Evidence map›Paper›PMID 29976629›Full record

ArticleCancer genomics & proteomics

The Dual PI3K/mToR Inhibitor Omipalisib/GSK2126458 Inhibits Clonogenic Growth in Oncogenically-transformed Cells from Neurocutaneous Melanocytosis.

Dipanjan Basu, Cláudia M Salgado, Bruce Bauer, Yasmin Khakoo, Janki R Patel, Ryan M Hoehl, Dominique M Bertolini, Joie Zabec, Morgan R Brzozowski, Miguel Reyes-Múgica

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. 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 20% 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, 23 citations in OpenAlex.

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  11. Neurocutaneous melanocytosis (melanosis).Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020
    Article
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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 1 institution in 1 country.

Dipanjan BasuDepartment of Pathology, Children's Hospital of Pittsburgh, Pittsburgh, PA, U.S.A basud@upmc.edu.
Cláudia M SalgadoDepartment of Pathology, Children's Hospital of Pittsburgh, Pittsburgh, PA, U.S.A.
Bruce BauerDivision of Plastic and Reconstructive Surgery, North Shore University Health System, Northbrook, IL, U.S.A.
Yasmin KhakooDepartment of Pediatrics and Neurology, Memorial Sloan Kettering Cancer Center, New York, NY, U.S.A.
Janki R PatelDietrich School of Arts and Sciences, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Ryan M HoehlDietrich School of Arts and Sciences, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Dominique M BertoliniDietrich School of Arts and Sciences, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Joie ZabecDietrich School of Arts and Sciences, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Morgan R BrzozowskiDietrich School of Arts and Sciences, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Miguel Reyes-MúgicaDepartment of Pathology, Children's Hospital of Pittsburgh, Pittsburgh, PA, U.S.A.
Children's Hospital of Pittsburgh · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

backgroundOmipalisib has been found to affect the viability of cancer cells. However, its effect on clonogenicity - a feature of cancer stem cells, is not clear. Cells isolated from neurocutaneous melanocytosis (NCM) patients' lesions grow clonogenically. The aim of this study was to investigate the effect of omipalisib treatment on clonogenic growth of NCM cells in vitro. MATERIALS AND

methodsClonogenic growth efficiency was evaluated by colony formation assays with or without specific growth factors. Activation of MEK and Akt was determined by immunoblots. Colony formation and cell viability were assessed upon pharmacological inhibition of MEK, Akt and mToR.

resultsClonogenicity appeared to depend on bFGF and IGF1signaling through ERK and Akt. Omipalisib treatment prevented colony formation and induced autophagic cell death.

conclusionSignaling through Akt is important for survival of clonogenic cells in NCM, and omipalisib treatment as a monotherapy or in combination with MEK162 could be an effective therapeutic strategy to inhibit clonogenic growth.

Indexed as

Phosphoinositide-3 Kinase InhibitorsApoptosisBenzenesulfonamidesCell ProliferationCell Transformation, NeoplasticFemaleHumansInfantMelanomaMelanosisNeurocutaneous SyndromesProto-Oncogene Proteins c-aktPyridazinesQuinolinesSignal TransductionSkin NeoplasmsBenzenesulfonamidesMTOR protein, humanomipalisibPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktPyridazinesQuinolinesSulfonamidesTOR Serine-Threonine KinasesClonogenicityMEK162neurocutaneous melanocytosisomipalisib

Identifiers

PMID29976629
PMCPMC6070711
OpenAlexW2858643434

What OpenQuestion 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 OpenQuestion graph.