Evidence map›Paper›PMID 34913283›Full record

ArticleYonsei medical journal2022

Primary Tumor Suppression and Systemic Immune Activation of Macrophages through the Sting Pathway in Metastatic Skin Tumor.

Chun-Bong Synn, Dong Kwon Kim, Jae Hwan Kim, Youngseon Byeon, Young Seob Kim, Mi Ran Yun, Ji Min Lee, Wongeun Lee, Eun Ji Lee, Seul Lee and 8 more

Open access · goldAbstract read
In one paragraph

Article in Yonsei medical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Role of STING in the treatment of non-small cell lung cancer.Cell communication and signaling : CCS · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Engineering complexity in human tissue models of cancer.Advanced drug delivery reviews · 2022
    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

18 authors at 3 institutions in 1 country.

Chun-Bong Synn *Department of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-5159-4644
Dong Kwon Kim *Department of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-1407-2369
Jae Hwan KimDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0003-3988-8134
Youngseon ByeonDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-6436-591X
Young Seob KimDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0003-2565-2315
Mi Ran YunJEUK Institute for Cancer Research, Gumi, Korea.ORCID https://orcid.org/0000-0002-2398-3287
Ji Min LeeBrain Korea, 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-5680-7239
Wongeun LeeJEUK Institute for Cancer Research, Gumi, Korea.ORCID https://orcid.org/0000-0002-1571-2129
Eun Ji LeeDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-4362-939X
Seul LeeDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-8185-9981
You-Won LeeDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-6334-5581
Doo Jae LeeWide River Institute of Immunology, Seoul National University, Hongcheon, Korea.ORCID https://orcid.org/0000-0001-7820-5995
Hyun-Woo KimWide River Institute of Immunology, Seoul National University, Hongcheon, Korea.ORCID https://orcid.org/0000-0002-9286-6164
Chang Gon KimYonsei Cancer Center, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-4929-8501
Min Hee HongYonsei Cancer Center, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0003-3490-2195
June Dong ParkWide River Institute of Immunology, Seoul National University, Hongcheon, Korea.ORCID https://orcid.org/0000-0001-8113-1384
Sun Min LimYonsei Cancer Center, Yonsei University College of Medicine, Seoul, Korea. LIMLOVE2008@yuhs.ac.ORCID https://orcid.org/0000-0001-7694-1593
Kyoung-Ho PyoDepartment of Medical Science, Yonsei University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-5428-0288
Yonsei University · KRSeoul National University · KRJeuk (South Korea) · KR

Funding

National Research Foundation of Korea 2019R1A2C4069993Yonsei University 6-2017-0104
6 · The paper itself

Abstract

purposeAgonists of the stimulator of interferon genes (STING) play a key role in activating the STING pathway by promoting the production of cytokines. In this study, we investigated the antitumor effects and activation of the systemic immune response of treatment with DMXAA (5,6-dimethylxanthenone-4-acetic acid), a STING agonist, in EML4-ALK lung cancer and CT26 colon cancer. MATERIALS AND

methodsThe abscopal effects of DMXAA in the treatment of metastatic skin nodules were assessed. EML4-ALK lung cancer and CT26 colon cancer models were used to evaluate these effects after DMXAA treatment. To evaluate the expression of macrophages and T cells, we sacrificed the tumor-bearing mice after DMXAA treatment and obtained the formalin-fixed paraffin-embedded (FFPE) tissue and tumor cells. Immunohistochemistry and flow cytometry were performed to analyze the expression of each FFPE and tumor cell.

resultsWe observed that highly infiltrating immune cells downstream of the STING pathway had increased levels of chemokines after DMXAA treatment. In addition, the levels of CD80 and CD86 in antigen-presenting cells were significantly increased after STING activation. Furthermore, innate immune activation altered the systemic T cell-mediated immune responses, induced proliferation of macrophages, inhibited tumor growth, and increased numbers of cytotoxic memory T cells. Tumor-specific lymphocytes also increased in number after treatment with DMXAA.

conclusionThe abscopal effect of DMXAA treatment on the skin strongly reduced the spread of EML4-ALK lung cancer and CT26 colon cancer through the STING pathway and induced the presentation of antigens.

Indexed as

Memory T CellsSkin NeoplasmsAnimalsImmunotherapyMacrophagesMembrane ProteinsMiceMembrane Proteinslung cancermacrophagesskin metastasisSTING agonistT cell-mediated immune response

Identifiers

PMID34913283
PMCPMC8688365
OpenAlexW4200576291

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.