Familial Nonmedullary Thyroid Cancer

Ron, Elaine; Kleinerman, Ruth A.; LiVolsi, Virginia A.; Fraumeni, Joseph F.

doi:10.1159/000226948

Cited by 56 publications

(13 citation statements)

References 3 publications

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“…Mainly, the function of miR-886-3p is unknown, the miR-886 gene's chromosomal location on 5q31 is shared with transforming growth factor β1, an important regulator in epithelial carcinogenesis, and the level of miR-886-3p expression difference between familial and sporadic papillary thyroid cancer was large (3-fold). Consistent with our findings, a recent study showed miR-886-3p was downregulated in squamous cell lung cancer compared with normal lung tissue, suggesting a potential tumor suppressor role for this miRNA [5]. Using two well-characterized thyroid cancer cell lines with differing levels of basal miR-866-3p expression, we demonstrated that miR-886-3p plays a critical role in cellular proliferation and migration, and regulates genes involved in the DNA replication and focal adhesion pathways.…”

Section: Discussionsupporting

confidence: 93%

“…Most cases of FNMTC are papillary thyroid cancer and have an autosomal dominant pattern of inheritance with incomplete penetrance. FNMTC accounts for up to 8% of all thyroid cancer cases [2], [3], [4], [5], [6]. In the familial cancer syndromes mentioned above, patients present with distinct extrathyroidal lesions and the susceptibility genes responsible for these syndromes are known.…”

Section: Introductionmentioning

confidence: 99%

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MiR-886-3p Regulates Cell Proliferation and Migration, and Is Dysregulated in Familial Non-Medullary Thyroid Cancer

et al. 2011

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BackgroundThe molecular basis and characteristics of familial non-medullary thyroid cancer are poorly understood. In this study, we performed microRNA (miRNA) profiling of familial and sporadic papillary thyroid cancer tumor samples.Methodology/Principal FindingsGenome wide miRNA profiling of sporadic and familial papillary thyroid cancer was performed. Differentially expressed miRNAs were validated by quantitative RT-PCR. Ectopic expression of miR-886-3p in thyroid cancer lines was performed to identify pathways targeted by the miRNA, as well as, to determine its effect on tumor cell biology. We found four differentially expressed miRNAs between familial and sporadic papillary thyroid cancer tumor samples. MiR-886-3p and miR-20a were validated to be differentially expressed by 3- and 4-fold, respectively. Pathway analysis of genome-wide expression data on cells overexpressing miR-886-3p and target prediction analysis showed genes involved in DNA replication and focal adhesion pathways were regulated by miR-886-3p. Overexpression of miR-886-3p in thyroid cancer cell lines significantly inhibited cellular proliferation, the number and size of spheroids and cellular migration. Additionally, overexpression of miR-886-3p increased the number of cells in S phase.Conclusions/SignificanceOur findings for the first time suggest that miR-886-3p plays an important role in thyroid cancer tumor cell biology and regulates genes involved in DNA replication and focal adhesion. Thus, miR-886-3p may play a role in the initiation and or progression of papillary thyroid cancer.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

MiR-886-3p Regulates Cell Proliferation and Migration, and Is Dysregulated in Familial Non-Medullary Thyroid Cancer

et al. 2011

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“…The association between breast cancer and laryngeal cancer has not been noted before in systematic studies, although there is anecdotal evidence of a laryngealcancer excess in high-risk breast-cancer families, including at least one family linked to BRCAZ (Wooster et al, 1994). The association between breast cancer and thyroid cancer is consistent with the observations of Goldgar et al (1994) and Ron et al (1991), and with the finding of an increased risk of breast cancer in papillary thyroid-cancer cases (Hrafnkelsson et aL, 1989). This association might be a reflection of the involvement of both breast and thyroid cancer in Cowden's syndrome (Lloyd and Dennis, 1963).…”

