Evidence map›Paper›PMID 41646102›Full record

ArticleESMO real world data and digital oncology2024

The impact of targeted therapies on molecular alterations identified by an institutional molecular tumor board: an approach based on ESCAT classification.

K Rahmani Narj Abadi, C Dupain, I Guillou, R Sanchez, K Nedara, G Marret, S Hescot, M-P Sablin, Z Castel-Ajgal, C Neuzillet and 24 more

Abstract read
In one paragraph

Article in ESMO real world data and digital oncology, 2024. 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. Article
  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

34 authors.

K Rahmani Narj AbadiDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
C DupainDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
I GuillouDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
R SanchezDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
K NedaraDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
G MarretDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
S HescotDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
M-P SablinDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
Z Castel-AjgalDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
C NeuzilletDepartment of Medical Oncology, Institut Curie, Paris & Saint Cloud, France.
E BorcomanDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
D Bello RoufaiDepartment of Medical Oncology, Institut Curie, Paris & Saint Cloud, France.
M RodriguesDepartment of Medical Oncology, Institut Curie, Paris & Saint Cloud, France.
A Asnacios LecerfDepartment of Medical Oncology, Institut Curie, Paris & Saint Cloud, France.
C CallensDepartment of Genetics, Institut Curie, Paris, France.
O Trabelsi-GratiDepartment of Genetics, Institut Curie, Paris, France.
S MelaabiDepartment of Genetics, Institut Curie, Paris, France.
K DriouchDepartment of Genetics, Institut Curie, Paris, France.
S AntonioDepartment of Genetics, Institut Curie, Paris, France.
E LemaitreDepartment of Genetics, Institut Curie, Paris, France.
M NijnikoffDepartment of Pathology, Institut Curie, PSL Research University, Paris, France.
A Vincent SalomonDepartment of Pathology, Institut Curie, PSL Research University, Paris, France.
Y AlloryDepartment of Pathology, Institut Curie, Saint-Cloud, France.
J CyrtaDepartment of Pathology, Institut Curie, PSL Research University, Paris, France.
H GhazelianDepartment of Pathology, Institut Curie, PSL Research University, Paris, France.
E GirardBioinformatics Core Facility, INSERM U900, Mines Paris Tech, Institut Curie, Paris, France.
N ServantBioinformatics Core Facility, INSERM U900, Mines Paris Tech, Institut Curie, Paris, France.
D Stoppa-LyonnetDepartment of Genetics, Institut Curie, Paris, France.
J WongDepartment of Genetics, Institut Curie, Paris, France.
A HamzaDepartment of Genetics, Institut Curie, Paris, France.
J Masliah-PlanchonDepartment of Genetics, Institut Curie, Paris, France.
M KamalDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
I BiècheDepartment of Genetics, Institut Curie, Paris, France.
C Le TourneauDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The European Society of Medical Oncology Scale for Clinical Actionability of Molecular Targets (ESCAT) classification system provides a standardized framework for categorizing genomic alterations (GAs) of patients with recurrent, metastatic, or rare cancer. This study aimed to present outcomes of patients discussed at the molecular tumor board (MTB) in general and according to ESCAT. Patients and methods: We included 1226 patients with recurrent and/or metastatic cancer presented at the MTB from 2018 to 2022. Clinical and demographic data collected included age, gender, type of specimen, tumor type, number of prior treatments received, techniques used for molecular analyses, GAs identified, MTB recommendations, and inclusion or not into a clinical trial. The clinical endpoints collected were overall response rate (ORR), progression-free survival (PFS), and overall survival (OS), and were correlated with ESCAT. Results: Successful molecular profiling was carried out in 895 of 1226 (73%) patients. Actionable GAs were found in 595 (49%) patients, and 206 (17%) patients were oriented to matched therapies. Eventually, 101 (8%) patients received a matched therapy. For these patients, PFS and OS were significantly longer for GAs classified as ESCAT tiers I/II, compared with tiers III/IV ( Conclusions: Detection of actionable GAs through MTB molecular screening enabled to treat 8% of patients with matched therapy. Patients treated with matched therapy based on ESCAT tiers I/II had statistically longer PFS and OS, compared with ESCAT tiers III/IV.

Indexed as

actionable genomic alterationclinical trialESCAT classificationmolecular tumor boardprecision medicine

Identifiers

PMID41646102
PMCPMC12836618

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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.