Evidence map›Paper›PMID 29904909›Full record

ArticleJournal of cellular physiology2018

Inactivation of Tp53 and Pten drives rapid development of pleural and peritoneal malignant mesotheliomas.

Eleonora Sementino, Craig W Menges, Yuwaraj Kadariya, Suraj Peri, Jinfei Xu, Zemin Liu, Richard G Wilkes, Kathy Q Cai, Frank J Rauscher, Andres J Klein-Szanto and 1 more

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  9. Review
  10. Genomics and Functional Genomics of Malignant Pleural Mesothelioma.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Article
  13. Review
  14. Antagonists of growth hormone-releasing hormone (GHRH) inhibit the growth of human malignant pleural mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Review
  16. 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

11 authors at 2 institutions in 1 country.

Eleonora SementinoCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Craig W MengesCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.ORCID 0000-0002-8305-9811
Yuwaraj KadariyaCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Suraj PeriDepartment of Biostatistics and Bioinformatics, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Jinfei XuCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Zemin LiuCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Richard G WilkesCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Kathy Q CaiHistopathology Facility, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Frank J RauscherGene Expression and Regulation Program, Wistar Institute, Philadelphia, Pennsylvania.
Andres J Klein-SzantoHistopathology Facility, Fox Chase Cancer Center, Philadelphia, Pennsylvania.
Joseph R TestaCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.ORCID 0000-0003-1301-5175
Fox Chase Cancer Center · USThe Wistar Institute · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Pathogenesis of Malignant Mesothelioma by the Human Polycomb Complex BAP1-ASXLR01CA175691 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI RAUSCHER III, FRANK JOSEPH, TESTA, JOSEPH R. · 2014 to 2018
$2.7M
NCI NIH HHS P30 CA006927NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA175691
6 · The paper itself

Abstract

Malignant mesothelioma (MM) is a therapy-resistant cancer arising primarily from the lining of the pleural and peritoneal cavities. The most frequently altered genes in human MM are cyclin-dependent kinase inhibitor 2A (CDKN2A), which encodes components of the p53 (p14ARF) and RB (p16INK4A) pathways, BRCA1-associated protein 1 (BAP1), and neurofibromatosis 2 (NF2). Furthermore, the p53 gene (TP53) itself is mutated in ~15% of MMs. In many MMs, the PI3K-PTEN-AKT-mTOR signaling node is hyperactivated, which contributes to tumor cell survival and therapeutic resistance. Here, we demonstrate that the inactivation of both Tp53 and Pten in the mouse mesothelium is sufficient to rapidly drive aggressive MMs. Pten

Indexed as

AnimalsCarcinogenesisCell ProliferationDisease Models, AnimalHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantMicePeritoneal NeoplasmsPleural NeoplasmsPTEN PhosphohydrolaseSignal TransductionTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1 protein, humanPTEN PhosphohydrolasePten protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin ThiolesteraseBap1genomic instabilitymesotheliomap53Pten

Identifiers

PMID29904909
PMCPMC6168364
OpenAlexW2808091376

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.