Evidence map›Paper›PMID 37047788›Full record

ArticleInternational journal of molecular sciences2023

Azacitidine Is Synergistically Lethal with XPO1 Inhibitor Selinexor in Acute Myeloid Leukemia by Targeting XPO1/eIF4E/c-MYC Signaling.

Huideng Long, Yue Hou, Jun Li, Chunhua Song, Zheng Ge

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 19 citations in OpenAlex.

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  5. c-Medical sciences (Basel, Switzerland) · 2026
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  12. CRM1 regulates androgen receptor stability and impacts DNA repair pathways in prostate cancer, independent of the androgen receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

5 authors at 2 institutions in 2 countries.

Huideng LongDepartment of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing 210009, China.
Yue HouDepartment of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing 210009, China.ORCID 0000-0002-0806-9083
Jun LiDepartment of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing 210009, China.
Chunhua SongHershey Medical Center, Pennsylvania State University Medical College, Hershey, PA 17033, USA.
Zheng GeDepartment of Hematology, Zhongda Hospital, School of Medicine, Southeast University, Institute of Hematology Southeast University, Nanjing 210009, China.ORCID 0000-0001-8028-1612
Zhongda Hospital Southeast University · CNPennsylvania State University · US

Funding

Jiangsu Province "333" project BRA2019103Jiangsu Provincial Medical Key Discipline (Laboratory) Cultivation Unit JSDW202212Medical research key projects - Jiangsu Commission of Health ZD2021003Milstein Medical Asian American Partnership (MMAAP) Foundation Research Project Award in Hematology 2017The National Natural Science Foundation of China 82070166
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a high-mortality malignancy with poor outcomes. Azacitidine induces cell death and demonstrates treatment effectiveness against AML. Selinexor (KPT-330) exhibited significant benefits in combination with typical induction treatment for AML patients. Here, we explore the antitumor effect of KPT-330 combined with AZA in AML through CCK-8, flow cytometry, RT-qPCR, western blot, and RNA-seq. Our results showed that KPT-330 combined with AZA synergistically reduced cell proliferation and induced apoptosis in AML primary cells and cell lines. Compared to the control, the KPT-330 plus AZA down-regulates the expression of XPO1, eIF4E, and c-MYC in AML. Moreover, the knockdown of c-MYC could sensitize the synergy of the combination on suppression of cell proliferation and promotion of apoptosis in AML. Moreover, the expression of

Indexed as

Antineoplastic AgentsLeukemia, Myeloid, AcuteApoptosisAzacitidineCell Line, TumorEukaryotic Initiation Factor-4EHumansHydrazinesKaryopherinsProto-Oncogene Proteins c-mycSignal TransductionTriazolesAntineoplastic AgentsAzacitidineEukaryotic Initiation Factor-4EHydrazinesKaryopherinsProto-Oncogene Proteins c-mycselinexorTriazolesacute myeloid leukemiaapoptosisazacitidinec-MYCeIF4EXPO-1 inhibitor

Identifiers

PMID37047788
PMCPMC10094826
OpenAlexW4362671075

What Socratic 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 Socratic graph.