Evidence map›Paper›PMID 20186503›Full record

ArticleEndocrine pathology2010

Mutational and immunohistochemical study of the PI3K/Akt pathway in papillary thyroid carcinoma in Greece.

Elias Sozopoulos, Helen Litsiou, Gerassimos Voutsinas, Nikolaos Mitsiades, Nikolaos Anagnostakis, Thomais Tseva, Efstratios Patsouris, Sofia Tseleni-Balafouta

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Article in Endocrine pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 34% 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Comparative evaluation of strategies for quantifying signaling pathway proteins in Ewing sarcoma.Applied immunohistochemistry & molecular morphology : AIMM · 2014
    Article
  8. Concomitant RAS, RET/PTC, or BRAF mutations in advanced stage of papillary thyroid carcinoma.Thyroid : official journal of the American Thyroid Association · 2014
    Article
  9. Article
  10. Article
  11. Article
  12. 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 at 5 institutions in 2 countries.

Elias Sozopoulos1st Department of Pathology, Medical School, University of Athens, M. Asias 75, Athens, 11527, Greece. elsozopoulos@yahoo.gr
Helen Litsiou
Gerassimos Voutsinas
Nikolaos Mitsiades
Nikolaos Anagnostakis
Thomais Tseva
Efstratios Patsouris
Sofia Tseleni-Balafouta
National and Kapodistrian University of Athens · GRAthens Medical Center · GRAthens State University · USHarvard University · USNational Centre of Scientific Research "Demokritos" · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PI3K/Akt signaling pathway plays critical role in many cell processes. There is indication that enhanced activation of PI3K/Akt cascade is implicated in thyroid tumors. Aim of this study was to evaluate the mutational status and expression of PI3K/Akt pathway mediators in papillary thyroid carcinoma in Greece. We evaluated the presence of mutations in PIK3CA (exons 9 and 20), AKT1 (exons 6-11), AKT2 (exons 6-11), AKT3 (exons 5-10), PTEN (exons 3-8), and PDPK1 (exons 4-10) genes in 83 papillary thyroid carcinomas by DNA sequencing. The expression levels of phospho-Akt and insulin-like growth factor I receptor (IGF-IR) were evaluated by immunohistochemistry. PIK3CA mutations were found in three samples. The analysis of AKT1 revealed one silent mutation in exon 9 (G726A) in 16 samples. One specimen carried an AKT3 mutation. One missense mutation was found in one sample in PTEN. No mutations were found in AKT2 and PDPK1. Increased levels of phosphorylated total Akt and IGF-IR were identified in some papillary cancers. Our findings indicate that PI3K/Akt signaling pathway is activated in some papillary tumors. However, mutations in genes coding most mediators of the pathway have not been proven to be the major modus of enhanced activation. These data suggest a potential role for PI3K/Akt-mediated signaling in papillary thyroid tumors.

Indexed as

3-Phosphoinositide-Dependent Protein KinasesAdenocarcinoma, PapillaryAdolescentAdultAgedBase SequenceClass I Phosphatidylinositol 3-KinasesDNA Mutational AnalysisFemaleGreeceHumansImmunohistochemistryMaleMiddle AgedPhosphatidylinositol 3-KinasesPolymerase Chain Reaction3-Phosphoinositide-Dependent Protein KinasesAKT1 protein, humanAKT2 protein, humanAKT3 protein, humanClass I Phosphatidylinositol 3-KinasesPDPK1 protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanReceptor, IGF Type 1

Identifiers

PMID20186503
OpenAlexW2061385475

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.