Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 16986502

[Thyroid microcarcinoma].

D S Lantsov
View original source ↗Export metadata ↓

Abstract

The WHO classification of thyroid tumors defines papillary microcarcinoma as papillary carcinoma, 1 cm or less in diameter. Many Russian and foreign authors include follicular and medullary types. The limiting size which permits a tumor to be considered microcarcinoma if it measures either 1 cm or 1.5 cm. A number of investigators terminologically use the data of a clinical observation of patients. In this connection, there is a great variety of terms used to define thyroid microcarcinoma. This tumor is a common random finding in the gland removed for various disease or examined at autopsy. According to autopsies, the incidence of thyroid microcarcinoma ranges from 1 to 36%. A great deal of papers and studies are dedicated to the etiology and pathogenesis of thyroid microcarcinoma and the potentialities of its early diagnosis and adequate treatment. However, little attention is given to the histological structure and proliferative activity of this tumor and their impact on prognosis and data are at times slightly contradictory or inadequately complete.

Explore related subjects

Carcinoma, PapillaryHumansThyroid NeoplasmsEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D S Lantsov. [Thyroid microcarcinoma].. https://pubmed.ncbi.nlm.nih.gov/16986502/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Radiation safety protocol for high dose 131I therapy of thyroid carcinoma in patients on hemodialysis for chronic renal failure.

Iodine ablation therapy for thyroid cancer on patients receiving dialysis poses unique radiation safety challenges. Exposure to gamma and beta negative particles by the hemodialysis (HD) staff is a concern that has not been well studied. A 53-y-old male patient on HD for chronic renal failure was scheduled for 131I high dose therapy as treatment for thyroid papillary carcinoma. The patient was on HD every other day, prior to ablation. A high dose of 131I (3,607.5 MBq) was required. The patient was admitted for 131I therapy, and continued HD. Thyroid cancer ablation therapy was administered according to our institutional protocol. New radiation safety measures were developed and implemented in order to give the patient an optimal treatment dose, reduce radiation to the patient (critical organs and whole body), and to protect the HD personnel. This included placing two lead shields between the patient and the HD nurse, and HD monitoring by two alternating nurses to reduce their radiation exposure. Film badges were used to measure radiation exposure to the nursing staff. Dosimetry calculations were obtained to determine radiation absorbed doses by the optic lens, skin, and whole body. Quality control verification for this shielding arrangement proved to be effective in protecting the HD staff against gamma and beta negative radiation from recent 131I high dose therapy. Implementation of this model proved to be an effective and adequate radiation safety protocol for limiting radiation exposure to the HD staff. The patient was given 3607.5 MBq for optimal treatment after HD. Hemodialysis was repeated after approximately 48 and 96 h to remove excess 131I and reduce radiation to the patient.

Carcinoma, Papillary↗
PubMed2007

Thyroid hormone receptor beta mutations in the 'hot-spot region' are rare events in thyroid carcinomas.

Thyroid cancer constitutes the most frequent endocrine neoplasia. Targeted expression of rearranged during transfection (RET)/papillary thyroid carcinoma (PTC) and V600E V-raf murine sarcoma viral oncogene homolog B1 (BRAF) to the thyroid glands of transgenic mice results in tumours similar to those of human PTC, providing evidence for the involvement of these oncogenes in PTC. Kato et al. developed a mouse model that mimics the full spectrum of the human follicular form of thyroid cancer (FTC). FTC rapidly develops in these mice through introduction of the thyroid hormone receptor beta (THRB)(PV) mutant on the background of the inactivated THRB wt locus. Our aim was to verify if, in the context of human follicular thyroid carcinogenesis, THRB acted as a tumour suppressor gene. We screened for mutations of the THRB gene in the hot-spot region, spanning exons 7-10, in 51 thyroid tumours and six thyroid cancer cell lines by PCR and direct sequencing. We did not find mutations in any of the tumours or cell lines analysed. Our findings suggest that, in contrast to the findings on the THRB-mutant transgenic mice, THRB gene mutations are not a relevant mechanism for human thyroid carcinogenesis.

Carcinoma, Papillary↗