Evidence map›Paper›PMID 42097147›Full record

ArticleCell reports. Medicine2026

A human iPSC-derived sensory neuron platform for high-throughput discovery of neuroprotectants against chemotherapy-induced peripheral neuropathy.

Veselina Petrova, Caitlin E Mills, Clemens Hug, Aysel Cetinkaya-Fisgin, Jennifer Splaine, Sepideh Fouladzadeh, Sara Hakim, Rasheen Powell, Shannon Zhen, Mirra Chung and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

23 authors.

Veselina PetrovaF.M. Kirby Neurobiology Center, Program in Neurobiology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
Caitlin E MillsLaboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston, MA, USA; Department of Systems Biology, Harvard Medical School, Boston, MA, USA.
Clemens HugLaboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston, MA, USA.
Aysel Cetinkaya-FisginDepartment of Neurology, Neuromuscular Division, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Jennifer SplaineICCB-Longwood Screening Facility, Harvard Medical School, 250 Longwood Avenue, Boston, MA, USA.
Sepideh FouladzadehDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Sara HakimF.M. Kirby Neurobiology Center, Program in Neurobiology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
Rasheen PowellF.M. Kirby Neurobiology Center, Program in Neurobiology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
Shannon ZhenF.M. Kirby Neurobiology Center, Program in Neurobiology, Boston Children's Hospital, Boston, MA, USA.
Mirra ChungLaboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston, MA, USA; Department of Systems Biology, Harvard Medical School, Boston, MA, USA.
Gary A BradshawLaboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston, MA, USA.
Tao DengNational Center for Advancing Translational Sciences (NCATS), Division of Preclinical Innovation, Stem Cell Translation Laboratory (SCTL), National Institutes of Health (NIH), Rockville, MD, USA.
Ilyas SingecNational Center for Advancing Translational Sciences (NCATS), Division of Preclinical Innovation, Stem Cell Translation Laboratory (SCTL), National Institutes of Health (NIH), Rockville, MD, USA.
Qing WangDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA, USA.
Riki KawaguchiDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA, USA.
Harathi JonnagaddalaDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Lee B BarrettF.M. Kirby Neurobiology Center, Program in Neurobiology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
Jennifer A SmithICCB-Longwood Screening Facility, Harvard Medical School, 250 Longwood Avenue, Boston, MA, USA.
Marian KalocsayDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Benjamin M GyoriDepartment of Bioengineering, Northeastern University, Boston, MA, USA; Khoury College of Computer Sciences, Northeastern University, Boston, MA, USA.
Ahmet HokeDepartment of Neurology, Neuromuscular Division, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Peter K SorgerLaboratory of Systems Pharmacology, Harvard Program in Therapeutic Science, Harvard Medical School, Boston, MA, USA; Department of Systems Biology, Harvard Medical School, Boston, MA, USA.
Clifford J WoolfF.M. Kirby Neurobiology Center, Program in Neurobiology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA. Electronic address: clifford.woolf@childrens.harvard.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a major dose-limiting side effect of cancer treatment, yet the lack of predictive human models continues to hinder therapeutic progress. Here, we establish a scalable and reproducible model of paclitaxel-induced axon degeneration and neurotoxicity in human iPSC-derived sensory neurons, suitable for high-throughput identification of neuroprotective compounds. Using this platform, we screen a library of 192 kinase inhibitors and identify 19 hits that commonly inhibit three STE20 kinases-MAP4K4, MINK1, and TNIK. Genetic knockdown studies reveal that multi-kinase inhibition of these kinases is required for neuroprotection against paclitaxel. Consistently, selective pharmacological inhibition of the identified STE20 kinases rescues paclitaxel-induced axon degeneration in iPSC-derived sensory neurons and primary human dorsal root ganglia (DRG) and preserves intraepidermal nerve fiber density in a mouse model of CIPN. Together, these findings establish a translational human sensory neuron platform that enables target validation and drug discovery for CIPN.

Indexed as

Antineoplastic AgentsHigh-Throughput Screening AssaysInduced Pluripotent Stem CellsNeuroprotective AgentsPeripheral Nervous System DiseasesSensory Receptor CellsAnimalsAxonsDisease Models, AnimalDrug DiscoveryGanglia, SpinalHumansMicePaclitaxelProtein Kinase InhibitorsAntineoplastic AgentsNeuroprotective AgentsPaclitaxelProtein Kinase Inhibitorsaxon degenerationchemotherapy-induced peripheral neuropathyhigh-throughput screeningiPSC-derived sensory neuronsneuroprotective small moleculesSTE20 kinases

Identifiers

PMID42097147
PMCPMC13198234

What OpenQuestion holds

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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.