Evidence map›Paper›PMID 27875244›Full record

ArticleEndocrine-related cancer2017

A six-genotype genetic prognostic model for papillary thyroid cancer.

Xiaopei Shen, Rengyun Liu, Mingzhao Xing

Open access · bronzeAbstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrine-related cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 4 pooled it
6.7field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 4 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Xiaopei ShenLaboratory for Cellular and Molecular Thyroid ResearchDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Rengyun LiuLaboratory for Cellular and Molecular Thyroid ResearchDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mingzhao XingLaboratory for Cellular and Molecular Thyroid ResearchDivision of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA mxing1@jhmi.edu.
Johns Hopkins University · US

Funding

Genetic & Epigenetic Events in Papillary Thyroid CancerR01CA113507 · NCI · JOHNS HOPKINS UNIVERSITY · PI XING, MICHAEL MINGZHAO · 2006 to 2015
$2.2M
TERT Promoter Mutations in Thyroid CancerR01CA189224 · NCI · JOHNS HOPKINS UNIVERSITY · PI XING, MICHAEL MINGZHAO · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA113507NCI NIH HHS R01 CA189224
6 · The paper itself

Abstract

A unique prognostic role of the genetic duet of BRAF V600E and TERT promoter mutations in papillary thyroid cancer (PTC) has been recently established, but the role of RAS mutation in this genetic interplay remains to be established. Using The Cancer Genome Atlas (TCGA) data of patients with PTC from 19 medical centers, we investigated the interactions among the three mutations in clinical outcomes of PTC. We found that BRAF and RAS mutations were mutually exclusive, but both were associated with TERT promoter mutations, with the genetic duet of BRAF/RAS and TERT mutations occurring in 34/388 (8.76%) patients. BRAF/RAS or TERT mutation had no or minimal effect alone, whereas coexisting BRAF/RAS and TERT mutations had a robust synergistic effect on poor clinicopathologic outcomes of PTC, including disease recurrence and patient mortality. For example, PTC recurrence rate was 52% with coexisting BRAF V600E/RAS and TERT promoter mutations vs 6.9% with no mutation, corresponding to a HR of 8.17 (95% CI 3.09-21.58), which remained significant at 14.71 (95% CI 2.79-77.61) after adjustment for clinicopathologic factors and institution. BRAF/RAS mutation or TERT mutation alone minimally affected Kaplan-Meier patient survival curves, whereas the genetic duet was associated with a sharp curve decline. Thus, by confirming and expanding previous findings in single-institution studies, this multicenter data analysis establishes a six-genotype genetic prognostic model for poor outcomes of PTC with a risk order of genetic duet of BRAF V600E/RAS mutation and TERT mutation >>>>BRAF V600E = TERT mutation alone >RAS mutation alone = wild-type genes.

Indexed as

Carcinoma, PapillaryGenotypeHumansKaplan-Meier EstimateModels, BiologicalMutationNeoplasm Recurrence, LocalPrognosisPromoter Regions, GeneticProto-Oncogene Proteins B-rafras ProteinsTelomeraseThyroid Cancer, PapillaryThyroid NeoplasmsBRAF protein, humanProto-Oncogene Proteins B-rafras ProteinsTelomeraseTERT protein, humanBRAF V600E mutationprognostic molecular markersRAS mutationTERT promoter mutationthyroid cancer

Identifiers

PMID27875244
PMCPMC5132178
OpenAlexW2549607136

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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.