Evidence map›Paper›PMID 38151286›Full record

ArticleCancer genomics & proteomics

Lianbo Li, Kosuke Kanemitsu, Koji Ohnishi, Rin Yamada, Hiromu Yano, Yukio Fujiwara, Yuji Miyamoto, Yoshiki Mikami, Taizo Hibi, Hideo Baba and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. 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
2.5field-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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Frontiers in immunology · 2025
    Article
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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

11 authors at 3 institutions in 1 country.

Lianbo Li *Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kosuke Kanemitsu *Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Koji OhnishiDepartment of Pathology, Aichi Medical University School of Medicine, Nagakute, Japan.
Rin YamadaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Hiromu YanoDepartment 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.
Yuji MiyamotoDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Honjo, Japan.
Yoshiki MikamiDepartment of Diagnostic Pathology, Kumamoto University Hospital, Kumamoto, Japan.
Taizo HibiDepartment of Pediatric Surgery and Transplantation, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan.
Hideo BabaDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Honjo, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; ycomo@kumamoto-u.ac.jp.
Kumamoto University · JPKumamoto University Hospital · JPAichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimCXCL10, a member of the CXC chemokine family, plays a crucial role in immune response by facilitating the chemotaxis of CXCR3-positive immune cells. We examined the expression of CXCL10 to unravel its functional significance in colorectal cancer. MATERIALS AND

methodsBioinformatics analysis was performed to investigate CXCL10 expression and its clinicopathological relevance. Subsequently, we examined the correlation between the serum levels of CXCL10 and its expression within cancer tissues.

resultsAnalysis of the TCGA database revealed that elevated CXCL10 expression in CRC tissues correlates with improved long-term survival and is inversely associated with lymph node infiltration and metastasis. Insights from Gene Ontology and Kyoto Encyclopedia of Genes and Genomes further established a connection between increased CXCL10 and co-regulated gene expression with enhanced immune activation and regulation, mediated by the inhibition of the NOD-like receptor signaling pathway. Single-cell analysis pinpointed myeloid cells and macrophages as the primary sources of CXCL10. Immunohistochemical assessments revealed that a subset of cancer cells and macrophages are positive for CXCL10 expression. CXCL10-positive cells are predominantly located at the invasive front of the tumor. Intriguingly, our findings reveal an inverse correlation between serum CXCL10 levels and its expression in cancer tissues.

conclusionThe expression of CXCL10 may play a role in mediating the inflammatory responses at the invasive front in colorectal cancer and is observed to be inversely correlated with serum CXCL10 levels. It is pivotal to elucidate the distinct roles of CXCL10 in colorectal cancer, particularly different functions of cancer-tissue CXCL10 from serum CXCL10.

Indexed as

Chemokine CXCL10Colorectal NeoplasmsHumansSignal TransductionChemokine CXCL10CXCL10 protein, humancolorectal cancerCXCL10invasive frontmacrophagestumor microenvironment

Identifiers

PMID38151286
PMCPMC10756351
OpenAlexW4390267769

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.