Evidence map›Paper›PMID 38750114›Full record

ArticleBritish journal of cancer2024

Synergistic antitumor activity by dual blockade of CCR1 and CXCR2 expressed on myeloid cells within the tumor microenvironment.

Hideyuki Masui, Kenji Kawada, Yoshiro Itatani, Hideyo Hirai, Yuki Nakanishi, Yoshiyuki Kiyasu, Keita Hanada, Michio Okamoto, Wataru Hirata, Yasuyo Nishikawa and 4 more

Abstract read
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Neutrophil and Colorectal Cancer.International journal of molecular sciences · 2024
    Review
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

14 authors.

Hideyuki MasuiDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kenji KawadaDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan. kkawada@kuhp.kyoto-u.ac.jp.ORCID 0000-0003-4336-6937
Yoshiro ItataniDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hideyo HiraiLaboratory of Stem Cell Regulation, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Yuki NakanishiDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID 0000-0001-5493-6312
Yoshiyuki KiyasuDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Keita HanadaDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Michio OkamotoDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Wataru HirataDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yasuyo NishikawaDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Naoko SugimotoDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takuya TamuraDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yoshiharu SakaiDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kazutaka ObamaDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemokine signaling within the tumor microenvironment can promote tumor progression. Although CCR1 and CXCR2 on myeloid cells could be involved in tumor progression, it remains elusive what effect would be observed if both of those are blocked.

methodsWe employed two syngeneic colorectal cancer mouse models: a transplanted tumor model and a liver metastasis model. We generated double-knockout mice for CCR1 and CXCR2, and performed bone marrow (BM) transfer experiments in which sub-lethally irradiated wild-type mice were reconstituted with BM from either wild-type, Ccr1

resultsMyeloid cells that express MMP2, MMP9 and VEGF were accumulated around both types of tumors through CCR1- and CXCR2-mediated pathways. Mice reconstituted with Ccr1

conclusionDual blockade of CCR1 and CXCR2 pathways in myeloid cells could be an effective therapy against colorectal cancer.

Indexed as

Mice, KnockoutMyeloid CellsReceptors, CCR1Receptors, Interleukin-8BTumor MicroenvironmentAnimalsCD8-Positive T-LymphocytesCell Line, TumorColorectal NeoplasmsLiver NeoplasmsMiceMice, Inbred C57BLCcr1 protein, mouseCxcr2 protein, mouseReceptors, CCR1Receptors, Interleukin-8B

Identifiers

PMID38750114
PMCPMC11231281

What OpenQuestion holds

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Registered trials

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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.