Evidence map›Paper›PMID 22312249›Full record

ReviewInternational journal of molecular sciences2012

Molecular basis of medullary thyroid carcinoma: the role of RET polymorphisms.

Lucieli Ceolin, Débora R Siqueira, Mírian Romitti, Carla V Ferreira, Ana Luiza Maia

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02363647 (Personalized Cancer Therapy for Patients With Metastatic Medullary Thyroid or Metastatic Colon Cancer), which is not on this map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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.

NCT02363647 naterminatednot on this mapstarted 2015, after this paper: background citation

Personalized Cancer Therapy for Patients With Metastatic Medullary Thyroid or Metastatic Colon Cancer

TypeinterventionalSponsorIcahn School of Medicine at Mount SinaiRan2015 to 2022Enrolled10ConditionsMedullary Thyroid Cancer, Colon CancerArmsTumor Genomic Analysis
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Quantitative assessment of the association between L769L and S836S polymorphisms at RET gene and medullary thyroid carcinoma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Modifier Role of CommonInternational journal of molecular sciences · 2021
    Trial
  3. Tumour-agnostic kinase inhibitors.Nature reviews. Drug discovery · 2025
    Review
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  12. Development of an AmpliSeqFrontiers in pharmacology · 2018
    Article
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  14. Review
  15. Article
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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 2 institutions in 1 country.

Lucieli CeolinThyroid Section, Endocrine Division, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos 2350, 90035-003, Porto Alegre, RS, Brazil; E-Mails: lu.ceolin@gmail.com (L.C.); deborarsiqueira@yahoo.com.br (D.R.S.); mirianromitti@bol.com.br (M.R.); carlinhavaz@yahoo.com.br (C.V.F.).
Débora R Siqueira
Mírian Romitti
Carla V Ferreira
Ana Luiza Maia
Hospital de Clínicas de Porto Alegre · BRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Medullary thyroid carcinoma is a rare malignant tumor originating in parafollicular C cells. It accounts for 5 to 8% of all thyroid cancers. MTC develops in either sporadic (75%) or hereditary form (25%). Genetic and molecular studies have demonstrated the involvement of the RET proto-oncogene in hereditary MTC and, less often, in its sporadic form. Although a strong genotype-phenotype correlation has been described, wide clinical heterogeneity is observed among families with the same RET mutation or even in carriers of the same kindred. In recent years, several single nucleotide polymorphisms of the RET gene have been described in the general population as well as in patients with MTC. Some studies have reported associations between the presence of polymorphisms and development or progression of MTC. Nonetheless, other studies failed to demonstrate any effect of the RET variants. Differences in the genetic background of distinct populations or methodological approaches have been suggested as potential reasons for the conflicting results. Here, we review current knowledge concerning the molecular pathogenesis of sporadic and hereditary MTC. In particular, we analyze the role of RET polymorphisms in the clinical presentation and prognosis of MTC based on the current literature.

Indexed as

Polymorphism, GeneticCarcinoma, NeuroendocrineGenetic Association StudiesGenotypeGuanine Nucleotide Exchange FactorsHumansProto-Oncogene MasProto-Oncogene Proteins c-retThyroid NeoplasmsGuanine Nucleotide Exchange FactorsMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-retmedullary thyroid carcinomaprognosisRET polymorphisms

Identifiers

PMID22312249
PMCPMC3269683
OpenAlexW2116485788

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.