Parental cancer and risk of papillary and follicular thyroid carcinoma

Galanti, Maria Rosaria; Ekbom, Anders; Grimelius, Lars; Yuen, Jeanette

doi:10.1038/bjc.1997.76

Cited by 56 publications

(25 citation statements)

References 29 publications

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“…Approximately 3%-5% of patients with thyroid cancer report a family history of the same disease (8,9). There are several rare familial syndromes that are associated with a high prevalence of thyroid cancer, in several cases associated with familial adenomatous polyposis.…”

Section: Genetic Aspectsmentioning

confidence: 98%

Epidemiology and Primary Prevention of Thyroid Cancer

Nagataki

Nyström

2002

Thyroid

134

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The purpose of this review is to provide an account of our present knowledge about the epidemiology of nonmedullary thyroid carcinoma, to discuss the effects of environment, lifestyle and radiation on the risk of developing thyroid cancer, and to discuss aspects on primary prevention of the disease. In areas not associated with nuclear fallout, the annual incidence of thyroid cancer ranges between 2.0-3.8 cases per 100,000 in women and 1.2-2.6 per 100,000 in men, women of childbearing age being at highest risk. Low figures are found in some European countries (Denmark, Holland, Slovakia) and high figures are found in Iceland and Hawaii. Differences in iodine intake may be one factor explaining the geographic variation, high iodine intake being associated with a slightly increased risk of developing thyroid cancer. In general, lifestyle factors have only a small effect on the risk of thyroid cancer, a possible protective effect of tobacco smoking has been recently reported. Because of the (small) increase in risk of thyroid cancer associated with iodination programs, these should be supervised, so that the population does not receive excess iodine. The thyroid gland is highly sensitive to radiation-induced oncogenesis. This is verified by numerous reports from survivors after Hiroshima and Nagasaki, the Nevada, Novaja Semlja and Marshal Island atmospheric tests, and the Chernobyl plant accident, as well as by investigations of earlier medical use of radiation for benign diseases in childhood. These reports are summarized in the review. There appears to be a dose-response relation for the risk of developing cancer after exposure to radioactive radioiodine. The thyroid gland of children is especially vulnerable to the carcinogenic action of ionizing radiation. Thus, the incidence of thyroid cancer in children in the Belarus area was less than 1 case per million per year before the Chernobyl accident, increasing to a peak exceeding 100 per million per year in certain areas after the accident. It is a social obligation of scientists to inform the public and politicians of these risks. All nuclear power plants should have a program in operation for stockpiling potassium iodide for distribution within 1-2 days after an accident.

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Section: Genetic Aspectsmentioning

confidence: 98%

Epidemiology and Primary Prevention of Thyroid Cancer

Nagataki

Nyström

2002

Thyroid

134

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“…Thus, the large cohort of patients who underwent childhood irradiation for benign medical conditions such as thymic enlargement and acne between 1920 and 1960 are now between the ages of 45 and 85, and this population still has an increased risk of developing thyroid carcinoma. Epidemiologic studies have demonstrated a 4-fold to 10-fold increased risk of well-differentiated thyroid cancer in first-degree relatives of subjects with this neoplasia (9,10). In contrast to the well-described molecular pathology associated with medullary thyroid carcinoma, the molecular and clinical genetics of thyroid follicular cell cancer have only recently been partially unveiled (Table 1) (11,12).…”

Section: Introductionmentioning

confidence: 94%

Follicular Neoplasms of the Thyroid: What to Recommend

Carling

Udelsman

2005

Thyroid

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Follicular neoplasms of the thyroid are usually diagnosed following fine-needle aspiration (FNA) biopsy of a dominant thyroid nodule. An FNA diagnosis of a follicular neoplasm represents a heterogeneous group of lesions including benign follicular hyperplasia, follicular adenomas, follicular carcinomas, and the follicular variant of papillary carcinoma. Hürthle cell neoplasms are also often included in this group. Because the criteria for malignancy in both follicular and Hürthle cell neoplasms requires vascular or capsular invasion seen on permanent histology, the majority of these patients undergo surgical resection. Intraoperative frozen section analysis of follicular neoplasms rarely renders informative information. Approximately 20% of these lesions prove to be malignant and for lesions greater than 1.0 cm in size, the majority of surgeons and endocrinologists recommend a total thyroidectomy. Postoperative treatment generally includes therapeutic doses of 131I for follicular carcinomas.

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“…There is increasing evidence that there is a familial component to PTC, with between 3.5-6.2% of PTC patients having one or more first degree relatives with thyroid carcinoma (2)(3)(4)(5)(6). Familial aggregations have been noted (7)(8)(9) and we reported the first recognised families predisposed to an autosomal dominant form of PTC with associated multinodular goitre (MNG) (10) (Fig.…”

Section: Introductionmentioning

confidence: 99%

At least three genes account for familial papillary thyroid carcinoma: TCO and MNG1 excluded as susceptibility loci from a large Tasmanian family

Mckay¹,

Williamson

Lesueur

et al. 1999

European Journal of Endocrinology

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Recent studies have mapped two susceptibility loci which appear to account for familial multinodular goitre (MNG1) and a variant of familial papillary thyroid cancer (PTC), with associated multinodular goitre (TCO). A Tasmanian family (Tas1) has been identified with an autosomal dominant form of PTC.This study has examined the MNG1 and TCO loci to determine if they are similarly predisposing the Tas1 family to PTC. Linkage analysis using identical microsatellite markers described in the two previous studies was used to determine the significance of these loci in the Tasmanian family. The resultant LOD scores were sufficiently negative using multipoint parametric analysis to exclude these two loci from involvement in the Tasmanian family.In addition, six candidate genes, RET, TRK, MET, TSHR, APC and PTEN were also excluded as susceptibility genes in Tas1 by using microsatellites that are positioned in or in close proximity to these genes. These results suggest that there are at least three susceptibility genes that predispose families to familial PTC.

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Parental cancer and risk of papillary and follicular thyroid carcinoma

Cited by 56 publications

References 29 publications

Epidemiology and Primary Prevention of Thyroid Cancer

Epidemiology and Primary Prevention of Thyroid Cancer

Follicular Neoplasms of the Thyroid: What to Recommend

At least three genes account for familial papillary thyroid carcinoma: TCO and MNG1 excluded as susceptibility loci from a large Tasmanian family

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