Evidence map›Paper›PMID 34731936›Full record

ArticleEndocrinology and metabolism (Seoul, Korea)2021

Whole-Exome Sequencing in Papillary Microcarcinoma: Potential Early Biomarkers of Lateral Lymph Node Metastasis.

Mijin Kim, Chae Hwa Kwon, Min Hee Jang, Jeong Mi Kim, Eun Heui Kim, Yun Kyung Jeon, Sang Soo Kim, Kyung-Un Choi, In Joo Kim, Meeyoung Park and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Endocrinology and metabolism (Seoul, Korea), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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

11 authors at 2 institutions in 1 country.

Mijin KimDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Chae Hwa KwonBiomedical Research Institute, Pusan National University Hospital, Pusan National University School of Medicine, Busan, Korea.
Min Hee JangDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Jeong Mi KimDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Eun Heui KimDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Yun Kyung JeonDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Sang Soo KimDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Kyung-Un ChoiDepartment of Pathology, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
In Joo KimDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Meeyoung ParkResearch Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Korea.
Bo Hyun KimDepartment of Internal Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
Pusan National University Hospital · KRPusan National University Yangsan Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEarly identification of patients with high-risk papillary thyroid microcarcinoma (PTMC) that is likely to progress has become a critical challenge. We aimed to identify somatic mutations associated with lateral neck lymph node (LN) metastasis (N1b) in patients with PTMC.

methodsWhole-exome sequencing (WES) of 14 PTMCs with no LN metastasis (N0) and 13 N1b PTMCs was performed using primary tumors and matched normal thyroid tissues.

resultsThe mutational burden was comparable in N0 and N1b tumors, as the median number of mutations was 23 (range, 12 to 46) in N0 and 24 (range, 12 to 50) in N1b PTMC (P=0.918). The most frequent mutations were detected in PGS1, SLC4A8, DAAM2, and HELZ in N1b PTMCs alone, and the K158Q mutation in PGS1 (four patients, Fisher's exact test P=0.041) was significantly enriched in N1b PTMCs. Based on pathway analysis, somatic mutations belonging to the receptor tyrosine kinase-RAS and NOTCH pathways were most frequently affected in N1b PTMCs. We identified four mutations that are predicted to be pathogenic in four genes based on Clinvar and Combined Annotation-Dependent Depletion score: BRAF, USH2A, CFTR, and PHIP. A missense mutation in CFTR and a nonsense mutation in PHIP were detected in N1b PTMCs only, although in one case each. BRAF mutation was detected in both N0 and N1b PTMCs.

conclusionThis first comprehensive WES analysis of the mutational landscape of N0 and N1b PTMCs identified pathogenic genes that affect biological functions associated with the aggressive phenotype of PTMC.

Indexed as

Lymph NodesBiomarkersCarcinoma, PapillaryExome SequencingHumansLymphatic MetastasisThyroid NeoplasmsBiomarkersBiomarkersMutationNeoplasm metastasisPapillary thyroid microcarcinomaWhole exome sequencing

Identifiers

PMID34731936
PMCPMC8566127
OpenAlexW3208252307

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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.