Evidence map›Paper›PMID 31695411›Full record

ArticleOncoTargets and therapy2019

PD-1 inhibitors dependent CD8

Chang E Gao, Ming Zhang, Qian Song, Jian Dong

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Galectin-1 fosters an immunosuppressive microenvironment in colorectal cancer by reprogramming CD8Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

4 authors at 2 institutions in 1 country.

Chang E GaoThe First Affiliated Hospital of Kunming Medical University, Department of Medical Oncology, Kunming, Yunnan 650031, People's Republic of China.
Ming ZhangYunnan Cancer Hospital & the Third Affiliated Hospital of Kunming Medical University & Yunnan Cancer Center, Cancer Research Institute, Kunming, Yunnan 650018, People's Republic of China.
Qian SongYunnan Cancer Hospital & the Third Affiliated Hospital of Kunming Medical University & Yunnan Cancer Center, Department of Radiation Oncology, Kunming, Yunnan 650018, People's Republic of China.
Jian DongYunnan Cancer Hospital & the Third Affiliated Hospital of Kunming Medical University & Yunnan Cancer Center, Department of Medical Oncology, Kunming, Yunnan 650018, People's Republic of China.
Kunming Medical University · CNFirst Affiliated Hospital of Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColon cancer is a common digestive tract malignancy which ranks as the third leading cause of cancer death worldwide. A current focus of anti-cancer research is harnessing the patient's own immune system for therapy. Programmed cell death protein 1 (PD-1), an immune suppressor, is upregulated in various activated immune cells, such as T cells, and in viral infections and tumors. PURPOSE: The objective of this study was to investigate the function of PD-1 inhibitor on the metastasisi of mouse colon cancer cells. PATIENTS AND

methodsIn the present study, we established an in situ colon cancer mouse model using the CT26 cell line. Hematoxylin-eosin (HE) staining was performed to detect colon cancer cell metastasis. The levels of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-12 (IL-12) in serum and mesenteric lymph nodes (MLNs) were detected by Enzyme-linked immunosorbent assay (ELISA). CD44

resultsWe found that anti-PD-1 therapy inhibited colon cancer cells metastasis to the small intestine, liver, and lung, and lengthened the survival time of mice. However, the depletion of CD8 suppressed the activity of anti-PD-1 antibodies. In response to anti-PD-1 immunotherapy, the levels of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-12 (IL-12) in serum and mesenteric lymph nodes (MLNs) were significantly increased, while IL-6, IL-17, and transforming growth factor-β (TGF-β) were decreased. CD8 depletion had the opposite effect. In addition, anti-PD-1 treatment significantly increased CD44

conclusionThese results suggest that PD-1 inhibitors rely on CD8+ T cells to exert anti-tumor immunity in colon cancer.

Indexed as

CD8 depletioncolon cancerIFN-γmetastasisprogrammed death 1 (PD-1)TNF-α

Identifiers

PMID31695411
PMCPMC6717878
OpenAlexW2970955296

What OpenQuestion holds

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LicenceCC BY-NC
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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.