Evidence map›Paper›PMID 23544172›Full record

ArticleTranslational oncology2013

Notch pathway is activated by MAPK signaling and influences papillary thyroid cancer proliferation.

Alex Shimura Yamashita, Murilo Vieira Geraldo, Cesar Seigi Fuziwara, Marco Aurélio Vamondes Kulcsar, Celso Ubirajara Moretto Friguglietti, Ricardo Borges da Costa, Gilson Soares Baia, Edna Teruko Kimura

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Article in Translational oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

50 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Expression of CLDN1 and EGFR in PTC.Discover oncology · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Notch signaling, hypoxia, and cancer.Frontiers in oncology · 2023
    Review
  13. The effect of NrfBMC cancer · 2022
    Article
  14. Article
  15. Article
  16. Molecular therapy. Nucleic acids · 2021
    Article
  17. Article
  18. Notch Signaling in Thyroid Cancer.Advances in experimental medicine and biology · 2021
    Review
  19. Article
  20. 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

8 authors.

Alex Shimura YamashitaDepartment of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Sã Paulo, Brazil.
Murilo Vieira Geraldo
Cesar Seigi Fuziwara
Marco Aurélio Vamondes Kulcsar
Celso Ubirajara Moretto Friguglietti
Ricardo Borges da Costa
Gilson Soares Baia
Edna Teruko Kimura

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutually exclusive genetic alterations in the RET, RAS, or BRAF genes, which result in constitutively active mitogen-activated protein kinase (MAPK) signaling, are present in about 70% of papillary thyroid carcinomas (PTCs). However, the effect of MAPK activation on other signaling pathways involved in oncogenic transformation, such as Notch, remains unclear. In this study, we tested the hypothesis that the MAPK pathway regulates Notch signaling and that Notch signaling plays a role in PTC cell proliferation. Conditional induction of MAPK signaling oncogenes RET/PTC3 or BRAF(T1799A) in normal rat thyroid cell line mediated activation of Notch signaling, upregulating Notch1 receptor and Hes1, the downstream effector of Notch pathway. Conversely, pharmacological inhibition of MAPK reduced Notch signaling in PTC cell. Thyroid tumor samples from transgenic mice expressing BRAF(T1799A) and primary human PTC samples showed high levels of Notch1 expression. Down-regulation of Notch signaling by γ-secretase inhibitor (GSI) or NOTCH1 RNA interference reduces PTC cell proliferation. Moreover, the combination of GSI with a MAPK inhibitor enhanced the growth suppression in PTC cells. This study revealed that RET/PTC and BRAF(T1799A) activate Notch signaling and promote tumor growth in thyroid follicular cell. Taken together, these data suggest that Notch signaling may be explored as an adjuvant therapy for thyroid papillary cancer.

Identifiers

PMID23544172
PMCPMC3610552

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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.