Evidence map›Paper›PMID 28469959›Full record

ArticleAmerican journal of cancer research2017

Treatment with the C-C chemokine receptor type 5 (CCR5)-inhibitor maraviroc suppresses growth and induces apoptosis of acute lymphoblastic leukemia cells.

Jie Zi, Shushu Yuan, Jianlin Qiao, Kai Zhao, Linyan Xu, Kunming Qi, Kailin Xu, Lingyu Zeng

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2017. 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
1.1field-weighted citation impact, top 23% 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, 34 citations in OpenAlex.

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  14. Reduction of leukemic burden via bone-targeted nanoparticle delivery of an inhibitor of C-chemokine (C-C motif) ligand 3 (CCL3) signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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  19. The G protein coupled receptor CCR5 in cancer.Advances in cancer research · 2020
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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

8 authors at 1 institution in 1 country.

Jie ZiBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Shushu YuanBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Jianlin QiaoBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Kai ZhaoBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Linyan XuBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Kunming QiDepartment of Hematology, The Affiliated Hospital of Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Kailin XuBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Lingyu ZengBlood Diseases Institute, Xuzhou Medical UniversityNo. 99, West Huaihai Road, Xuzhou, Jiangsu Province, China.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) is the most common hematological malignancy diagnosed in children and is a malignant disorder that originates from one single hematopoietic precursor committed to B- or T-cell lineage. C-C chemokine receptor type 5 (CCR5) is a chemokine and chemokine receptor pair playing critical roles in tumorigenesis. A highly potent competitive antagonist of CCR5, maraviroc, recently has been identified with suppression of cancer cells aggressive in a variety of cancers. However, the effects of maraviroc on ALL cells have not yet been defined. Here we report that CCR5 selective inhibitor significantly inhibited ALL cells SUP-B15 growth and induced SUP-B15 cells to undergo cell apoptosis. This cell apoptosis was associated with increased levels of cleavage of caspase-3 and caspase-9, and Poly (ADP-ribose) polymerase (PARP). Moreover, we demonstrated that maraviroc strongly inhibited SUP-B15 cells migration to C-X-C motif chemokine ligand 12 (CXCL12) and CXCL13, and adhesion to fibronectin and vascular cell adhesion molecule 1 (VCAM-1) in vitro. Importantly, CCR5-activated signaling proteins Janus Kinase 1 (JAK1), JAK2 and signal transducer and activator of transcription (STAT3) were inhibited by maraviroc. Finally, maraviroc suppressed the growth of SUP-B15 xenograft tumors in athymic mice. Collectively, this study demonstrated that CCR5 inhibition by maraviroc has the potential for the treatment of human ALL.

Indexed as

ALLCCR5JAKmaravirocSTAT3

Identifiers

PMID28469959
PMCPMC5411794
OpenAlexW2981253396

What OpenQuestion holds

Textmetadata
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.