Evidence map›Paper›PMID 24497931›Full record

ArticlePloS one2014

CXCR7 is highly expressed in acute lymphoblastic leukemia and potentiates CXCR4 response to CXCL12.

Rita de Cássia Carvalho Melo, Ana Leda Longhini, Carolina Louzão Bigarella, Mariana Ozello Baratti, Fabiola Traina, Patrícia Favaro, Paula de Melo Campos, Sara Teresinha Olalla Saad

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. The antitumor effects of WNT5A against hematological malignancies.Journal of cell communication and signaling · 2023
    Article
  5. Article
  6. CXCL12-CXCR4/CXCR7 Axis in Cancer: from Mechanisms to Clinical Applications.International journal of biological sciences · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Cells · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Rita de Cássia Carvalho MeloCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Ana Leda LonghiniCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Carolina Louzão BigarellaCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Mariana Ozello BarattiCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Fabiola TrainaCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Patrícia FavaroCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil ; Departamento de Ciências Biológicas, Universidade Federal de São Paulo, Diadema, São Paulo, Brasil.
Paula de Melo CamposCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Sara Teresinha Olalla SaadCentro de Hematologia e Hemoterapia, Universidade de Campinas, Campinas, São Paulo, Brasil.
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, a novel CXCL12-binding receptor, has been identified. This CXCL12-binding receptor commonly known as CXCR7 (CXC chemokine receptor 7), has lately, based on a novel nomenclature, has received the name ACKR3 (atypical chemokine receptor 3). In this study, we aimed to investigate the expression of CXCR7 in leukemic cells, as well as its participation in CXCL12 response. Interesting, we clearly demonstrated that CXCR7 is highly expressed in acute lymphoid leukemic cells compared with myeloid or normal hematopoietic cells and that CXCR7 contributed to T-acute lymphoid leukemic cell migration induced by CXCL12. Moreover, we showed that the cellular location of CXCR7 varied among T-lymphoid cells and this finding may be related to their migration capacity. Finally, we hypothesized that CXCR7 potentiates CXCR4 response and may contribute to the maintenance of leukemia by initiating cell recruitment to bone marrow niches that were once occupied by normal hematopoietic stem cells.

Indexed as

AdultAgedAged, 80 and overBenzylaminesBlotting, WesternBone MarrowCell Line, TumorCell MovementChemokine CXCL12CyclamsFemaleFlow CytometryGene Expression Regulation, LeukemicHeterocyclic CompoundsHumansJurkat CellsACKR3 protein, humanBenzylaminesChemokine CXCL12CyclamsHeterocyclic CompoundsplerixaforReceptors, CXCRReceptors, CXCR4

Identifiers

PMID24497931
PMCPMC3908922
OpenAlexW2023808388

What OpenQuestion 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 OpenQuestion graph.