Evidence map›Paper›PMID 28487980›Full record

ArticleMolecular medicine reports2017

Combination of bortezomib and daunorubicin in the induction of apoptosis in T-cell acute lymphoblastic leukemia.

Xin Du, Jia Tong, Hongying Lu, Cong He, Shenghong Du, Peimin Jia, Weili Zhao, Hanzhang Xu, Junmin Li, Zhixiang Shen and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. [Effect of bortezomib in inducing apoptosis of imatinib-resistant K562 cells and the mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    Article
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

13 authors at 2 institutions in 1 country.

Xin DuState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Jia TongState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Hongying LuState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Cong HeState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Shenghong DuState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Peimin JiaState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Weili ZhaoState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Hanzhang XuHongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Department of Pathophysiology, Chemical Biology Division of Shanghai Universities E‑Institutes, Key Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Junmin LiState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Zhixiang ShenState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Yingli WuHongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Department of Pathophysiology, Chemical Biology Division of Shanghai Universities E‑Institutes, Key Laboratory of Cell Differentiation and Apoptosis of The Chinese Ministry of Education, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Jianhua TongState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Li ZhouState Key Laboratory of Medical Genomics, Department of Hematology, Faculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Ruijin Hospital · CNTongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite advances in the treatment of T‑cell acute lymphoblastic leukemia (T‑ALL), the outcome of T‑ALL treatment remains unsatisfactory, therefore, more effective treatment is urgently required. The present study examined the cytotoxicities of bortezomib in combination with daunorubicin against human Jurkat and Molt‑4 T‑ALL cells and primary T‑ALL cells. Compared with treatment alone, co‑exposure of cells to bortezomib and daunorubicin resulted in a significant increase in cell death in the Jurkat cells, as evidenced by the increased percentage of Annexin V‑positive cells, the formation of apoptotic bodies. In addition, the administration sequence of bortezomib and daunorubicin had an effect on cell viability. Treatment with bortezomib followed by daunorubicin treatment was more effective, compared with treatment with daunorubicin followed by bortezomib. Co-treatment with bortezomib and daunorubicin markedly enhanced the activation of caspase‑3, ‑8 and ‑9, which was reversed by the pan‑caspase inhibitor, Z‑VAD‑FMK. In addition, cotreatment with bortezomib and daunorubicin enhanced the collapse of mitochondrial transmembrane potential and upregulated the proapoptotic protein, B‑cell lymphoma 2 (Bcl‑2)‑interacting mediator of cell death (Bim), but not Bcl‑2 or Bcl‑extra large. Consistent with this, it was demonstrated that cotreatment of bortezomib and daunorubicin efficiently induced apoptosis in primary T‑ALL cells, and cell death was associated with the collapse of mitochondrial transmembrane potential and the upregulation of Bim. Taken together, these findings indicated that the combination of bortezomib and daunorubicin significantly enhanced their apoptosis‑inducing effect in T‑ALL cells, which may warrant further investigation in preclinical and clinical investigations.

Indexed as

Antineoplastic AgentsApoptosisBcl-2-Like Protein 11BortezomibCaspasesCell Line, TumorCell ProliferationCell SurvivalDaunorubicinDrug SynergismGene ExpressionHumansJurkat CellsMembrane Potential, MitochondrialPrecursor T-Cell Lymphoblastic Leukemia-LymphomaAntineoplastic AgentsBcl-2-Like Protein 11BortezomibCaspasesDaunorubicin

Identifiers

PMID28487980
PMCPMC5482122
OpenAlexW2613043762

What OpenQuestion holds

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LicenceCC BY-NC-ND
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 OpenQuestion graph.