC and associated with a trend toward improved RFS with the addition of cetuximab to adjuvant FOLFOX. Conversely, cetuximab seems detrimental in patients with GA tumors. These data may help to improve patient selection in future adjuvant clinical trials testing anti-EGFR therapies.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsColonic NeoplasmsAdultAgedCetuximabChemotherapy, AdjuvantErbB ReceptorsFemaleFluorouracilHumansLeucovorinMaleMiddle AgedNeoplasm StagingOrganoplatinum CompoundsCetuximabEGFR protein, humanErbB ReceptorsFluorouracilLeucovorinOrganoplatinum Compoundsadjuvantcetuximabcolon cancermolecular hyperselectionnegative hyperselection

Identifiers

PMID41167084
PMCPMC12607000

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Registered trials

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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.