Evidence map›Paper›PMID 41945265›Full record

ArticleNano convergence2026

Multimodal gene and targeted drug therapy for chronic myelogenous leukemia using BIM/MCL-1 chimeric nanoparticle: computational target analysis and therapeutic validation.

Margaret L Lugin, Winnie Lei, Rebecca T Lee, Jee Young Chung, Nicholas M Katritsis, Woochang Hwang, Angela G Fleischman, Namshik Han, Young Jik Kwon

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nano convergence, 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

5 · Who and what money

Authors and funding

9 authors.

Margaret L Lugin *Department of Chemical and Biomolecular Engineering, University of California, Irvine, CA, 92697, USA.
Winnie Lei *The Milner Therapeutics Institute, University of Cambridge, Cambridge, CB2 0AW, UK.
Rebecca T Lee *Department of Biomedical Engineering, University of California, Irvine, CA, 92697, USA.
Jee Young ChungDepartment of Pharmaceutical Sciences, University of California, Irvine, CA, 92697, USA.
Nicholas M KatritsisThe Milner Therapeutics Institute, University of Cambridge, Cambridge, CB2 0AW, UK.
Woochang HwangThe Milner Therapeutics Institute, University of Cambridge, Cambridge, CB2 0AW, UK.
Angela G FleischmanDivision of Hematology/Oncology, Department of Medicine, University of California, Irvine, CA, 92697, USA. agf@uci.edu.
Namshik HanThe Milner Therapeutics Institute, University of Cambridge, Cambridge, CB2 0AW, UK. nh417@cam.ac.uk.
Young Jik KwonDepartment of Chemical and Biomolecular Engineering, University of California, Irvine, CA, 92697, USA. kwonyj@uci.edu.ORCID http://orcid.org/0000-0003-4086-6995

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
CARCINOGENESIST32CA009054 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI EDINGER, AIMEE L, FRUMAN, DAVID ALEXANDER · 1985 to 2025
$8.6M
Preclinical Validation of Dual-Modal Nanotherapy for Chronic Myeloid Neoplasms and BeyondR21CA228099 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KWON, YOUNG JIK · 2019 to 2020
$351k
Ministry of Science and ICT, South Korea RS-2025-25427881Naational Institute of Health P30CA062203National Research Foundation of Korea RS-2025-18362970NCI NIH HHS 1R21CA228099-01A1NCI NIH HHS P30 CA062203NCI NIH HHS R21 CA228099NCI NIH HHS T32 CA009054NCI NIH HHS T32CA009054
6 · The paper itself

Abstract

Developing an efficient and safe therapy necessitates a mechanistic understanding of the complex underlying pathology and manipulation of the multiple pathways at the molecular and genetic level. Network-based simulation of chronic myeloid leukemia (CML), a relatively well-understood cancer model, revealed the dynamics of simultaneously expressing pro-apoptotic BIM (Bcl-2 interacting mediator of cell death) and silencing pro-survival MCL-1 (myeloid cell leukemia-1) in combination with the breakpoint cluster region (BCR)-Abelson (ABL)-targeted tyrosine kinase inhibitor dasatinib. Viral/nonviral chimeric nanoparticles (ChNPs) composed of a BIM-expressing adeno-associated virus (AAV) core and a degradable polymeric shell that encapsulates MCL-1 siRNA (BIM/MCL-1 ChNPs) selectively killed BCR-ABL + CML cells in combination with dasatinib. In a mouse CML model, the BIM/MCL-1 ChNPs and dasatinib combination therapy suppressed proliferation of BCR-ABL + hematopoietic cells and prevented leukemic infiltration of organs. The enhanced anti-leukemic effect was further pronounced in an acute phase model of the disease. This study investigated a strategy of developing a versatile and tunable multimodal therapy assisted by a computational toolset that analyzes the molecular foundation of a disease and predicts therapeutic response. The interdisciplinary approach developed and validated in this study can be used in discovering new therapies for cancer and other diseases.

Indexed as

Chronic myeloid leukemiaCombined gene and targeted therapyDasatinibMulti- omics network analysisSimultaneous BIM expression and MCL-1 silencingSynergized apoptosisViral/nonviral chimeric nanoparticles

Identifiers

PMID41945265
PMCPMC13057112

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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.