Evidence map›Paper›PMID 29526163›Full record

ReviewJournal of biomedical science2018

Mechanisms of human telomerase reverse transcriptase (hTERT) regulation: clinical impacts in cancer.

Ricardo Leão, Joana Dias Apolónio, Donghyun Lee, Arnaldo Figueiredo, Uri Tabori, Pedro Castelo-Branco

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of biomedical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 4 pooled it
13.4field-weighted citation impact, top 1% 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

158 citing papers in PubMed, 4 syntheses or guidelines pooled it, 252 citations in OpenAlex.

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98 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

6 authors at 4 institutions in 3 countries.

Ricardo LeãoDivision of Urology, Department of Surgery Princess Margaret Cancer Centre, University Health Network, 610 University Ave 3-130, Toronto, ON, M5G 2M9, Canada. romaoleao@gmail.com.ORCID http://orcid.org/0000-0003-3719-717X
Joana Dias ApolónioRegenerative Medicine Program, Department of Biomedical Sciences and Medicine, University of Algarve, Edifício 2 - Ala Norte, 8005-139, Faro, Portugal.
Donghyun LeeArthur and Sonia Labatt Brain Tumor Research Center, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Arnaldo FigueiredoFaculty of Medicine, University of Coimbra, R. Larga, 3004-504, Coimbra, Coimbra, Portugal.
Uri TaboriArthur and Sonia Labatt Brain Tumor Research Center, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Pedro Castelo-BrancoRegenerative Medicine Program, Department of Biomedical Sciences and Medicine, University of Algarve, Edifício 2 - Ala Norte, 8005-139, Faro, Portugal.
Algarve Biomedical Center · PTUniversity of Toronto · CAUniversity Health Network · CAUniversity of Coimbra · PT

Funding

Fundação para a Ciência e a Tecnologia PD/BD/105899/2014Fundação para a Ciência e a Tecnologia SFRH/BD/102232/2014Fundação para a Ciência e a Tecnologia UID/BIM/04773/2013
6 · The paper itself

Abstract

backgroundLimitless self-renewal is one of the hallmarks of cancer and is attained by telomere maintenance, essentially through telomerase (hTERT) activation. Transcriptional regulation of hTERT is believed to play a major role in telomerase activation in human cancers. MAIN BODY: The dominant interest in telomerase results from its role in cancer. The role of telomeres and telomere maintenance mechanisms is well established as a major driving force in generating chromosomal and genomic instability. Cancer cells have acquired the ability to overcome their fate of senescence via telomere length maintenance mechanisms, mainly by telomerase activation. hTERT expression is up-regulated in tumors via multiple genetic and epigenetic mechanisms including hTERT amplifications, hTERT structural variants, hTERT promoter mutations and epigenetic modifications through hTERT promoter methylation. Genetic (hTERT promoter mutations) and epigenetic (hTERT promoter methylation and miRNAs) events were shown to have clinical implications in cancers that depend on hTERT activation. Knowing that telomeres are crucial for cellular self-renewal, the mechanisms responsible for telomere maintenance have a crucial role in cancer diseases and might be important oncological biomarkers. Thus, rather than quantifying TERT expression and its correlation with telomerase activation, the discovery and the assessment of the mechanisms responsible for TERT upregulation offers important information that may be used for diagnosis, prognosis, and treatment monitoring in oncology. Furthermore, a better understanding of these mechanisms may promote their translation into effective targeted cancer therapies.

conclusionHerein, we reviewed the underlying mechanisms of hTERT regulation, their role in oncogenesis, and the potential clinical applications in telomerase-dependent cancers.

Indexed as

CarcinogenesisGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansNeoplasmsTelomeraseTelomeraseTERT protein, humanCancer biomarkersTelomeraseTelomerase regulationTelomeres

Identifiers

PMID29526163
PMCPMC5846307
OpenAlexW2806751322

What OpenQuestion holds

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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.