Evidence map›Paper›PMID 29209896›Full record

ReviewHormones & cancer2018

BRAF-Oncogene-Induced Senescence and the Role of Thyroid-Stimulating Hormone Signaling in the Progression of Papillary Thyroid Carcinoma.

F I Moulana, A A H Priyani, M V C de Silva, R S Dassanayake

Open access · greenAbstract readReview
In one paragraph

Review in Hormones & cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. BRAFJournal of cancer research and clinical oncology · 2021
    Article
  9. Review
  10. Observational
  11. Review
  12. Article
  13. VASN promotes YAP/TAZ and EMT pathway in thyroid carcinogenesis in vitro.American journal of translational research · 2019
    Article
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

F I MoulanaThe Biochemistry and Molecular Biology unit, Department of Chemistry, Faculty of Science, University of Colombo, Colombo, Sri Lanka.
A A H PriyaniDepartment of Pathology, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka.
M V C de SilvaDepartment of Pathology, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka.
R S DassanayakeThe Biochemistry and Molecular Biology unit, Department of Chemistry, Faculty of Science, University of Colombo, Colombo, Sri Lanka. rsdassanayake@chem.cmb.ac.lk.
University of Colombo · LK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogene-induced senescence (OIS) explains the phenomenon of cellular senescence triggered by the action of oncogenes. It is a mechanism adopted by a cell to inhibit progression of benign tumors into malignancy, occurs in premalignant lesions, and is almost never present in malignant lesions. BRAF mutations occur in about 40-45% of all papillary thyroid carcinomas (PTCs) and of which 99.7% is the BRAFV600E mutation. A unique phenotype of the BRAFV600E mutation is the upregulation of the thyroid-stimulating hormone receptor (TSHR) on thyrocyte membranes. Despite the overexpression of the receptor, BRAFV600E cells undergo cell cycle arrest leading to OIS via a negative feedback signaling mechanism. A simultaneous increase in serum thyroid-stimulating hormone (TSH) in response to hypothyroidism (common in autoimmune diseases such as Hashimoto's thyroiditis) would cause senescent tumor cells to overcome OIS and proceed towards malignancy, hence showing the importance of TSH/TSHR signaling in the development of PTCs. Increase in TSH/TSHR signaling triggers an increase in levels of downstream enzymes such as manganese superoxide dismutase (MnSOD) and dual-specific phosphatase 6 (DUSP6) which eventually results in the production of oncogenic proteins such as c-Myc. Therefore, the detection of these genetic alterations as effective biomarkers for premalignant lesions of PTC is important in clinical settings and techniques such as polymerase chain reaction-mediated restriction fragment length polymorphism (PCR-RFLP) and real-time PCR can be used to detect the BRAFV600E point mutation and overexpression of TSHR, MnSOD, and DUSP6, respectively.

Indexed as

Cellular SenescenceDisease ProgressionDual Specificity Phosphatase 6HumansMutationProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mycReceptors, G-Protein-CoupledSignal TransductionSuperoxide DismutaseThyroid Cancer, PapillaryThyrotropinBRAF protein, humanDual Specificity Phosphatase 6DUSP6 protein, humanMYC protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mycReceptors, G-Protein-CoupledSuperoxide DismutaseThyrotropin

Identifiers

PMID29209896
PMCPMC10355898
OpenAlexW2774017426

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.