Evidence map›Paper›PMID 24300787›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014

PID1 (NYGGF4), a new growth-inhibitory gene in embryonal brain tumors and gliomas.

Anat Erdreich-Epstein, Nathan Robison, Xiuhai Ren, Hong Zhou, Jingying Xu, Tom B Davidson, Mathew Schur, Floyd H Gilles, Lingyun Ji, Jemily Malvar and 10 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  13. MEK Inhibition Suppresses Growth of Atypical Teratoid/Rhabdoid Tumors.Journal of neuropathology and experimental neurology · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 2 countries.

Anat Erdreich-EpsteinAuthors' Affiliations: Departments of Pediatrics, Pathology, Radiology, and Neurosurgery, at the Saban Research Institute at Children's Hospital Los Angeles, Norris Comprehensive Cancer Center; Departments of Preventive Medicine and Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California; Division of Pediatric Neurooncology at the German Cancer Research Center DKFZ; and Department of Pediatric Hematology and Oncology, Heidelberg University Hospital, Heidelberg, Germany.
Nathan Robison
Xiuhai Ren
Hong Zhou
Jingying Xu
Tom B Davidson
Mathew Schur
Floyd H Gilles
Lingyun Ji
Jemily Malvar
Gregory M Shackleford
Ashley S Margol
Mark D Krieger
Alexander R Judkins
David T W Jones
Stefan M Pfister
Marcel Kool
Richard Sposto
Shahab Asgharzadeh
Shahab Asgharazadeh
University of Southern California · USUniversity Hospital Heidelberg · DEGerman Cancer Research Center · DEHeidelberg University · DE

Funding

Training Physician Scientists in Pediatric OncologyT32CA009659 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI DECLERCK, YVES A · 1991 to 2020
$2.2M
Tumor-Inhibitory Effects of P1D1 in GliomasR21NS077007 · NINDS · CHILDREN'S HOSPITAL OF LOS ANGELES · PI ERDREICH-EPSTEIN, ANAT · 2011 to 2012
$440k
NCI NIH HHS T32 CA009659NINDS NIH HHS 1R21NS077007-01NINDS NIH HHS R21 NS077007
6 · The paper itself

Abstract

purposeWe present here the first report of PID1 (Phosphotyrosine Interaction Domain containing 1; NYGGF4) in cancer. PID1 was identified in 2006 as a gene that modulates insulin signaling and mitochondrial function in adipocytes and muscle cells. EXPERIMENTAL DESIGN AND

resultsUsing four independent medulloblastoma datasets, we show that mean PID1 mRNA levels were lower in unfavorable medulloblastomas (groups 3 and 4, and anaplastic histology) compared with favorable medulloblastomas (SHH and WNT groups, and desmoplastic/nodular histology) and with fetal cerebellum. In two large independent glioma datasets, PID1 mRNA was lower in glioblastomas (GBM), the most malignant gliomas, compared with other astrocytomas, oligodendrogliomas and nontumor brains. Neural and proneural GBM subtypes had higher PID1 mRNA compared with classical and mesenchymal GBM. Importantly, overall survival and radiation-free progression-free survival were longer in medulloblastoma patients whose tumors had higher PID1 mRNA (univariate and multivariate analyses). Higher PID1 mRNA also correlated with longer overall survival in patients with glioma and GBM. In cell culture, overexpression of PID1 inhibited colony formation in medulloblastoma, atypical teratoid rhabdoid tumor (ATRT), and GBM cell lines. Increasing PID1 also increased cell death and apoptosis, inhibited proliferation, induced mitochondrial depolaization, and decreased serum-mediated phosphorylation of AKT and ERK in medulloblastoma, ATRT, and/or GBM cell lines, whereas siRNA to PID1 diminished mitochondrial depolarization.

conclusionsThese data are the first to link PID1 to cancer and suggest that PID1 may have a tumor inhibitory function in these pediatric and adult brain tumors.

Indexed as

Carrier ProteinsCell Line, TumorCerebellar NeoplasmsChild, PreschoolDisease-Free SurvivalFemaleGene ExpressionHumansKaplan-Meier EstimateMaleMedulloblastomaNeoplasms, Germ Cell and EmbryonalProportional Hazards ModelsRNA, MessengerCarrier ProteinsPID1 protein, humanRNA, Messenger

Identifiers

PMID24300787
PMCPMC3962776
OpenAlexW2099447701

What OpenQuestion holds

Textmetadata
LicenceTDM
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.