Evidence map›Paper›PMID 39754975›Full record

ArticleESMO open2025

Longer survival with precision medicine in late-stage cancer patients.

C K Mapendano, A K Nøhr, M Sønderkær, A Pagh, A Carus, T Lörincz, C A Haslund, L Ø Poulsen, A Ernst, J S Bødker and 6 more

Abstract read
In one paragraph

Article in ESMO open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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

  1. Pooled it
  2. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    Review
  3. Observational
  4. Observational
  5. Review
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

16 authors.

C K MapendanoDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark.
A K NøhrCenter for Clinical Data Science, Aalborg University and Aalborg University Hospital, Aalborg, Denmark.
M SønderkærMolecular Diagnostics and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
A PaghDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark.
A CarusDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
T LörinczDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark.
C A HaslundDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark.
L Ø PoulsenDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
A ErnstMolecular Diagnostics and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
J S BødkerMolecular Diagnostics and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
S C DahlCenter for Clinical Data Science, Aalborg University and Aalborg University Hospital, Aalborg, Denmark.
L SundeDepartment of Clinical Medicine, Aalborg University, Aalborg, Denmark; Department of Clinical Genetics and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark.
A H BrügmannDepartment of Clinical Medicine, Aalborg University, Aalborg, Denmark; Department of Pathology, Aalborg University Hospital, Aalborg, Denmark.
C VesteghemCenter for Clinical Data Science, Aalborg University and Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
I S PedersenMolecular Diagnostics and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark.
M LadekarlDepartment of Oncology and Clinical Cancer Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Aalborg, Denmark. Electronic address: morten.ladekarl@rn.dk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn a per-protocol analysis of molecularly profiled patients with treatment-refractory, end-stage cancer discussed at the National Molecular Tumor Board (NMTB), we aimed to assess the overall survival (OS) outcome of targeted treatment compared with no targeted treatment. MATERIALS AND

methodsPatients were prospectively included at a single oncological center. Whole exome and RNA sequencing (tumor-normal) were carried out, and cases were presented at the NMTB for discussion of targeted treatment. Treatment was available through a basket trial, by compassionate use or in early clinical trials.

resultsOne hundred and ninety-six patients were included from 2020 to 2023. In all but three patients a driver variant was disclosed, while 42% had simultaneous affection of more than three oncogenic pathways. In 42% of patients a druggable target was identified but two-thirds did not receive the suggested treatment. The fraction of patients initiating treatment yearly rose from 8% to 22%. For patients treated (N = 30), the clinical benefit rate was 44% and median time on treatment was 3.5 months. Druggable targets were enriched in lung cancers, while patients receiving or not receiving targeted treatment had similar clinical characteristics. The median OS was longer for patients receiving targeted treatment (15 months), but similar for patients with no druggable target and suggested targeted treatment not initiated (5 and 6 months, respectively) (P = 0.004). In multivariate analysis, targeted treatment (hazard ratio 0.43, confidence interval 0.25-0.72), few metastatic sites, and adenocarcinoma histology were predictive of improved OS while alterations of the RTK/RAS pathway were prognostically unfavorable.

conclusionsTissue-agnostic targeted treatment based on molecular tumor profiling is possible in an increasing fraction of end-stage cancer patients. In those who receive targeted treatment, results strongly suggest a significant survival benefit.

Indexed as

NeoplasmsPrecision MedicineAdultAgedAged, 80 and overFemaleHumansMaleMiddle AgedMolecular Targeted TherapyNeoplasm StagingProspective Studiesclinical trialmolecular pathway analysisprecision medicineprognosistissue agnostic

Identifiers

PMID39754975
PMCPMC11758131

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.