Analysis of mutations in genes of the follicle-stimulating hormone receptor signaling pathway in ovarian granulosa cell tumors

被引：39

作者：

Ligtenberg, MJ

Siers, M

Themmen, APN

Hanselaar, TG

Willemsen, W

Brunner, HG ^{[1
]}

机构：

[1] Univ Nijmegen Hosp, Dept Human Genet 417, NL-6525 GA Nijmegen, Netherlands

[2] Univ Nijmegen Hosp, Dept Pathol, NL-6525 GA Nijmegen, Netherlands

[3] Univ Nijmegen Hosp, Dept Gynaecol, NL-6525 GA Nijmegen, Netherlands

[4] Erasmus Univ, Dept Endocrinol & Reprod, NL-3015 GE Rotterdam, Netherlands

来源：

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM | 1999年 / 84卷 / 06期

关键词：

D O I：

10.1210/jc.84.6.2233

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

It has been suggested that ovarian granulosa cell tumors may result from unopposed hyperstimulation, either by excessive gonadotropin stimulation, by activating mutations of the FSH receptor gene, or of the G protein subunits, Gs alpha or Gi alpha 2. We have examined the entire open reading frame of the FSH receptor gene in ovarian granulosa cell tumors. In addition, these tumors were evaluated for the known oncogenic G protein mutations Gsp and Gip2. Normal results were obtained in all 23 ovarian granulosa cell tumors. We conclude that mutations of the FSH receptor G protein signaling pathway do not play any major role in the genesis of these tumors.

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收藏

页码：2233 / 2234

页数：2

相关论文

共 11 条

[1] No evidence of a role for mutations or polymorphisms of the follicle-stimulating hormone receptor in ovarian granulosa cell tumors [J].

Fuller, PJ ;

Verity, K ;

Shen, Y ;

Mamers, P ;

Jobling, T ;

Burger, HG .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (01) :274-279

[2] Absence of mutations in the FSH receptor in ovarian granulosa cell tumors [J].

Kotlar, T ;

Young, RH ;

Albanese, C ;

Crowley, WF ;

Scully, RE ;

Jameson, JL .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (08) :3001-3001

[3] A mutation in the follicle-stimulating hormone receptor occurs frequently in human ovarian sex cord tumors [J].

Kotlar, TJ ;

Young, RH ;

Albanese, C ;

Crowley, WF ;

Scully, RE ;

Jameson, JL .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1997, 82 (04) :1020-1026

[4]

LIU G, 1998, 80 ANN M END SOC NEW, P62

[5] 2 G-PROTEIN ONCOGENES IN HUMAN ENDOCRINE TUMORS [J].

LYONS, J ;

LANDIS, CA ;

HARSH, G ;

VALLAR, L ;

GRUNEWALD, K ;

FEICHTINGER, H ;

DUH, QY ;

CLARK, OH ;

KAWASAKI, E ;

BOURNE, HR ;

MCCORMICK, F .

SCIENCE, 1990, 249 (4969) :655-659

[6] SOMATIC MUTATIONS IN THE THYROTROPIN RECEPTOR GENE CAUSE HYPERFUNCTIONING THYROID ADENOMAS [J].

PARMA, J ;

DUPREZ, L ;

VANSANDE, J ;

COCHAUX, P ;

GERVY, C ;

MOCKEL, J ;

DUMONT, J ;

VASSART, G .

NATURE, 1993, 365 (6447) :649-651

[7]

RUSSO D, 1995, ONCOGENE, V11, P1907

[8] Absence of the previously reported G protein oncogene (gip2) in ovarian granulosa cell tumors [J].

Shen, Y ;

Mamers, P ;

Jobling, T ;

Burger, HG ;

Fuller, PJ .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1996, 81 (11) :4159-4161

[9] Association of a human G-protein β3 subunit variant with hypertension [J].

Siffert, W ;

Rosskopf, D ;

Siffert, G ;

Busch, S ;

Moritz, A ;

Erbel, R ;

Sharma, AM ;

Ritz, E ;

Wichmann, HE ;

Jakobs, KH ;

Horsthemke, B .

NATURE GENETICS, 1998, 18 (01) :45-48

[10] Screening male intracytoplasmic sperm injection candidates for mutations of the follicle stimulating hormone receptor gene [J].

Tuerlings, JHAM ;

Ligtenberg, MJL ;

Kremer, JAM ;

Siers, M ;

Meuleman, EJH ;

Braat, DDHM ;

Hoefsloot, LH ;

Merkus, HMWM ;

Brunner, HG .

HUMAN REPRODUCTION, 1998, 13 (08) :2098-2101