Evidence map›Paper›PMID 36272973›Full record

ArticleNature communications2022

PD-L1-directed PlGF/VEGF blockade synergizes with chemotherapy by targeting CD141

Duk Ki Kim, Juhee Jeong, Dong Sun Lee, Do Young Hyeon, Geon Woo Park, Suwan Jeon, Kyung Bun Lee, Jin-Young Jang, Daehee Hwang, Ho Min Kim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
9.3field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 95 citations in OpenAlex.

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  13. Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 2026
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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 4 institutions in 2 countries.

Duk Ki Kim *Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.
Juhee Jeong *Department of Anatomy and Cell Biology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Dong Sun LeeCenter for Biomolecular and Cellular Structure, Institute for Basic Science (IBS), Daejeon, 34126, Republic of Korea.
Do Young HyeonSchool of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Geon Woo ParkDepartment of Anatomy and Cell Biology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Suwan JeonDepartment of Anatomy and Cell Biology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Kyung Bun LeeDepartment of Pathology, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Jin-Young JangDepartment of Surgery and Cancer Research Institute, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.ORCID 0000-0003-3312-0503
Daehee HwangSchool of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Ho Min KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea. hm_kim@kaist.ac.kr.ORCID 0000-0003-0029-3643
Keehoon JungDepartment of Anatomy and Cell Biology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea. keehoon.jung@snu.ac.kr.ORCID 0000-0002-2199-5292
Seoul National University · KRInstitute for Basic Science · KRKorea Advanced Institute of Science and Technology · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year overall survival rate. Patients with PDAC display limited benefits after undergoing chemotherapy or immunotherapy modalities. Herein, we reveal that chemotherapy upregulates placental growth factor (PlGF), which directly activates cancer-associated fibroblasts (CAFs) to induce fibrosis-associated collagen deposition in PDAC. Patients with poor prognosis have high PIGF/VEGF expression and an increased number of PIGF/VEGF receptor-expressing CAFs, associated with enhanced collagen deposition. We also develop a multi-paratopic VEGF decoy receptor (Ate-Grab) by fusing the single-chain Fv of atezolizumab (anti-PD-L1) to VEGF-Grab to target PD-L1-expressing CAFs. Ate-Grab exerts anti-tumor and anti-fibrotic effects in PDAC models via the PD-L1-directed PlGF/VEGF blockade. Furthermore, Ate-Grab synergizes with gemcitabine by relieving desmoplasia. Single-cell RNA sequencing identifies that a CD141

Indexed as

Antineoplastic AgentsCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalPancreatic NeoplasmsSingle-Chain AntibodiesFemaleFibrosisHumansPlacenta Growth FactorReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor AAntineoplastic AgentsPlacenta Growth FactorReceptors, Vascular Endothelial Growth FactorSingle-Chain AntibodiesVascular Endothelial Growth Factor A

Identifiers

PMID36272973
PMCPMC9588060
OpenAlexW4307138125

What OpenQuestion holds

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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.