Evidence map›Paper›PMID 33112820›Full record

ArticleEndocrine connections2020

Akt1 genetic variants confer increased susceptibility to thyroid cancer.

Thomas Crezee, Mirela Petrulea, Doina Piciu, Martin Jaeger, Jan W A Smit, Theo S Plantinga, Carmen E Georgescu, Romana Netea-Maier

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Journal of Korean medical science · 2025
    Article
  3. 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

8 authors at 4 institutions in 2 countries.

Thomas CrezeeDepartment of Pathology, Radboud University Medical Center, Nijmegen, The Netherlands.
Mirela PetruleaDepartment of Endocrinology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Doina PiciuDepartment of Endocrinology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Martin JaegerRadboud Institute for Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands.
Jan W A SmitDivision of Endocrinology, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Theo S PlantingaDepartment of Pathology, Radboud University Medical Center, Nijmegen, The Netherlands.
Carmen E GeorgescuDepartment of Endocrinology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Romana Netea-MaierRadboud Institute for Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands.
Iuliu Hațieganu University of Medicine and Pharmacy · ROInstitute of Oncology Prof. Dr. Ion Chiricuta · RORadboud University Medical Center · NLRadboud Institute for Molecular Life Sciences · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The PI3K-Akt-mTOR pathway plays a central role in the development of non-medullary thyroid carcinoma (NMTC). Although somatic mutations have been identified in these genes in NMTC patients, the role of germline variants has not been investigated. Here, we selected frequently occurring genetic variants in AKT1, AKT2, AKT3, PIK3CA and MTOR and have assessed their effect on NMTC susceptibility, progression and clinical outcome in a Dutch discovery cohort (154 patients, 188 controls) and a Romanian validation cohort (159 patients, 260 controls). Significant associations with NMTC susceptibility were observed for AKT1 polymorphisms rs3803304, rs2494732 and rs2498804 in the Dutch discovery cohort, of which the AKT1 rs3803304 association was confirmed in the Romanian validation cohort. No associations were observed between PI3K-Akt-mTOR polymorphisms and clinical parameters including histology, TNM staging, treatment response and clinical outcome. Functionally, cells bearing the associated AKT1 rs3803304 risk allele exhibit increased levels of phosphorylated Akt protein, potentially leading to elevated signaling activity of the oncogenic Akt pathway. All together, germline encoded polymorphisms in the PI3K-Akt-mTOR pathway could represent important risk factors in development of NMTC.

Indexed as

genetic variationnon-medullary thyroid cancerPI3K/Akt/mTORsusceptibility

Identifiers

PMID33112820
PMCPMC7774771
OpenAlexW3092575530

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.