Evidence map›Paper›PMID 33816301›Full record

ArticleFrontiers in oncology2021

Targeting the MDSCs of Tumors In Situ With Inhibitors of the MAPK Signaling Pathway to Promote Tumor Regression.

Jiayun Yu, Hanwen Li, Zongliang Zhang, Weimin Lin, Xiawei Wei, Bin Shao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. 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

6 authors at 3 institutions in 1 country.

Jiayun YuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Hanwen LiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Zongliang ZhangDepartment of Radiotherapy, Cancer Center, State Key Laboratory of Biotherapy and Cancer Center, Laboratory of Aging Research and Cancer Drug Target, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Weimin LinState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Xiawei WeiDepartment of Radiotherapy, Cancer Center, State Key Laboratory of Biotherapy and Cancer Center, Laboratory of Aging Research and Cancer Drug Target, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.
Bin ShaoState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Sichuan University · CNState Key Laboratory of Oral DiseasesState Key Laboratory of Biotherapy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are one of the major components of the tumor microenvironment. Evidence has shown differences in the functions and fates of MDSCs in the tumor tissue and the periphery. However, the exact mechanism that regulates MDSC function has not been completely clarified. In this study, we performed RNA sequencing of MDSCs derived from the spleen and tumor. Based on the results of our RNA-seq analysis, mitogen-activated protein kinases (MAPK) were significantly increased in tumor polymorphonuclear MDSCs (PMN-MDSCs) and monocytic MDSCs (M-MDSCs). Subsequently, 3 major MAPK pathways, including extracellular signal-regulated protein kinases (ERK), p38 and c-Jun NH2-terminal kinases (JNK), were studied to analyze the role of MAPKs in MDSCs. The ERK 1/2 inhibitor SCH772984 and the JNK inhibitor SP600125 significantly increased the apoptosis of both PMN-MDSCs and M-MDSCs

Indexed as

apoptosislymphocytemitogen-activated protein kinasesmyeloid-derived suppressor cellstumor microenvironment

Identifiers

PMID33816301
PMCPMC8016393
OpenAlexW3138615402

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.