Evidence map›Paper›PMID 16532025›Full record

ArticleOncogene2006

H-RAS 81 polymorphism is significantly associated with aneuploidy in follicular tumors of the thyroid.

P Castro, P Soares, L Gusmão, R Seruca, M Sobrinho-Simões

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Variations inMolecular and clinical oncology · 2022
    Article
  3. Identification of a novelOncology letters · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Lack of mutational events of RAS genes in sporadic thyroid cancer but high risk associated with HRAS T81C single nucleotide polymorphism (case-control study).Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  9. Article
  10. Article
  11. Article
  12. Molecular pathology of thyroid cancer: diagnostic and clinical implications.Best practice & research. Clinical endocrinology & metabolism · 2008
    Review
  13. 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

5 authors at 1 institution in 1 country.

P CastroInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal.
P Soares
L Gusmão
R Seruca
M Sobrinho-Simões
Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follicular thyroid tumors are often aneuploid. It was advanced that chromosomal instability is closely associated to RAS mutations, but such association remains unproven. H-RAS can be alternatively spliced in two different proteins, p21 and p19, the former being the active protein. In order to investigate the relationship between RAS mutational status and ploidy in thyroid tumors, we analysed RAS genes in a series of 99 follicular lesions (14 nodular goiters, 70 follicular adenomas and 15 follicular carcinomas), eight thyroid carcinoma cell lines and a control group of 102 blood donors, correlating the presence of RAS mutations with the ploidy of the tumors and evaluating the two spliced forms of H-RAS. Overall, 20% of the follicular tumors harbored RAS mutations and 62% of the patients with follicular tumors (and 51% of blood donors) harbored the H-RAS 81T --> C polymorphism. The presence of RAS mutations was not associated with aneuploidy. The H-RAS polymorphism did not seem to confer a higher propensity for neoplastic transformation as it was also found in hyperplastic lesions, but was strongly associated with aneuploidy (P<0.0001). The presence of the H-RAS 81T --> C polymorphism was associated with significantly higher amounts of total H-RAS mRNA expression, higher amounts of p21 isoform and a higher fraction of neoplastic cells in S phase. Our results suggest that the H-RAS 81T --> C polymorphism may induce aneuploidy through overexpression of the active p21 isoform of H-RAS.

Indexed as

Genes, rasPolymorphism, GeneticAdenocarcinoma, FollicularAllelesAlternative SplicingAneuploidyGenes, NeoplasmHumansModels, GeneticMutationPloidiesPolymorphism, Single-Stranded Conformationalras ProteinsReverse Transcriptase Polymerase Chain ReactionThyroid Neoplasmsras Proteins

Identifiers

PMID16532025
OpenAlexW1991883683

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.