Evidence map›Paper›PMID 42566094›Full record

ArticleMolecular biology reports2026

Synergistic apoptotic induction in acute lymphoblastic leukemia cells: exploring the role of EAAT1 inhibition by UCPH-101 in combination with asparaginase.

Masoumeh Fardi, Mohsen Hamidpour, Morteza Fardi, Elham Gholipour, Mehdi Allahbakhshian Farsani

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

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5 · Who and what money

Authors and funding

5 authors.

Masoumeh FardiDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohsen HamidpourDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Morteza FardiDepartment of Animal Genomics and Bioinformatics, Animal Biotechnology Research Institute, Agricultural Research, Education and Extension Organization (AREEO), Agricultural Biotechnology Research Institute of Iran (ABRII), Rasht, Iran.
Elham GholipourHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehdi Allahbakhshian FarsaniDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Allahbakhshian@sbmu.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDespite advances in treating acute lymphoblastic leukemia (ALL), resistance to asparaginase (ASNase) remains a major clinical hurdle. Recent evidence suggests that leukemic cells may evade ASNase-induced cytotoxicity by upregulating the glutamate/aspartate transporter EAAT1 (SLC1A3). This study aimed to evaluate whether pharmacological inhibition of EAAT1 using UCPH-101 could enhance the inhibitory effects of ASNase in T-ALL models.

methodsUsing patient-derived samples and established T-ALL cell lines (MOLT-4 and Jurkat) we assessed the effects of ASNase and UCPH-101, both alone and in combination. Combinations were designed based on IC

resultsSynergy analysis based on CI values revealed synergistic interactions (CI < 1) at sub and supra IC

conclusionThese findings demonstrate that EAAT1 inhibition augments ASNase anti-leukemic activity in preclinical ALL models, revealing a metabolic vulnerability that can be exploited therapeutically. The mechanistic insights reported herein support further exploration of EAAT1-targeted strategies to improve outcomes in T-ALL.

Indexed as

ApoptosisAsparaginaseExcitatory Amino Acid Transporter 1Precursor Cell Lymphoblastic Leukemia-LymphomaCell Line, TumorCell SurvivalDrug SynergismHumansJurkat CellsAsparaginaseExcitatory Amino Acid Transporter 1SLC1A3 protein, humanAcute lymphoblastic leukemiaAsparaginase (ASNase)Combination therapyEAAT1SLC1A3UCPH-101

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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.