Evidence map›Paper›PMID 27472284›Full record

ArticleACS nano2016

Viral/Nonviral Chimeric Nanoparticles To Synergistically Suppress Leukemia Proliferation via Simultaneous Gene Transduction and Silencing.

Cheol Am Hong, Soo Kyung Cho, Julius A Edson, Jane Kim, Dominique Ingato, Bryan Pham, Anthony Chuang, David A Fruman, Young Jik Kwon

Abstract read
In one paragraph

Article in ACS nano, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
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

7 citing papers in PubMed, 28 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Cheol Am HongDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Soo Kyung ChoDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Julius A EdsonDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Jane KimDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Dominique IngatoDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Bryan PhamDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Anthony ChuangDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
David A FrumanDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
Young Jik KwonDepartment of Pharmaceutical Sciences, ‡Department of Chemical Engineering and Materials Science, §Department of Biological Sciences, ∥Division of Hematology/Oncology, ⊥Department of Molecular Biology and Biochemistry, and #Department of Biomedical Engineering, University of California , Irvine, California 92697, United States.
University of California, Irvine · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
TOR kinase inhibitors for leukemia therapy: mechanisms of action and resistanceR01CA158383 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI FRUMAN, DAVID ALEXANDER · 2012 to 2016
$1.5M
NCI NIH HHS P30 CA062203NCI NIH HHS R01 CA158383
6 · The paper itself

Abstract

Single modal cancer therapy that targets one pathological pathway often turns out to be inefficient. For example, relapse of chronic myelogenous leukemia (CML) after inhibiting BCR-ABL fusion protein using tyrosine kinase inhibitors (TKI) (e.g., Imatinib) is of significant clinical concern. This study developed a dual modal gene therapy that simultaneously tackles two key BCR-ABL-linked pathways using viral/nonviral chimeric nanoparticles (ChNPs). Consisting of an adeno-associated virus (AAV) core and an acid-degradable polymeric shell, the ChNPs were designed to simultaneously induce pro-apoptotic BIM expression by the AAV core and silence pro-survival MCL-1 by the small interfering RNA (siRNA) encapsulated in the shell. The resulting BIM/MCL-1 ChNPs were able to efficiently suppress the proliferation of BCR-ABL+ K562 and FL5.12/p190 cells in vitro and in vivo via simultaneously expressing BIM and silencing MCL-1. Interestingly, the synergistic antileukemic effects generated by BIM/MCL-1 ChNPs were specific to BCR-ABL+ cells and independent of a proliferative cytokine, IL-3. The AAV core of ChNPs was efficiently shielded from inactivation by anti-AAV serum and avoided the generation of anti-AAV serum, without acute toxicity. This study demonstrates the development of a synergistically efficient, specific, and safe therapy for leukemia using gene carriers that simultaneously manipulate multiple and interlinked pathological pathways.

Indexed as

Gene SilencingNanoparticlesTransduction, GeneticAntineoplastic AgentsApoptosisBenzamidesCell ProliferationDrug Resistance, NeoplasmFusion Proteins, bcr-ablGenetic TherapyHumansK562 CellsLeukemiaPiperazinesProtein Kinase InhibitorsPyrimidinesAntineoplastic AgentsBenzamidesFusion Proteins, bcr-ablPiperazinesProtein Kinase InhibitorsPyrimidinesAAV transductionBIM expressioncore−shell nanoparticleshybrid vectorMCL-1 silencingRNA interferencesynergistic leukemia gene therapy

Identifiers

PMID27472284
PMCPMC5602606
OpenAlexW2494734027

What OpenQuestion holds

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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.