Evidence map›Paper›PMID 37056380›Full record

ArticleCell reports methods2023

Phenotypic deconvolution in heterogeneous cancer cell populations using drug-screening data.

Alvaro Köhn-Luque, Even Moa Myklebust, Dagim Shiferaw Tadele, Mariaserena Giliberto, Leonard Schmiester, Jasmine Noory, Elise Harivel, Polina Arsenteva, Shannon M Mumenthaler, Fredrik Schjesvold and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports methods, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

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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

15 authors at 5 institutions in 3 countries.

Alvaro Köhn-LuqueOslo Centre for Biostatistics and Epidemiology, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway.
Even Moa MyklebustOslo Centre for Biostatistics and Epidemiology, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway.
Dagim Shiferaw TadeleDepartment of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, 0379 Oslo, Norway.
Mariaserena GilibertoDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Leonard SchmiesterOslo Centre for Biostatistics and Epidemiology, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway.
Jasmine NooryInstitute for Mathematics and its Applications, School of Mathematics, University of Minnesota, Minneapolis, MN 55455, USA.
Elise HarivelOslo Centre for Biostatistics and Epidemiology, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway.
Polina ArsentevaOslo Centre for Biostatistics and Epidemiology, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway.
Shannon M MumenthalerLawrence J. Ellison Institute for Transformative Medicine, Los Angeles, CA 90064, USA.
Fredrik SchjesvoldKG Jebsen Center for B-Cell Malignancies, Institute for Clinical Medicine, University of Oslo, 0450 Oslo, Norway.
Kjetil TaskénDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Jorrit M EnserinkDepartment of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, 0379 Oslo, Norway.
Kevin LederCollege of Science and Engineering, University of Minnesota, Minneapolis, MN 55455, USA.
Arnoldo FrigessiOslo Centre for Biostatistics and Epidemiology, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway.
Jasmine FooInstitute for Mathematics and its Applications, School of Mathematics, University of Minnesota, Minneapolis, MN 55455, USA.
Oslo University Hospital · NOUniversity of Oslo · NOUniversity of Minnesota · USUniversité de Bourgogne · FRUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor heterogeneity is an important driver of treatment failure in cancer since therapies often select for drug-tolerant or drug-resistant cellular subpopulations that drive tumor growth and recurrence. Profiling the drug-response heterogeneity of tumor samples using traditional genomic deconvolution methods has yielded limited results, due in part to the imperfect mapping between genomic variation and functional characteristics. Here, we leverage mechanistic population modeling to develop a statistical framework for profiling phenotypic heterogeneity from standard drug-screen data on bulk tumor samples. This method, called PhenoPop, reliably identifies tumor subpopulations exhibiting differential drug responses and estimates their drug sensitivities and frequencies within the bulk population. We apply PhenoPop to synthetically generated cell populations, mixed cell-line experiments, and multiple myeloma patient samples and demonstrate how it can provide individualized predictions of tumor growth under candidate therapies. This methodology can also be applied to deconvolution problems in a variety of biological settings beyond cancer drug response.

Indexed as

Antineoplastic AgentsNeoplasmsCell LineEarly Detection of CancerGenomicsHumansAntineoplastic Agentsdeconvolutiondrug resistancedrug screeningmechanistic modelingmultiple myelomatumor heterogeneitytumor profiling

Identifiers

PMID37056380
PMCPMC10088094
OpenAlexW4323310383

What OpenQuestion holds

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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.