Latency Period of Thyroid Neoplasia After Radiation Exposure

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

To determine the temporal sequence for developing benign and malignant thyroid neoplasms after radiation. Therapeutic radiation is associated with thyroid neoplasms in humans and animals. Some question whether thyroid cancers develop de novo or from benign thyroid neoplasms. Little information, however, is available concerning the time to development of benign and malignant thyroid neoplasms after radiation exposure. We retrospectively analyzed the records of 171 consecutive patients who had a history of exposure to radiation and were treated surgically at University of California, San Francisco-affiliated hospitals for thyroid neoplasms between 1960 and 1999. There were 66 men and 105 women aged 9 to 80 years (mean, 47.0 years). One hundred patients had benign and 71 had malignant tumors (58 papillary cancers, 10 follicular cancers, 1 Hurthle cell cancer, 1 medullary cancer, and 1 carcinosarcoma). The mean latency period for benign tumors was longer than that for malignant lesions (mean, 34.1 and 28.4 years, P = 0.018; median, 38.0 years and 30.0 years, P = 0.001). Follicular carcinomas developed sooner (mean, 20.5 years; median, 20 years) than did follicular adenomas (mean, 35.3 years; median, 36.5 years; P = 0.003, P = 0.0009). Patients with papillary thyroid cancers presenting as occult papillary cancers (<1 cm) and as a dominant nodule had similar latency periods (mean, 34.0 and 28.0 years P = 0.29; median, 37.5 and 30.5 years, P = 0.09), respectively. Although there could be selection bias regarding referral of patients, our data document that malignant thyroid tumors after radiation exposure, including follicular carcinomas, present earlier than do benign thyroid tumors. Occult and manifest papillary thyroid cancers present at about the same time interval after radiation exposure. Our findings question whether benign thyroid neoplasms progress to malignant thyroid neoplasms and that most occult thyroid cancers do not progress to malignant thyroid cancers in radiation-exposed patients.

Related collections

Most cited references 17

Record: found
Abstract: found
Article: not found

High prevalence of mutations of the p53 gene in poorly differentiated human thyroid carcinomas.

A Karmakar, K Matsuo, LIGANG CHEN … (1992)

The development and progression of thyroid tumors is signaled by phenotype-specific mutations of genes involved in growth control. Molecular events associated with undifferentiated thyroid cancer are not known. We examined normal, benign, and malignant thyroid tissue for structural abnormalities of the p53 tumor suppressor gene. Mutations were detected by single-strand conformation polymorphisms of PCR-amplified DNA, using primers bracketing the known hot spots on either exons 5, 6, 7, or 8. The prevalence of mutations was as follows: normal thyroid 0/6; follicular adenomas 0/31; papillary carcinomas 0/37; medullary carcinomas 0/2; follicular carcinomas 1/11; anaplastic carcinomas 5/6; thyroid carcinoma cell lines 3/4. Positive cases were confirmed by direct sequencing of the PCR products. All five anaplastic carcinoma tissues and the anaplastic carcinoma cell line ARO had G:C to A:T transitions leading to an Arg to His substitution at codon 273. In both tumors and cell lines, examples of heterozygous and homozygous p53 mutations were identified. The only thyroid carcinoma cell line in which p53 mutations were not detected in exons 5-8 had markedly decreased p53 mRNA levels, suggesting the presence of a structural abnormality of either p53 itself or of some factor controlling its expression. The presence of p53 mutations almost exclusively in poorly differentiated thyroid tumors and thyroid cancer cell lines suggests that inactivation of p53 may confer these neoplasms with aggressive properties, and further loss of differentiated function.

0 comments Cited 81 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: not found
Article: not found

Thyroid follicular cell carcinogenesis*1

R. Hill (1989)

0 comments Cited 16 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Origin and Progression of Thyroid Epithelial Tumours: Cellular and Molecular Mechanisms

David Wynford-Thomas (1997)

Tumours of the thyroid follicular cell are proving to be one of the most informative models for ‘dissecting’ the molecular genetics of multi-stage human tumorigenesis. Early thyroid tumour development is closely correlated with mutation of five alternative genes, ras, ret, trk, gsp and the TSH receptor, associated with different tumour phenotypes, providing an excellent example of genotype/phenotype correlation. For two of these genes, ras and ret, there is also direct experimental evidence from gene transfer studies that they are sufficient to initiate tumorigenesis, one of very few situations where such proof of causality has been obtained for a human tumour. Much less is known of the molecular basis of malignant transformation in thyroid. However, the rare, further progression to undifferentiated (anaplastic) cancer provides a particularly clear-cut illustration of the role of the tumour-suppressor gene p53 in human cancer. Furthermore, in vitro data suggest the intriguing possibility that the anaplastic phenotype results from a combination of p53 mutation together with a spontaneous switch in differentiation programme, i.e. co-operation between a genetic and an epigenetic event.