Genetic Predisposition for Nonmedullary Thyroid Cancer

被引：18

作者：

Nagy, Rebecca ^{[1
,2
,3
,4
,5
]}

Ringel, Matthew D. ^{[1
,2
,3
,4
,6
]}

机构：

[1] Ohio State Univ, Div Human Genet, Coll Med, Columbus, OH 43210 USA

[2] Arthur G James Comprehens Canc Ctr, Columbus, OH 43210 USA

[3] Richard G Solove Res Inst, Columbus, OH 43210 USA

[4] Ohio State Univ, Dept Internal Med, Coll Med, Div Endocrinol Diabet & Metab, Columbus, OH 43210 USA

[5] Ohio State Univ, Dept Internal Med, Div Human Genet, Wexner Med Ctr, Columbus, OH 43210 USA

[6] Ohio State Univ, Dept Internal Med, Div Endocrinol Metab & Diabet, Wexner Med Ctr, Columbus, OH 43210 USA

来源：

HORMONES & CANCER | 2015年 / 6卷 / 01期

关键词：

SINGLE-NUCLEOTIDE POLYMORPHISMS; CRIBRIFORM MORULAR VARIANT; GENOME-WIDE ASSOCIATION; FIRST-DEGREE RELATIVES; COMMON VARIANTS; CLINICAL CHARACTERISTICS; ENDOCRINE OVERACTIVITY; SUSCEPTIBILITY LOCUS; GERMLINE MUTATIONS; LINKAGE ANALYSIS;

D O I：

10.1007/s12672-014-0205-y

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Nonmedullary thyroid cancer (NMTC) can be sporadic or can occur as a component cancer as part of several well-described hereditary cancer syndromes. NMTC, particularly papillary thyroid cancer, also can occur by itself in families and is often termed familial NMTC or familial papillary thyroid cancer. The occurrence of NMTC in families, along with extensive population-based evidence from patients with sporadic thyroid cancer, together suggest that NMTC has a strong genetic component, only a small proportion of which has been characterized to date. Advances in genetic and genomic technology have rapidly advanced our understanding of the complex nature of NMTC susceptibility, although much remains to be explained. Herein, we describe the current state of knowledge, starting with a brief review of hereditary syndromic causes and moving on to describe recent data using modern genomic approaches to identifying genes involved in the predisposition to NMTC.

引用

页码：13 / 20

页数：8

共 76 条

[1] Thyroid Cancer Risk 40+ Years after Irradiation for an Enlarged Thymus: An Update of the Hempelmann Cohort [J].

Adams, Jacob ;

Shore, Roy E. ;

Dozier, Ann ;

Lipshultz, Steven E. ;

Schwartz, Ronald G. ;

Constine, Louis S. ;

Pearson, Thomas A. ;

Stovall, Marilyn ;

Thevenet-Morrison, Kelly ;

Fisher, Susan G. .

RADIATION RESEARCH, 2010, 174 (06) :753-762

[2]

Ai L, 2014, ENDOCRINE

[3] Common Variants of the Thyroglobulin Gene Are Associated with Differentiated Thyroid Cancer Risk [J].

Akdi, Abdelmounaim ;

Perez, Gisselle ;

Pastor, Susana ;

Castell, Juan ;

Biarnes, Josefina ;

Marcos, Ricard ;

Velazquez, Antonia .

THYROID, 2011, 21 (05) :519-525

[4] Investigation of insulin resistance gene polymorphisms in patients with differentiated thyroid cancer [J].

Akker, Mustafa ;

Guldiken, Sibel ;

Sipahi, Tammam ;

Palabiyik, Orkide ;

Tosunoglu, Ayhan ;

Celik, Ozlem ;

Tuncbilek, Nermin ;

Sezer, Atakan ;

Sut, Necdet .

MOLECULAR BIOLOGY REPORTS, 2014, 41 (05) :3541-3547

[5] Polymorphisms of DNA damage response genes in radiation-related and sporadic papillary thyroid carcinoma [J].

Akulevich, Natallia M. ;

Saenko, Vladimir A. ;

Rogounovitch, Tatiana I. ;

Drozd, Valentina M. ;

Lushnikov, Eugeny F. ;

Ivanov, Victor K. ;

Mitsutake, Norisato ;

Kominami, Ryo ;

Yamashita, Shunichi .

[6] Is familial non-medullary thyroid carcinoma more aggressive than sporadic thyroid cancer? A multicenter series [J].

Alsanea, O ;

Wada, N ;

Ain, K ;

Wong, M ;

Taylor, K ;

Ituarte, PHG ;

Treseler, PA ;

Weier, HU ;

Freimer, N ;

Siperstein, AE ;

Duh, QY ;

Takami, H ;

Clark, OH .

SURGERY, 2000, 128 (06) :1043-1050

[7] Cancer as a complex phenotype: Pattern of cancer distribution within and beyond the nuclear family [J].

Amundadottir, LT ;

Thorvaldsson, S ;

Gudbjartsson, DF ;

Sulem, P ;

Kristjansson, K ;

Arnason, S ;

Gulcher, JR ;

Bjornsson, J ;

Kong, A ;

Thorsteinsdottir, U ;

Stefansson, K .

PLOS MEDICINE, 2004, 1 (03) :229-236

[8]

[Anonymous], 2004, PATHOLOGY GENETICS T, P320

[9] Common genetic variants in metabolism and detoxification pathways and the risk of papillary thyroid cancer. [J].

Aschebrook-Kilfoy, Briseis ;

Neta, Gila ;

Brenner, Alina V. ;

Hutchinson, Amy ;

Pfeiffer, Ruth M. ;

Sturgis, Erich M. ;

Xu, Li ;

Wheeler, William ;

Doody, Michele M. ;

Chanock, Stephen J. ;

Sigurdson, Alice J. .

[10] Familial nontoxic multinodular thyroid goiter locus maps to chromosome 149 but does not account for familial nonmedullary thyroid cancer [J].

Bignell, GR ;

Canzian, F ;

Shayeghi, M ;

Stark, M ;

Shugart, YY ;

Biggs, P ;

Mangion, J ;

Hamoudi, R ;

Rosenblatt, J ;

Buu, P ;

Sun, S ;

Stoffer, SS ;

Goldgar, DE ;

Romeo, G ;

Houlston, RS ;

Narod, SA ;

Stratton, MR ;

Foulkes, WD .

AMERICAN JOURNAL OF HUMAN GENETICS, 1997, 61 (05) :1123-1130

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