Evidence map›Paper›PMID 31758086›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2020

Establishment of a Gorlin syndrome model from induced neural progenitor cells exhibiting constitutive GLI1 expression and high sensitivity to inhibition by smoothened (SMO).

Hajime Ikehara, Katsunori Fujii, Toshiyuki Miyashita, Yu Ikemoto, Marina Nagamine, Naoki Shimojo, Akihiro Umezawa

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

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  4. Review
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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

7 authors at 3 institutions in 1 country.

Hajime IkeharaCenter for Regenerative Medicine, National Center for Child Health and Development Research Institute, 2-10-1, Okura, Setagaya, Tokyo, 157-8535, Japan.
Katsunori FujiiDepartment of Pediatrics, Chiba University Graduate School of Medicine, Chiba, Japan.
Toshiyuki MiyashitaDepartment of Molecular Genetics, Kitasato University School of Medicine, Kanagawa, Japan.
Yu IkemotoCenter for Regenerative Medicine, National Center for Child Health and Development Research Institute, 2-10-1, Okura, Setagaya, Tokyo, 157-8535, Japan.
Marina NagamineCenter for Regenerative Medicine, National Center for Child Health and Development Research Institute, 2-10-1, Okura, Setagaya, Tokyo, 157-8535, Japan.
Naoki ShimojoDepartment of Pediatrics, Chiba University Graduate School of Medicine, Chiba, Japan.
Akihiro UmezawaCenter for Regenerative Medicine, National Center for Child Health and Development Research Institute, 2-10-1, Okura, Setagaya, Tokyo, 157-8535, Japan. umezawa@1985.jukuin.keio.ac.jp.
Chiba University · JPNational Center For Child Health and Development · JPKitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hedgehog signaling pathway is a vital factor for embryonic development and stem cell maintenance. Dysregulation of its function results in tumor initiation and progression. The aim of this research was to establish a disease model of hedgehog-related tumorigenesis with Gorlin syndrome-derived induced pluripotent stem cells (GS-iPSCs). Induced neural progenitor cells from GS-iPSCs (GS-NPCs) show constitutive high GLI1 expression and higher sensitivity to smoothened (SMO) inhibition compared with wild-type induced neural progenitor cells (WT-NPCs). The differentiation process from iPSCs to NPCs may have similarity in gene expression to Hedgehog signal-related carcinogenesis. Therefore, GS-NPCs may be useful for screening compounds to find effective drugs to control Hedgehog signaling activity.

Indexed as

Basal Cell Nevus SyndromeNeural Stem CellsSmoothened ReceptorZinc Finger Protein GLI1AnilidesCell DifferentiationCells, CulturedHumansModels, BiologicalPatched-1 ReceptorPyridinesSignal TransductionAnilidesGLI1 protein, humanHhAntag691Patched-1 ReceptorPTCH1 protein, humanPyridinesSmoothened ReceptorSMO protein, humanZinc Finger Protein GLI1GLI1hedgehog signaling pathwayinduced pluripotent stem cellsPTCH1vismodegib

Identifiers

PMID31758086
OpenAlexW2990626157

What Socratic holds

Textmetadata
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 Socratic graph.