Evidence map›Paper›PMID 28814980›Full record

ArticleClinical epigenetics2017

Cooperative effect of chidamide and chemotherapeutic drugs induce apoptosis by DNA damage accumulation and repair defects in acute myeloid leukemia stem and progenitor cells.

Yin Li, Yan Wang, Yong Zhou, Jie Li, Kai Chen, Leisi Zhang, Manman Deng, Suqi Deng, Peng Li, Bing Xu

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 76 citations in OpenAlex.

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  7. Disruption of mitochondrial oxidative phosphorylation by chidamide eradicates leukemic cells in AML.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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

10 authors at 4 institutions in 1 country.

Yin Li *Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 People's Republic of China.
Yan Wang *Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 People's Republic of China.
Yong Zhou *Department of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen, 361003 People's Republic of China.
Jie LiDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 People's Republic of China.
Kai ChenDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 People's Republic of China.
Leisi ZhangDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 People's Republic of China.
Manman DengDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen, 361003 People's Republic of China.
Suqi DengDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515 People's Republic of China.
Peng LiGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530 People's Republic of China.
Bing XuDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen, 361003 People's Republic of China.
Nanfang Hospital · CNFirst Affiliated Hospital of Xiamen University · CNChinese Academy of Sciences · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMany conventional chemotherapeutic drugs are known to be involved in DNA damage, thus ultimately leading to apoptosis of leukemic cells. However, they fail to completely eliminate leukemia stem cells (LSCs) due to their higher DNA repair capacity of cancer stem cells than that of bulk cancer cells, which becomes the root of drug resistance and leukemia recurrence. A new strategy to eliminate LSCs in acute myeloid leukemia (AML) is therefore urgently needed.

resultsWe report that a low-dose chidamide, a novel orally active benzamide-type histone deacetylase (HDAC) inhibitor, which selectively targets HDACs 1, 2, 3, and 10, could enhance the cytotoxicity of DNA-damaging agents (daunorubicin, idarubicin, and cytarabine) in CD34

conclusionsThese findings provide preclinical evidence for low-dose chidamide in combination with chemotherapeutic agents in treating recurrent/resistant AML as an alternative salvage regimen, especially those possessing stem and progenitor cells.

Indexed as

AdolescentAdultAminopyridinesAntineoplastic Combined Chemotherapy ProtocolsBenzamidesCell Line, TumorCell ProliferationCell SurvivalCytarabineDaunorubicinDNA DamageDNA RepairDrug TherapyFemaleHumansIdarubicinAminopyridinesBenzamidesCytarabineDaunorubicinIdarubicinN-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamideAcute myeloid leukemiaChidamideDNA damageDrug resistanceLeukemia stem and progenitor cells

Identifiers

PMID28814980
PMCPMC5556349
OpenAlexW2749124526

What OpenQuestion holds

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LicenceCC BY
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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.