Evidence map›Paper›PMID 32457900›Full record

ArticleFrontiers in cell and developmental biology2020

An FGFR/AKT/SOX2 Signaling Axis Controls Pancreatic Cancer Stemness.

Mei-Yu Quan, Qiang Guo, Jiayu Liu, Ruo Yang, Jing Bai, Wei Wang, Yaxin Cai, Rui Han, Yu-Qing Lv, Li Ding and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. FGFR Inhibitor AZD4547 Disrupts Inflammatory CAF Crosstalk With Cancer Cells and Macrophages and Attenuates Metastasis in Pancreatic Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 3 countries.

Mei-Yu QuanSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Qiang GuoSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Jiayu LiuInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Ruo YangSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Jing BaiSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Wei WangSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Yaxin CaiInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Rui HanSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Yu-Qing LvCenter for Precision Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Li DingDivision of Oncology Research and Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN, United States.
Daniel D BilladeauDivision of Oncology Research and Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN, United States.
Zhenkun LouDivision of Oncology Research and Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN, United States.
Saverio BellusciInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Xiaokun LiSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Jin-San ZhangSchool of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CNNovel (United States) · USWenzhou University · CNMayo Clinic · USUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stemness is associated with high malignancy and low differentiation, as well as therapeutic resistance of tumors including pancreatic ductal adenocarcinoma (PDAC). Fibroblast growth factors (FGFs) exert pleiotropic effects on a variety of cellular processes and functions including embryonic stem cell pluripotency and cancer cell stemness via the activation of four tyrosine kinase FGF receptors (FGFRs). FGF ligands have been a major component of the cocktail of growth factors contained in the cancer stemness-inducing (CSI) and organoid culture medium. Although FGF/FGFR signaling has been hypothesized to maintain cancer stemness, its function in this process is still unclear. We report that inhibition of FGF/FGFR signaling impairs sphere-forming ability of PDAC

Indexed as

FGFRpancreatic cancerSOX2sphere-formation assaystemness

Identifiers

PMID32457900
PMCPMC7221133
OpenAlexW3022653165

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.