Evidence map›Paper›PMID 41792440›Full record

ArticleLeukemia2026

Enhancing tyrosine kinase inhibitor sensitivity by restoring IKAROS activity on GLUT1 expression and glycolysis in Philadelphia chromosome-positive acute lymphoblastic leukemia.

Linyao Zhang, Qi Han, Huimin Xiang, Rosa Lapalombella, Ann-Kathrin Eisfeld, Walter G Hanel, Jonathan E Brammer, Alice S Mims, Jennifer A Woyach, Chunhua Song and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Linyao Zhang *Department of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing, China.
Qi Han *Department of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing, China.
Huimin XiangDepartment of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing, China.
Rosa LapalombellaDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA.ORCID 0000-0001-6916-9400
Ann-Kathrin EisfeldDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA.ORCID 0000-0001-6442-1419
Walter G HanelDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA.ORCID 0000-0001-8982-6877
Jonathan E BrammerDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA.
Alice S MimsDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA.ORCID 0000-0002-8971-2199
Jennifer A WoyachDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA.ORCID 0000-0002-3403-9144
Chunhua SongDivision of Hematology, The Ohio State University Wexner Medical Center, The James Cancer Hospital, Columbus, OH, USA. chunhua.song@osumc.edu.ORCID 0000-0002-4081-2543
Zheng GeDepartment of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing, China. zhengge@seu.edu.cn.ORCID 0000-0001-8028-1612

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) are still less sensitive to tyrosine kinase inhibitors (TKIs). Ph+ ALL shows a high incidence of IKZF1 deletions. Casein kinase II (CK2)-mediated hyperphosphorylation of IKZF1, encoding protein IKAROS, contributes to its dysfunction, and CK2 inhibitor, CX-4945, restores IKAROS function in high-risk ALL. Here, we found that Ph+ ALL cells with IKZF1 deletion are inherently resistant to TKIs. The combination of TKIs (imatinib or ponatinib) with CX-4945 significantly extended the survival and reduced the tumor burden in the IKZF1 deletion (Ik6

Indexed as

Glucose Transporter Type 1GlycolysisIkaros Transcription FactorPhiladelphia ChromosomePrecursor Cell Lymphoblastic Leukemia-LymphomaProtein Kinase InhibitorsAnimalsApoptosisCell Line, TumorDrug Resistance, NeoplasmHumansImatinib MesylateImidazolesMiceNaphthyridinesPhenazinesGlucose Transporter Type 1Ikaros Transcription FactorIKZF1 protein, humanImatinib MesylateImidazolesNaphthyridinesPhenazinesProtein Kinase InhibitorssilmitasertibTyrosine Kinase Inhibitors

Identifiers

PMID41792440
PMCPMC13056559

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.