Evidence map›Paper›PMID 34873056›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Predicting patient response with models trained on cell lines and patient-derived xenografts by nonlinear transfer learning.

Soufiane M C Mourragui, Marco Loog, Daniel J Vis, Kat Moore, Anna G Manjon, Mark A van de Wiel, Marcel J T Reinders, Lodewyk F A Wessels

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% of its field
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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  18. Cell cycle plasticity underlies fractional resistance to palbociclib in ER+/HER2- breast tumor cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

8 authors at 4 institutions in 3 countries.

Soufiane M C MourraguiDivision of Molecular Carcinogenesis, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.ORCID 0000-0001-6920-2696
Marco LoogDepartment of Electrical Engineering, Mathematics and Computer Science, Delft University of Technology, 2628 XE Delft, The Netherlands.ORCID 0000-0002-1298-8461
Daniel J VisDivision of Molecular Carcinogenesis, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
Kat MooreDivision of Molecular Carcinogenesis, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
Anna G ManjonDivision of Cell Biology, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.ORCID 0000-0003-3255-5062
Mark A van de WielEpidemiology and Biostatistics, Amsterdam University Medical Center, 1105 AZ Amsterdam, The Netherlands.
Marcel J T ReindersDepartment of Electrical Engineering, Mathematics and Computer Science, Delft University of Technology, 2628 XE Delft, The Netherlands; l.wessels@nki.nl m.j.t.reinders@tudelft.nl.ORCID 0000-0002-1148-1562
Lodewyk F A WesselsDivision of Molecular Carcinogenesis, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; l.wessels@nki.nl m.j.t.reinders@tudelft.nl.
The Netherlands Cancer Institute · NLLeiden University Medical Center · NLUniversity of Cambridge · GBUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preclinical models have been the workhorse of cancer research, producing massive amounts of drug response data. Unfortunately, translating response biomarkers derived from these datasets to human tumors has proven to be particularly challenging. To address this challenge, we developed TRANSACT, a computational framework that builds a consensus space to capture biological processes common to preclinical models and human tumors and exploits this space to construct drug response predictors that robustly transfer from preclinical models to human tumors. TRANSACT performs favorably compared to four competing approaches, including two deep learning approaches, on a set of 23 drug prediction challenges on The Cancer Genome Atlas and 226 metastatic tumors from the Hartwig Medical Foundation. We demonstrate that response predictions deliver a robust performance for a number of therapies of high clinical importance: platinum-based chemotherapies, gemcitabine, and paclitaxel. In contrast to other approaches, we demonstrate the interpretability of the TRANSACT predictors by correctly identifying known biomarkers of targeted therapies, and we propose potential mechanisms that mediate the resistance to two chemotherapeutic agents.

Indexed as

AnimalsAntineoplastic AgentsBiomarkers, PharmacologicalCell Line, TumorDeep LearningDisease Models, AnimalDrug Screening Assays, AntitumorForecastingGene Expression ProfilingHeterograftsHumansModels, TheoreticalAntineoplastic AgentsBiomarkers, Pharmacologicalcancerclinical drug responsemodel systemstransfer learningtranslational medicine

Identifiers

PMID34873056
PMCPMC8670522
OpenAlexW4200333648

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.