Evidence map›Paper›PMID 11376121›Full record

ReviewMolecular pathology : MP2001

The IGF system in thyroid cancer: new concepts.

V Vella, L Sciacca, G Pandini, R Mineo, S Squatrito, R Vigneri, A Belfiore

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular pathology : MP, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04298684 (Efficacy of Metformin Versus Sitagliptin on Benign Thyroid Nodules Size in Type 2 Diabetes), which is not on this map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 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.

NCT04298684 phase4unknown statusstarted 2021, after this paper: background citation

Efficacy of Metformin Versus Sitagliptin on Benign Thyroid Nodules Size in Type 2 Diabetes: a 2-years Prospective Multicentric Study

Ran2021Enrolled90Registered outcomes9Posted comparisons0ConditionsDiabetes Mellitus, Type 2, Thyroid Nodule (Benign)ArmsMetformin, Sitagliptin
PMID 26154837PMID 27987248PMID 18346005PMID 9839117PMID 3899825PMID 30233494PMID 29858981PMID 29158735PMID 28196954PMID 25734734PMID 24927125PMID 2480830other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Serum Insulin, Glucose, Indices of Insulin Resistance, and Risk of Lung Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2017
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  18. Obesity and Thyroid Cancer Risk: An Update.International journal of environmental research and public health · 2022
    Review
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  20. Review

14 more citing papers are in PubMed but not listed here.

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

7 authors.

V VellaCattedra di Endocrinologia, Istituto di Medicina Interna, Malattie Endocrine e del Metabolismo, University of Catania, Ospedale Garibaldi, Catania, Italy.
L Sciacca
G Pandini
R Mineo
S Squatrito
R Vigneri
A Belfiore

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, the activation of the insulin-like growth factor (IGF) system in cancer has emerged as a key factor for tumour progression and resistance to apoptosis. Therefore, a variety of strategies have been developed to block the type I IGF receptor (IGF-I-R), which is thought to mediate the biological effects of both IGF-I and IGF-II. However, recent data suggest that the IGF signalling system is complex and that other receptors are involved. To unravel the complexity of the IGF system in thyroid cancer, IGF-I and IGF-II production, and the expression and function of their cognate receptors were studied. Both IGFs were found to be locally produced in thyroid cancer: IGF-I by stromal cells and IGF-II by malignant thyrocytes. Values were significantly higher in malignant tissue than in normal tissue. IGF-I-Rs were overexpressed in differentiated papillary carcinomas but not in poorly differentiated or undifferentiated tumours, whereas insulin receptors (IRs) were greatly overexpressed in all tumour hystotypes, with a trend for higher values in dedifferentiated tumours. As a consequence of IR overexpression, high amounts of IR/IGF-I-R hybrids (which bind IGF-I with high affinity) were present in all thyroid cancer histotypes. Because of recent evidence that isoform A of IR (IR-A) is a physiological receptor for IGF-II in fetal life, the relative abundance of IR-A in thyroid cancer was measured. Preliminary data indicate that overexpressed IRs mainly occur as IR-A in thyroid cancer. These data indicate that both IR/IGF-I-R hybrids and IR-A play an important role in the overactivation of the IGF system in thyroid cancer and in IGF-I mitogenic signalling in these tumours. J Clin PATHOL: Mol Pathol

Indexed as

Carcinoma, PapillaryCase-Control StudiesEnzyme-Linked Immunosorbent AssayHumansInsulin-Like Growth Factor IInsulin-Like Growth Factor IIProtein IsoformsReceptor, IGF Type 1Receptor, IGF Type 2Receptor, InsulinStromal CellsThyroid GlandThyroid NeoplasmsTumor Cells, CulturedInsulin-Like Growth Factor IInsulin-Like Growth Factor IIProtein IsoformsReceptor, IGF Type 1Receptor, IGF Type 2Receptor, Insulin

Identifiers

PMID11376121
PMCPMC1187048

What OpenQuestion holds

Textmetadata
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.