Evidence map›Paper›PMID 29996478›Full record

ReviewCancers2018

Epithelioid Hemangioendothelioma as a Model of YAP/TAZ-Driven Cancer: Insights from a Rare Fusion Sarcoma.

John M Lamar, Vijeyaluxmy Motilal Nehru, Guy Weinberg

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06680401 (The Evaluation of Cytokines and Hormones as Biomarkers for Epithelioid Haemangioendothelioma and Generation of Patient-derived Preclinical Models to Assess the Activity of Anticancer Agents and Validate Novel Therapeutic Targets), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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.

NCT06680401 recruitingnot on this mapstarted 2021, after this paper: background citation

The Evaluation of Cytokines and Hormones as Biomarkers for Epithelioid Haemangioendothelioma and Generation of Patient-derived Preclinical Models to Assess the Activity of Anticancer Agents and Validate Novel Therapeutic Targets

TypeobservationalSponsorFondazione IRCCS Istituto Nazionale dei Tumori, MilanoRan2021 to 2028Enrolled50ConditionsClinical Presentation, Natural History, Treatment Outcomes
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. [Vascular neoplasms of the liver].Pathologie (Heidelberg, Germany) · 2025
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  14. Genes & development · 2021
    Article
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  19. Vascular tumors of the mediastinum.Mediastinum (Hong Kong, China) · 2020
    Review
  20. Article
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

3 authors at 3 institutions in 1 country.

John M LamarDepartment of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA. lamarj@mail.amc.edu.ORCID 0000-0001-5406-8391
Vijeyaluxmy Motilal NehruDepartment of Oncology, University of Illinois College of Medicine, Chicago, IL 60612, USA. vmotil2@uic.edu.
Guy WeinbergDepartment of Anesthesiology, University of Illinois College of Medicine, and Jesse Brown VA Medical Center, Chicago, IL 60612, USA. guyw@uic.edu.
Albany Medical Center Hospital · USIllinois College · USUniversity of Illinois Urbana-Champaign · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelioid hemangioendothelioma (EHE) is a rare soft-tissue sarcoma involving cells with histologic markers that suggest an endothelial origin. Around 90% of EHEs are caused by the fusion of Transcriptional Co-activator with a PDZ-motif (TAZ) with Calmodulin Binding Transcription Activator 1 (CAMTA1), a central nervous system-specific transcription activator. The 10% of EHEs that lack the TAZ⁻CAMTA1 fusion instead have a fusion of Yes-associated Protein (YAP) and Transcription Factor E3 (TFE3) genes (YAP-TFE3). YAP and TAZ are well-defined downstream effectors in the Hippo pathway that promote cell growth when translocated to the nucleus. The TAZ⁻CAMTA1 fusion transcript is insensitive to the Hippo inhibitory signals that normally prevent this process and thus constitutively activates the TAZ transcriptome. In EHE, this causes tumors to form in a variety of organs and tissue types, most commonly the liver, lung, and bone. Its clinical course is unpredictable and highly variable. TAZ activation is known to contribute to key aspects of the cancer phenotype, including metastasis and fibrosis, and increased expression of TAZ is thought to be causally related to the progression of many cancers, including breast, lung, and liver. Therefore, understanding TAZ biology and the molecular mechanisms by which it promotes unregulated cell proliferation will yield insights and possibly improved treatments for both EHE as well as much more common cancers.

Indexed as

epithelioid hemangioendotheliomafusion sarcomaHippo signalingTAZtranscriptional coactivatorsYAP

Identifiers

PMID29996478
PMCPMC6070876
OpenAlexW2872830304

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.