Evidence map›Paper›PMID 35626065›Full record

ReviewCancers2022

Looking at Thyroid Cancer from the Tumor-Suppressor Genes Point of View.

Sadegh Rajabi, Catherine Alix-Panabières, Arshia Sharbatdar Alaei, Raziyeh Abooshahab, Heewa Shakib, Mohammad Reza Ashrafi

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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 5 institutions in 3 countries.

Sadegh RajabiTraditional Medicine and Materia Medica Research Center, Shahid Beheshti University of Medical Sciences, Tehran 19839-63113, Iran.ORCID 0000-0003-0177-7922
Catherine Alix-PanabièresLaboratory of Rare Human Circulating Cells (LCCRH), University Medical Centre of Montpellier, CEDEX 5, 34093 Montpellier, France.ORCID 0000-0002-6401-2903
Arshia Sharbatdar AlaeiDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran 19839-63113, Iran.
Raziyeh AbooshahabCurtin Medical School, Curtin University, Bentley, WA 6102, Australia.ORCID 0000-0001-7379-0339
Heewa ShakibCellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19857-17443, Iran.
Mohammad Reza AshrafiDepartment of Biochemistry, Afzalipoor Faculty of Medicine, Kerman University of Medical Sciences, Kerman 76169-13555, Iran.
Shahid Beheshti University of Medical Sciences · IRCentre National de la Recherche Scientifique · FRCurtin University · AUKerman University of Medical Sciences · IRResearch Institute for Endocrine Sciences · IR

Funding

C.A.-P. is supported by the ELBA project, which has received funding from the European Union Horizon 2020 Research and Innovation program under the Marie Skłodowska-Curie grant agreement No 765492 as well as by the National Institute of Cancer (INCa, http No 765492
6 · The paper itself

Abstract

Thyroid cancer is the most frequent endocrine malignancy and accounts for approximately 1% of all diagnosed cancers. A variety of mechanisms are involved in the transformation of a normal tissue into a malignant one. Loss of tumor-suppressor gene (TSG) function is one of these mechanisms. The normal functions of TSGs include cell proliferation and differentiation control, genomic integrity maintenance, DNA damage repair, and signaling pathway regulation. TSGs are generally classified into three subclasses: (i) gatekeepers that encode proteins involved in cell cycle and apoptosis control; (ii) caretakers that produce proteins implicated in the genomic stability maintenance; and (iii) landscapers that, when mutated, create a suitable environment for malignant cell growth. Several possible mechanisms have been implicated in TSG inactivation. Reviewing the various TSG alteration types detected in thyroid cancers may help researchers to better understand the TSG defects implicated in the development/progression of this cancer type and to find potential targets for prognostic, predictive, diagnostic, and therapeutic purposes. Hence, the main purposes of this review article are to describe the various TSG inactivation mechanisms and alterations in human thyroid cancer, and the current therapeutic options for targeting TSGs in thyroid cancer.

Indexed as

gene therapyinactivationmutationthyroid cancertumor-suppressor gene

Identifiers

PMID35626065
PMCPMC9139614
OpenAlexW4280598478

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.