Evidence map›Paper›PMID 26320182›Full record

ArticleOncotarget2015

Characterization of the metastatic phenotype of a panel of established osteosarcoma cells.

Ling Ren, Arnulfo Mendoza, Jack Zhu, Joseph W Briggs, Charles Halsey, Ellen S Hong, Sandra S Burkett, James Morrow, Michael M Lizardo, Tanasa Osborne and 4 more

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
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  12. Review
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  14. Whole-Exome Analysis and Osteosarcoma: A Game Still Open.International journal of molecular sciences · 2024
    Review
  15. Pharmacologic Inhibition of EIF4A Blocks NRF2 Synthesis to Prevent Osteosarcoma Metastasis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  16. Article
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  20. Article

22 more citing papers are in PubMed but not listed here.

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

14 authors at 6 institutions in 1 country.

Ling RenMolecular Oncology Section - Metastasis Biology Group, Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
Arnulfo MendozaMolecular Oncology Section - Metastasis Biology Group, Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
Jack ZhuGenetic Branch, National Cancer Institute, Bethesda, Maryland, USA.
Joseph W BriggsMolecular Oncology Section - Metastasis Biology Group, Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
Charles HalseyMolecular Pathology Unit, Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, Maryland, USA.
Ellen S HongMolecular Oncology Section - Metastasis Biology Group, Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
Sandra S BurkettComparative Molecular Cytogenetics Core Facility, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
James MorrowSchool of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Michael M LizardoMolecular Oncology Section - Metastasis Biology Group, Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
Tanasa OsborneNational Institute of Environmental Health, Research Triangle Park, North Carolina, USA.
Samuel Q LiSchool of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Hue H LuuDepartment of Orthopedic Surgery & Rehabilitation Medicine, University of Chicago, Medicine & Biological Sciences, Chicago, USA.
Paul MeltzerGenetic Branch, National Cancer Institute, Bethesda, Maryland, USA.
Chand KhannaMolecular Oncology Section - Metastasis Biology Group, Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA.
National Cancer Institute · USMolecular Oncology (United States) · USCase Western Reserve University · USCenter for Cancer Research · USNational Institute of Environmental Health Sciences · USUniversity of Chicago · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
Functional Genomics of SarcomaZIABC010759 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MELTZER, PAUL S. · 2009 to 2025
$22.3M
Defining novel drivers and predictive signatures of metastasis in osteosarcoma thF30CA186633 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MORROW, JAMES JULIUS · 2014 to 2017
$182k
Intramural NIH HHSNCI NIH HHS F30 CA186633NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

Osteosarcoma (OS) is the most common bone tumor in pediatric patients. Metastasis is a major cause of mortality and morbidity. The rarity of this disease coupled with the challenges of drug development for metastatic cancers have slowed the delivery of improvements in long-term outcomes for these patients. In this study, we collected 18 OS cell lines, confirmed their expression of bone markers and complex karyotypes, and characterized their in vivo tumorgenicity and metastatic potential. Since prior reports included conflicting descriptions of the metastatic and in vivo phenotypes of these models, there was a need for a comparative assessment of metastatic phenotypes using identical procedures in the hands of a single investigative group. We expect that this single characterization will accelerate the study of this metastatic cancer. Using these models we evaluated the expression of six previously reported metastasis-related OS genes. Ezrin was the only gene consistently differentially expressed in all the pairs of high/low metastatic OS cells. We then used a subtractive gene expression approach of the high and low human metastatic cells to identify novel genes that may be involved in OS metastasis. PHLDA1 (pleckstrin homology-like domain, family A) was identified as one of the genes more highly expressed in the high metastatic compared to low metastatic cells. Knocking down PHLDA1 with siRNA or shRNA resulted in down regulation of the activities of MAPKs (ERK1/2), c-Jun N-terminal kinases (JNK), and p38 mitogen-activated protein kinases (MAPKs). Reducing the expression of PHLDA1 also delayed OS metastasis progression in mouse xenograft models.

Indexed as

Cell MovementAnimalsBone NeoplasmsCell Line, TumorDisease ProgressionExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansJNK Mitogen-Activated Protein KinasesLung NeoplasmsMiceMice, Inbred BALB CMice, Inbred C3HNeoplasm InvasivenessOsteosarcomap38 Mitogen-Activated Protein KinasesExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPHLDA1 protein, humanTranscription Factorsbreast cancerDHTestrogen receptor-αintegrin αvβ3resveratrol

Identifiers

PMID26320182
PMCPMC4745740
OpenAlexW1908149944

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.