Evidence map›Paper›PMID 26662608›Full record

ArticleEndocrine pathology2016

STK11 Mutation Identified in Thyroid Carcinoma.

Shuanzeng Wei, Virginia A LiVolsi, Marcia S Brose, Kathleen T Montone, Jennifer J D Morrissette, Zubair W Baloch

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in Endocrine pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Genetic susceptibility to hereditary non-medullary thyroid cancer.Hereditary cancer in clinical practice · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Disease pattern in Danish patients with Peutz-Jeghers syndrome.International journal of colorectal disease · 2016
    Article
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 2 institutions in 1 country.

Shuanzeng WeiDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA, 19104, USA. weishuanzeng@hotmail.com.
Virginia A LiVolsiDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA, 19104, USA. linus@mail.med.upenn.edu.
Marcia S BroseDepartment of Otorhinolaryngology, Abramson Cancer Center of the University of Pennsylvania, Philadelphia, PA, USA. brosem@mail.med.upenn.edu.
Kathleen T MontoneDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA, 19104, USA. kmontone@mail.med.upenn.edu.
Jennifer J D MorrissetteDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA, 19104, USA. Jennifer.Morrissette@uphs.upenn.edu.
Zubair W BalochDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA, 19104, USA. baloch@mail.med.upenn.edu.
Hospital of the University of Pennsylvania · USUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peutz-Jeghers syndrome (PJS) is an autosomal-dominant disorder, in which germline mutation of serine threonine-protein kinase 11 (STK11) is identified in up to 90 % of the patients who meet clinical criteria for PJS. Hematoxylin and eosin (H&E) slides of the tumor were reviewed to confirm areas with at least 25 % of tumor cellularity. Then, the designated area was extracted for genomic DNA. Targeted next-generation sequencing analysis was performed using a 47-gene panel. Case 1 is a 71-year-old man with high grade follicular thyroid carcinoma with clear cell and oncocytic features. The carcinoma showed a missense mutation in TP53 (p.R342G, c.1024C > G) and a 16-nucleotide intronic deletion started next to the 3' of exon 6 (involving the canonical +1 and +2 bases of the splice donor site) in STK11 (p.?, c.862 + 1_862 + 16delGTGGGAGCCTCATCCC). Case 2 is a 76-year-old woman with tall cell variant papillary thyroid carcinoma. The carcinoma demonstrated a missense mutation in BRAF (p.V600E, c.1799T > A) and a missense mutation in STK11 (p.F354L, c.1062C > G). In summary, we present two elderly patients with thyroid carcinoma harboring STK11 mutation without clinical manifestation of PJS. The findings suggest that STK11 may play a role in thyroid carcinoma development.

Indexed as

Mutation, MissenseAdenocarcinoma, FollicularAgedAMP-Activated Protein Kinase KinasesBiomarkers, TumorCarcinomaCarcinoma, PapillaryFemaleHumansImmunohistochemistryMaleOligonucleotide Array Sequence AnalysisProtein Serine-Threonine KinasesThyroid Cancer, PapillaryThyroid NeoplasmsAMP-Activated Protein Kinase KinasesBiomarkers, TumorProtein Serine-Threonine KinasesSTK11 protein, humanCarcinomaLKB1MutationSTK11Thyroid

Identifiers

PMID26662608
OpenAlexW2191308414

What OpenQuestion holds

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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.