Evidence map›Paper›PMID 39564003›Full record

ArticleClinical & translational immunology2024

The contribution of the CRP/CD64 axis to renal cancer progression by inducing protumor activation of tumor-associated macrophages.

Cheng Pan, Yukio Fujiwara, Hiromu Yano, Toshiki Anami, Yuki Ibe, Lianbo Li, Yuji Miura, Takanobu Motoshima, Shigeyuki Esumi, Junji Yatsuda and 3 more

Abstract read
In one paragraph

Article in Clinical & translational immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Cheng PanDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Yukio FujiwaraDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.ORCID https://orcid.org/0000-0002-2074-0597
Hiromu YanoDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Toshiki AnamiDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Yuki IbeDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Lianbo LiDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Yuji MiuraDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Takanobu MotoshimaDepartment of Urology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Shigeyuki EsumiDepartment of Anatomy and Neurobiology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Junji YatsudaDepartment of Urology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Taizo HibiDepartment of Pediatric Surgery and Transplantation, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Tomomi KambaDepartment of Urology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences Kumamoto University Kumamoto Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: C-reactive protein (CRP) is a well-known acute-phase protein that increases remarkably under various inflammatory conditions and is elevated in patients with malignant tumors. In this study, we investigated the influence of CRP on the tumor microenvironment in clear cell renal cell carcinoma (ccRCC). Methods: This study explored CRP's role in ccRCC by co-culturing human macrophages with ccRCC cells and employing antibody blocking, RNA sequencing and Results: A co-culture study using human macrophages and RCC cell lines showed that CRP-stimulated macrophages secrete IL-6, which induces RCC proliferation via STAT3 activation. CRP-induced protumor activation of macrophages was suppressed by CD64 blocking antibodies. Furthermore, CRP elevates PD-L1 expression in macrophages via the CD64-STAT1 signalling pathway. Statistical analysis of TCGA data indicated that increased CD64 expression was associated with a worse clinical course in ccRCC. Immunohistochemical analysis of pathological specimens revealed that high CD64 expression in tumor-associated macrophages (TAMs), and a high density of CD64 Conclusions: The CRP-CD64 signal was linked to the protumor activation of TAMs and could be a promising target for anticancer immunotherapy in ccRCC.

Indexed as

CD64CRPIL6macrophagePD‐L1renal cell carcinoma

Identifiers

PMID39564003
PMCPMC11574560

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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.