Microsatellite instability in thyroid tumours and tumour-like lesions

Abstract

Summary Fifty-one thyroid tumours and tumour-like lesions were analysed for instability at ten dinucleotide microsatellite loci and at two coding mononucleotide repeats within the transforming growth factor β (TGF-β) type II receptor (TβRII) and insulin-like growth factor II (IGF-II) receptor (IGFIIR) genes respectively. Microsatellite instability (MI) was detected in 11 out of 51 cases (21.5%), including six (11.7%) with MI at one or two loci and five (9.8%) with Ml at three or more loci (RER + phenotype). No mutations in the TβRII and IGFIIR repeats were observed. The overall frequency of MI did not significantly vary in relation to age, gender, benign versus malignant status and tumour size. However, widespread MI was significantly more frequent in follicular adenomas and carcinomas than in papillary and Hürthle cell tumours: three out of nine tumours of follicular type (33.3%) resulted in replication error positive (RER + ), versus 1 out of 29 papillary carcinomas (3.4%, P = 0.01), and zero out of eight Hürthle cell neoplasms. Regional lymph node metastases were present in five MI-negative primary cancers and resulted in MI-positive in two cases.

Microsatellite instability and its correlation with clinicopathological features in a series of thyroid tumors prevalent in iodine deficient areas

“…Our present data is in concordance with the previous study using a different subset of markers (Soares et al, 1997). Another study described overall frequency of 21.5% in fifty-one thyroid tumors (Lazzereschi et al, 1999), which differs from ours. High frequency of MSI at BAT -40 and BAT -26 in present study sug-gests that the biochemical defects governing the spectrum of MSI in thyroid and colorectal cancer share some similarity that contradicts the previous finding (Onda et al, 2001).…”

“…MSI -H was found to be frequently associated with high-risk group cases. This finding is contradictory to the previous one where no associations between MSI status, patient's age, gender and tumor size were observed (Lazzereschi et al, 1999).…”

Foci formation of P53‐binding protein 1 in thyroid tumors: Activation of genomic instability during thyroid carcinogenesis

“…2 Thus, transfection of mutant HRAS V12 or mutant BRAF V600E induced GIN in a rat thyroid cell line, manifesting as loss of chromosomal material, mitotic bridge formation and misaligned chromosomes. [3][4][5] Recently, we found RET oncogene amplification in human thyroid cancers. 6 Oncogene amplification is common in solid tumors and correlates with a poor prognosis for patients with ovarian cancer (HER-2/neu), breast cancer (C-MYC, HER-2/neu), neuroblastoma (N-MYC), or small cell lung cancer (C-MYC).…”

Recent Developments in the Molecular Biology of the Thyroid

“…Microsatellite instability is common in certain inherited cancer syndromes (e.g., HNPCC) and some sporadic cancers. In thyroid tumors, it has been observed with a frequency of 14-33% in follicular carcinomas, and with lower prevalence in papillary carcinomas and oncocytic tumors [172,[184][185][186]. Overall, microsatellite mutations are uncommon in thyroid tumors and rarely involve multiple foci, which argues against the presence of significant DNA replication error in these tumors.…”