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Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue.

Bounacer A, Du Villard JA, Wicker R, Caillou B, Schlumberger M, Sarasin A, Suárez HG - Br. J. Cancer (2002)

Bottom Line: The RET proto-oncogene encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain.In human thyroid gland, the RET proto-oncogene is normally expressed in parafollicular C-cells.Several explanations for this association are discussed.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire d'Instabilité Génétique et Cancer (UPR 2169), Institut de Recherches sur le Cancer, C.N.R.S.-IFR 89, B.P. no 8, 94801 Villejuif Cedex, France. BounacerA@cf.ac.uk

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Frequency of radiation-induced (A) and sporadic (B) thyroid tumours (n=29) presenting a wild type allele A1, or mutated allele A2, or both (A1+A2) in the presence or absence of C-cell hyperplasia in peritumoural tissue. C-cell hyperplasia was associated with 55% (16/29) of the tumours in (A) and with only 7% (2/29) of the tumours in (B).
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fig2: Frequency of radiation-induced (A) and sporadic (B) thyroid tumours (n=29) presenting a wild type allele A1, or mutated allele A2, or both (A1+A2) in the presence or absence of C-cell hyperplasia in peritumoural tissue. C-cell hyperplasia was associated with 55% (16/29) of the tumours in (A) and with only 7% (2/29) of the tumours in (B).

Mentions: With the aim of determining a relationship between C-cell hyperplasia and the G691S RET SNP, we looked in the same thyroid sample for the polymorphism in the tumoural tissue and for the CCH in the surrounding peritumoural tissue. Our results showed that firstly, the majority of the radiation-induced tumours associated with a CCH (14/16: 88%), presented the polymorphism and interestingly, in 75% of the cases (12/16) only the mutated allele A2 was detected. Secondly, in the absence of CCH in peritumoural tissue only 14% (2/13) of the radiation-induced tumours presented a 691 RET sequence variant in heterozygote form (A1/A2) (Table 1 and Figure 2Figure 2


Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue.

Bounacer A, Du Villard JA, Wicker R, Caillou B, Schlumberger M, Sarasin A, Suárez HG - Br. J. Cancer (2002)

Frequency of radiation-induced (A) and sporadic (B) thyroid tumours (n=29) presenting a wild type allele A1, or mutated allele A2, or both (A1+A2) in the presence or absence of C-cell hyperplasia in peritumoural tissue. C-cell hyperplasia was associated with 55% (16/29) of the tumours in (A) and with only 7% (2/29) of the tumours in (B).
© Copyright Policy
Related In: Results  -  Collection

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fig2: Frequency of radiation-induced (A) and sporadic (B) thyroid tumours (n=29) presenting a wild type allele A1, or mutated allele A2, or both (A1+A2) in the presence or absence of C-cell hyperplasia in peritumoural tissue. C-cell hyperplasia was associated with 55% (16/29) of the tumours in (A) and with only 7% (2/29) of the tumours in (B).
Mentions: With the aim of determining a relationship between C-cell hyperplasia and the G691S RET SNP, we looked in the same thyroid sample for the polymorphism in the tumoural tissue and for the CCH in the surrounding peritumoural tissue. Our results showed that firstly, the majority of the radiation-induced tumours associated with a CCH (14/16: 88%), presented the polymorphism and interestingly, in 75% of the cases (12/16) only the mutated allele A2 was detected. Secondly, in the absence of CCH in peritumoural tissue only 14% (2/13) of the radiation-induced tumours presented a 691 RET sequence variant in heterozygote form (A1/A2) (Table 1 and Figure 2Figure 2

Bottom Line: The RET proto-oncogene encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain.In human thyroid gland, the RET proto-oncogene is normally expressed in parafollicular C-cells.Several explanations for this association are discussed.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire d'Instabilité Génétique et Cancer (UPR 2169), Institut de Recherches sur le Cancer, C.N.R.S.-IFR 89, B.P. no 8, 94801 Villejuif Cedex, France. BounacerA@cf.ac.uk

Show MeSH
Related in: MedlinePlus