Evidence map›Paper›PMID 23924149›Full record

ArticleThyroid : official journal of the American Thyroid Association2014

Thyrotropin signaling confers more aggressive features with higher genomic instability on BRAF(V600E)-induced thyroid tumors in a mouse model.

Florence Orim, Andrey Bychkov, Mika Shimamura, Masahiro Nakashima, Masahiro Ito, Michiko Matsuse, Tomomi Kurashige, Keiji Suzuki, Vladimir Saenko, Yuji Nagayama and 2 more

Open access · greenAbstract read
In one paragraph

Article in Thyroid : official journal of the American Thyroid Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. TSH-TSHR axis promotes tumor immune evasion.Journal for immunotherapy of cancer · 2022
    Article
  6. The Mysterious Universe of the TSH Receptor.Frontiers in endocrinology · 2022
    Review
  7. Prevalence ofGland surgery · 2020
    Review
  8. Article
  9. Review
  10. Increased Anaplastic Lymphoma Kinase Activity Induces a Poorly Differentiated Thyroid Carcinoma in Mice.Thyroid : official journal of the American Thyroid Association · 2019
    Article
  11. Article
  12. Article
  13. Review
  14. p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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

12 authors at 3 institutions in 2 countries.

Florence Orim1 Department of Radiation Medical Sciences, Nagasaki University , Nagasaki, Japan .
Andrey Bychkov
Mika Shimamura
Masahiro Nakashima
Masahiro Ito
Michiko Matsuse
Tomomi Kurashige
Keiji Suzuki
Vladimir Saenko
Yuji Nagayama
Shunichi Yamashita
Norisato Mitsutake
Nagasaki University · JPUniversity of Nagasaki · JPNagasaki Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe BRAF(V600E) mutation is the most common genetic alteration in papillary thyroid carcinomas (PTCs). Transgenic mice overexpressing BRAF(V600E) in their thyroids under control of the thyroglobulin promoter (Tg-BRAF2 mice) developed invasive PTCs with high penetrance. However, these mice showed elevated thyrotropin (TSH) levels, which also stimulate the proliferation of thyrocytes and tumorigenesis. The purpose of the present study was to investigate how TSH signaling cooperates with BRAF(V600E) in the process of thyroid carcinogenesis.

methodsWe crossed Tg-BRAF2 mice with TSH receptor knockout (TshR(-/-)) mice. Four genetically distinct mice groups-Braf(wt)/TshR(+/-) (group 1), Braf(wt)/TshR(-/-) (group 2), Tg-BRAF2/TshR(+/-) (group 3), and Tg-BRAF2/TshR(-/-) (group 4)--were sacrificed at 12 and 24 weeks of age. We performed histopathological analysis. Genomic instability was evaluated by immunofluorescence for p53-binding protein 1 (53BP1) and γH2AX. Invasiveness and genomic instability were also evaluated using thyroid PCCL3 cells expressing BRAF(V600E).

resultsGroups 3 and 4 developed distinct neoplasias comparable to human PTCs. Group 3 developed typically larger, more aggressive, invasive tumors compared to group 4. The frequency of 53BP1 and γH2AX foci-indicators of genomic instability--in group 3 was higher than that in group 4. TSH also enhanced invasiveness and genomic instability in PCCL3 cells with BRAF(V600E) expression.

conclusionsThese data demonstrate that the TSH signaling confers more aggressive features in BRAF(V600E)-induced thyroid tumors in mice. This might be due, in part, to accelerated genomic instability.

Indexed as

Genomic InstabilityAnimalsCarcinoma, PapillaryMiceMice, KnockoutMice, TransgenicMutationProto-Oncogene Proteins B-rafReceptors, ThyrotropinSignal TransductionThyroid NeoplasmsThyrotropinBraf protein, mouseProto-Oncogene Proteins B-rafReceptors, ThyrotropinThyrotropin

Identifiers

PMID23924149
PMCPMC3949501
OpenAlexW2158484636

What OpenQuestion holds

Textmetadata
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.