Section: Discussionsupporting

confidence: 82%

Cancer mortality in relatives of women with breast cancer: The OPCS study

et al. 1996

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Mortality from cancer and other causes in male and female first-degree relatives of women with breast cancer diagnosed before age 60 has been examined in a large population-based cohort study, providing estimates of familial risks free from ascertainment or recall bias. Relatives of 3,295 patients with breast cancer diagnosed in the UK between I954 and I98 I were identified through a register of households established in 1939. The I 1.678 first-degree relatives thus identified were followed up through national records until the end of 1992. Over this period 5,42 I deaths (including 1,527 cancer deaths) occurred in these relatives. Mortality from breast cancer was significantly raised in first-degree relatives (SMR 187,248 deaths), and there was also significant excess mortality from cancers of the larynx (SMR 177, I 7 deaths), endometrium (SMR I66,29 deaths) and unspecified neoplasms (SMR 153, 70 deaths). The SMR for ovarian cancer was 130, based on 58 deaths (p = 0.06). There was no marked excess for other sites or for non-neoplastic causes of death, but there was a significant deficit in mortality from cervical cancer (SMR 63, 18 deaths). The SMR for breast cancer increased significantly with decreasing age of the relative. After allowing for age, sisters of cases had a slightly (though non-significantly) higher risk than mothers (ratio of SMRs I .22). These results, together with penetrance estimates from linked families, suggest that approximately one woman in 800 carries BRCAI, the susceptibility gene on chromosome 17q, and that this gene causes about I% of all breast cancers. o 1996 Wiley-Liss, Inc.

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“…Most studies suggest that benign thyroid disease is also more common in families with FNMTC (3). Ron et al found an odd ratio of five for patient with another family member with thyroid cancer (40), Goldger et al using the Utah Population Database and Surveillance Epidemiology and End Results (SEER) data documented a 9 fold increase of thyroid cancer and an association with breast cancer (p < 0.001) (41).…”

Section: Historymentioning

confidence: 99%

Familial Non Medullary Thyroid Cancer*

Clark¹

2002

European Surg

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Summary: Background: There have been an increasing number of articles regarding patients with familial non medullary thyroid cancer (FNMTC) in the past few years. FNMTC has been defined as families with two or more first degree relatives having papillary or Hurthle cell thyroid cancer.  Methods: The history and new aspects of genetics, environment, pathology, management and clinical outcome of FNMTC are reviewed.  Results: The familial occurrence of NFMTC was first noted in 1995. In families with three or more members with NFMTC there appears to be an autosomal dominant type of inheritance with incomplete penetrance. 99.9 % of these patients have familial disease. FNMTC without any other associated syndrome accounts for about 5 % of patients with thyroid cancer of follicular cell origin (prevalence ranges between 3.5 and 6.2 %). When two members of a family have thyroid cancer about 50 % will have a susceptibility gene for thyroid cancer. FNMTC is rare in patients with follicular thyroid cancer. To date, genetic testing to document whether an individual of a family with familial papillary or Hurthle cell cancer without other syndromes has a specific germ line mutation is not available. In 1998 a linkage site locus (thyroid cancer oxyophilia – TCO gene) on chromosome 19p13.2 in a single French family with oxyophilia and trabecular thyroid cancers was identified. Individuals with the TCO linkage site have a relatively characteristic histologic pattern with trabecular and oncocytic neoplasms. Patients with papillary thyroid cancers and familial polyposis also have a distinct architecture and primarily occur in women. An experienced pathologist can make or at least suggest that the patient with this particular histological pattern should be screened for FNMTC. When total thyroidectomy with removal of regional lymphadenopathy can be done safely this is the preferred approach for patients with nodules in families with FNMTC as recommended for patients with thyroid nodules and a history of radiation exposure. For individuals in families with two or more other members with papillary or Hurthle cell thyroid cancer and a normal thyroid gland to palpation a baseline ultrasound examination is recommended, to document whether there are any thyroid nodules present. If occult nodules are present they can be observed with a repeat ultrasound examination in six months and then yearly to be sure they are not growing, or they can be biopsied by FNA under ultrasound guidance. Although occult thyroid cancers are usually of little clinical significance this may not be true for patients with FNMTC. Occult thyroid cancers in patients with FNMTC seem more aggressive and may be lethal.  Conclusions: Several groups continue to try to identify the genes responsible for the majority of families with FNMTC. Such studies are relatively expensive, but seem necessary to improve the care of patients with FNMTC.

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Familial Nonmedullary Thyroid Cancer

Cited by 56 publications

References 3 publications

MiR-886-3p Regulates Cell Proliferation and Migration, and Is Dysregulated in Familial Non-Medullary Thyroid Cancer

MiR-886-3p Regulates Cell Proliferation and Migration, and Is Dysregulated in Familial Non-Medullary Thyroid Cancer

Cancer mortality in relatives of women with breast cancer: The OPCS study

Familial Non Medullary Thyroid Cancer*

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