Evidence map›Paper›PMID 39523021›Full record

ArticleCell proliferation2025

Predicting tumour resistance to paclitaxel and carboplatin utilising genome-wide screening in haploid human embryonic stem cells.

Jonathan Nissenbaum, Emanuel Segal, Hagit Philip, Rivki Cashman, Tamar Golan-Lev, Benjamin E Reubinoff, Adi Turjeman, Ofra Yanuka, Elyad Lezmi, Oded Kopper and 1 more

Abstract read
In one paragraph

Article in Cell proliferation, 2025. 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

11 authors.

Jonathan NissenbaumNewStem LTD, Jerusalem, Israel.
Emanuel SegalThe Azrieli Center for Stem Cells and Genetic Research, Department of Genetics, Silberman Institute of Life Sciences, The Hebrew University, Jerusalem, Israel.
Hagit PhilipNewStem LTD, Jerusalem, Israel.
Rivki CashmanNewStem LTD, Jerusalem, Israel.
Tamar Golan-LevThe Azrieli Center for Stem Cells and Genetic Research, Department of Genetics, Silberman Institute of Life Sciences, The Hebrew University, Jerusalem, Israel.
Benjamin E ReubinoffHadassah Stem Cell Research Center, Goldyne Savad Institute of Gene Therapy, Department of Obstetrics and Gynecology, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Adi TurjemanThe Center for Genomic Technologies, The Hebrew University, Jerusalem, Israel.
Ofra YanukaThe Azrieli Center for Stem Cells and Genetic Research, Department of Genetics, Silberman Institute of Life Sciences, The Hebrew University, Jerusalem, Israel.
Elyad LezmiNewStem LTD, Jerusalem, Israel.
Oded KopperNewStem LTD, Jerusalem, Israel.
Nissim BenvenistyNewStem LTD, Jerusalem, Israel.ORCID https://orcid.org/0000-0001-8234-2685

Funding

Azrieli FoundationISF-Israel Precision Medicine Partnership (IPMP) Program 3605/21Israel Science Foundation 2054/22NewStem LTD
6 · The paper itself

Abstract

Taxanes and platinum molecules, specifically paclitaxel and carboplatin, are widely used anticancer drugs that induce cell death and serve as first-line chemotherapy for various cancer types. Despite the efficient effect of both drugs on cancer cell proliferation, many tumours have innate resistance against paclitaxel and carboplatin, which leads to inefficient treatment and poor survival rates. Haploid human embryonic stem cells (hESCs) are a novel and robust platform for genetic screening. To gain a comprehensive view of genes that affect or regulate paclitaxel and carboplatin resistance, genome-wide loss-of-function screens in haploid hESCs were performed. Both paclitaxel and carboplatin screens have yielded selected plausible gene lists and pathways relevant to resistance prediction. The effects of mutations in selected genes on the resistance to the drugs were demonstrated. Based on the results, an algorithm that can predict resistance to paclitaxel or carboplatin was developed. Applying the algorithm to the DNA mutation profile of patients' tumours enabled the separation of sensitive versus resistant patients, thus, providing a prediction tool. As the anticancer drugs arsenal can offer alternatives in case of resistance to either paclitaxel or carboplatin, an early prediction can provide a significant advantage and should improve treatment. The algorithm assists this unmet need and helps predict whether a patient will respond to the treatment and may have an immediate clinically actionable application.

Indexed as

Antineoplastic AgentsCarboplatinDrug Resistance, NeoplasmHuman Embryonic Stem CellsPaclitaxelAlgorithmsHaploidyHumansMutationNeoplasmsAntineoplastic AgentsCarboplatinPaclitaxel

Identifiers

PMID39523021
PMCPMC11882768

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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.