Evidence map›Paper›PMID 20001715›Full record

ReviewThyroid : official journal of the American Thyroid Association2009

Lessons from mouse models of thyroid cancer.

Caroline S Kim, Xuguang Zhu

Open access · greenAbstract readReview
In one paragraph

Review in Thyroid : official journal of the American Thyroid Association, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  9. Article
  10. Preclinical Imaging for the Study of Mouse Models of Thyroid Cancer.International journal of molecular sciences · 2017
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Promise and pitfalls of molecular markers of thyroid nodules.Indian journal of endocrinology and metabolism · 2012
    Article
  17. Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Caroline S KimMolecular Oncology Research Institute and Division of Endocrinology, Diabetes, and Metabolism, Tufts Medical Center , Boston, Massachusetts, USA.
Xuguang Zhu
National Cancer Institute · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

backgroundThyroid cancer is the most common endocrine tumor and is increasing in incidence. The aim of this study was to review mouse models of differentiated thyroid cancer and how they elucidate human thyroid cancer biology. SUMMARY: Differentiated thyroid cancer, primarily papillary and follicular, comprises the majority of thyroid cancers. There has been tremendous growth in the cross-talk between basic science and clinical practice for thyroid cancer management. Insight into the framework of genes responsible for differentiated thyroid cancer has been gained through the use of mouse models. Common genetic alterations found in human papillary thyroid cancer such as RET/PTC rearrangements or the BRAF(V600E) mutation have genetically modified mouse counterparts. These and other preclinical mouse models have validated the importance of the cyclic adenosine monophosphate (cAMP)/protein kinase A and mitogen-activated protein kinase (MAPK) signaling pathways in papillary thyroid cancer (PTC). RAS mutations have a role in both papillary and follicular thyroid cancer development. Mice with overactivation of the phosphatidylinol-3-kinase (PI3K)-AKT and/or thyrotropin-regulated signaling pathways have been found to develop follicular thyroid cancer. Additional mouse models of thyroid cancer that utilize inducible expression systems are in development or are being characterized and will better reflect the majority of human thyroid cancers which are non-hereditary. Advances in in vivo imaging of mice allow for earlier detection of metastasis and the ability to follow tumor growth or regression which may be used in evaluation of pharmaceutical agents.

conclusionsMouse models have expanded our understanding of the altered signaling pathways that contribute to thyroid cancer tumorigenesis and provide a powerful tool to develop novel diagnostic approaches and therapies.

Indexed as

Adenocarcinoma, FollicularAnimalsCarcinoma, PapillaryCyclic AMPHumansMAP Kinase Signaling SystemMiceMice, TransgenicModels, AnimalProto-Oncogene Proteins B-rafras ProteinsReceptors, ThyrotropinReceptor, trkASignal TransductionThyroid NeoplasmsBraf protein, mouseCyclic AMPProto-Oncogene Proteins B-rafras ProteinsReceptors, ThyrotropinReceptor, trkA

Identifiers

PMID20001715
PMCPMC2861953
OpenAlexW2017000262

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.