Evidence map›Paper›PMID 36902186›Full record

ArticleInternational journal of molecular sciences2023

ETC-159, an Upstream Wnt inhibitor, Induces Tumour Necrosis via Modulation of Angiogenesis in Osteosarcoma.

Kenon Chua, Arthur Yi Loong Sim, Eric Yew Meng Yeo, Muhammad Sufyan Bin Masroni, Wah Wah Naw, Sai Mun Leong, Kee Wah Lee, Huey Jin Lim, David M Virshup, Victor Kwan Min Lee

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Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% 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, 13 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Kenon ChuaProgramme in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore 169857, Singapore.
Arthur Yi Loong SimDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.ORCID 0000-0002-1487-3684
Eric Yew Meng YeoDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.
Muhammad Sufyan Bin MasroniDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.ORCID 0000-0003-0259-1724
Wah Wah NawDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.ORCID 0000-0002-3971-1577
Sai Mun LeongDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.
Kee Wah LeeDepartment of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, MD10, 4 Medical Drive, Singapore 117594, Singapore.
Huey Jin LimDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.
David M VirshupProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore 169857, Singapore.
Victor Kwan Min LeeDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Level 3 NUH Main Building, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.
National University of Singapore · SGDuke-NUS Medical School · SGSingHealth · SG

Funding

National Medical Research Council MOH-000156-00
6 · The paper itself

Abstract

There is an increasing urgency in the search for new drugs to target high-grade cancers such as osteosarcomas (OS), as these have limited therapeutic options and poor prognostic outlook. Even though key molecular events leading to tumorigenesis are not well understood, it is widely agreed that OS tumours are Wnt-driven. ETC-159, a PORCN inhibitor that inhibits the extracellular secretion of Wnt, has recently progressed on to clinical trials. In vitro and in vivo murine and chick chorioallantoic membrane xenograft models were established to examine the effect of ETC-159 on OS. Consistent with our hypothesis, we noted that ETC-159 treatment not only resulted in markedly decreased β-catenin staining in xenografts, but also increased tumour necrosis and a significant reduction in vascularity-a hereby yet undescribed phenotype following ETC-159 treatment. Through further understanding the mechanism of this new window of vulnerability, therapies can be developed to potentiate and maximize the effectiveness of ETC-159, further increasing its clinical utility for the treatment of OS.

Indexed as

AcyltransferasesBone NeoplasmsNeovascularization, PathologicOsteosarcomaWnt Signaling PathwayAnimalsbeta CateninCarcinogenesisCell Line, TumorCell ProliferationHeterocyclic Compounds, 4 or More RingsHumansMembrane ProteinsMiceNecrosisAcyltransferasesbeta CateninETC-159Heterocyclic Compounds, 4 or More RingsMembrane ProteinsPORCN protein, humanangiogenesisETC-159osteosarcomaWnt

Identifiers

PMID36902186
PMCPMC10003732
OpenAlexW4322774389

What OpenQuestion holds

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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.