XRCC1 T-77C polymorphism affects the genetic susceptibility for PTC development in men, the specific combination of XRCC1 haplotypes correlates with RET/PTC incidence, CDKN1B Val109Gly significantly influences the risk of developing PTC regardless of gender and in PTC cases, selected genotypes of TP53Arg72Pro and ATM Asp1853Asn were significantly associated with monitored tumour characteristics.
We studied point mutations in the p53 gene in 22 patients exposed in childhood to radiation in the head and neck area who later developed papillary thyroid cancers (RITC).
We investigated whether retroviral p53 transfection could enhance growth inhibition and chemosensitivity in a p53 mutant papillary thyroid cancer cell line (NPA).
We found that anlotinib inhibits the cell viability of papillary thyroid cancer and ATC cell lines, likely due to abnormal spindle assembly, G2/M arrest, and activation of TP53 upon anlotinib treatment.
To investigate whether the oxidative stress is involved in the evolution of Graves' disease (GD) and Hashimoto thyroiditis (HT) into Papillary Thyroid Carcinoma (PTC), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and cancer related proteins (Bcl-2, p53 and Ki-67) expressions were evaluated in these pathologies.
Thus, RV acts via a Ras-MAPK kinase-MAPK signal transduction pathway to increase p53 expression, serine phosphorylation of p53, and p53-dependent apoptosis in PTC and FTC cell lines.
The results showed that PIG3 was aberrantly overexpressed in the majority of specimens of PTC while the expression of p53 was lower in PTC compared with normal thyroid tissues.
The findings suggest TP53 allele combinations other than Arg/Arg may contribute to the risk of development of PTC in individuals exposed to radiation during their late childhood, adolescence or in young adulthood.
Since p53 is closely related to cellular apoptosis and no point mutation was observed in the transcripts expressed by malignant cells, apoptosis and/or the production of an angiogenesis inhibitor induced by wild-type p53 molecules may be related to the favorable prognosis of patients treated for papillary carcinoma of the thyroid.
Significantly increased PTC susceptibility was also associated with the TP-53Arg72Pro CC and CG/CC genotypes compared with the GG genotype (CC vs GG: adjusted OR = 2.04, 95%CI = 1.54-2.70; CG/CC vs GG: adjusted OR = 1.35, 95%CI = 1.11-1.67, respectively).
RASSF10 is Epigenetically Inactivated and Suppresses Cell Proliferation and Induces Cell Apoptosis by Activating the p53 Signalling Pathway in Papillary Thyroid Carcinoma Cancer.
Nuclear accumulation of immunoreactive p53 protein is associated with two established indicators of poor prognosis in papillary carcinoma of the thyroid.
Mutations in the p53 tumour-suppressor gene (exons 5-8) were investigated in 31 Belarussian childhood thyroid tumours (24 cases of papillary thyroid carcinoma, 3 benign tumours and 2 cases each of thyroiditis and goiter); 33 thyroid tumours from juveniles and adults without radiation exposures (25 carcinomas of various histological types, including 11 papillary carcinomas and 8 adenomas) and 6 tumours from adults (4 papillary carcinomas, 1 adenoma, 1 goiter) served as controls.
Mutations in p53 exons 6 and 7 have been reported in the childhood papillary thyroid carcinomas in Belarus presumably as a result of radioiodine fall-out.
LOH analysis showed that the PTC retained chromosome arm 17p (where the p53 gene resides), whereas the carcinoma was associated with the loss of this allele.