Evidence map›Paper›PMID 41125871›Full record

ArticleNature biomedical engineering2026

Comprehensive resistance profiling of chronic myeloid leukaemia associated ABL1 variants against five tyrosine kinase inhibitors using prime editing.

Yusang Jung, Goosang Yu, Hyeong-Cheol Oh, Jueng-Hu Lee, Eunhye Jeon, Juhyeon Bae, Taebo Sim, Hyongbum Henry Kim

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Article in Nature biomedical engineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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.

Yusang Jung *Department of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0003-1897-0649
Goosang Yu *Department of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0002-3650-1822
Hyeong-Cheol OhDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0001-9031-6540
Jueng-Hu LeeDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Eunhye JeonGraduate School of Medical Science, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0001-8206-8620
Juhyeon BaeGraduate School of Medical Science, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.
Taebo SimGraduate School of Medical Science, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0003-3015-2059
Hyongbum Henry KimDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea. hkim1@yuhs.ac.ORCID http://orcid.org/0000-0002-4693-738X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There are four generations of tyrosine kinase inhibitors (TKIs) that target BCR-ABL1 mutations, a fusion oncogene, in chronic myeloid leukaemia, but predicting the resistance profiles of these TKIs for patients with ABL1 mutations is sometimes difficult, especially when the mutations are not included by clinical guidelines. Here we use prime editing to generate 97% (2,802/2,892) of all possible single-nucleotide variants in the sequence encoding the ABL1 kinase domain, which covers 98% (1,954/1,998) of all possible corresponding single amino acid variants. We evaluated their effects on resistance to five TKIs (imatinib, nilotinib, bosutinib, ponatinib and asciminib), spanning all four TKI generations by using K562 cells. We identified 361 pairs of resistance-conferring single amino acid variants and the corresponding TKIs. Our comprehensive resistance map will complement clinical guidelines in drug selection for patients with chronic myeloid leukaemia based on ABL1 mutations, facilitating precision medicine.

Indexed as

Drug Resistance, NeoplasmFusion Proteins, bcr-ablGene EditingLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsProto-Oncogene Proteins c-ablAniline CompoundsHumansImatinib MesylateImidazolesK562 CellsMutationNiacinamideNitrilesPyrazolesPyridazinesABL1 protein, humanAniline CompoundsasciminibbosutinibFusion Proteins, bcr-ablImatinib MesylateImidazolesNiacinamidenilotinibNitrilesponatinibProtein Kinase InhibitorsProto-Oncogene Proteins c-ablPyrazolesPyridazinesPyrimidinesQuinolinesTyrosine Kinase Inhibitors

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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.