Phenotypes associated with this allele

• Allele Symbol: Inha^tm1Bay
• Allele Name: targeted mutation 1, Baylor College of Medicine
• Allele ID: MGI:1857202
• Summary: 11 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Inha^tm1Bay/Inha^tm1Bay	involves: 129S6/SvEvTac * 129S7/SvEvBrd	MGI:4418906
hm2	Inha^tm1Bay/Inha^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:2662287
cx3	Esr1^tm1Ksk/Esr1^tm1Ksk Esr2^tm1Unc/Esr2^tm1Unc Inha^tm1Bay/Inha^tm1Bay	involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd	MGI:4418901
cx4	Esr1^tm1Ksk/Esr1^tm1Ksk Esr2^tm1Unc/Esr2^tm1Unc Inha^tm1Bay/Inha^+	involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd	MGI:4418903
cx5	Esr1^tm1Ksk/Esr1^tm1Ksk Inha^tm1Bay/Inha^tm1Bay	involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd	MGI:4418905
cx6	Esr2^tm1Unc/Esr2^tm1Unc Inha^tm1Bay/Inha^tm1Bay	involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd	MGI:4418907
cx7	Inha^tm1Bay/Inha^tm1Bay Smad3^tm1Par/Smad3^tm1Par	involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/Sv * C57BL/6	MGI:3790431
cx8	Inha^tm1Bay/Inha^tm1Bay Smad3^tm1Par/Smad3^+	involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/Sv * C57BL/6	MGI:3790432
cx9	Amhr2^tm1Bhr/Amhr2^tm1Bhr Inha^tm1Bay/Inha^tm1Bay	involves: 129S7/SvEvBrd	MGI:3042187
cx10	Amhr2^tm1Bhr/Amhr2^tm1Bhr Inha^tm1Bay/Inha^+	involves: 129S7/SvEvBrd * C57BL/6	MGI:3042188
cx11	Gnrh1^hpg/Gnrh1^hpg Inha^tm1Bay/Inha^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6 * HPG/Bm	MGI:2662292

Genotype
MGI:4418906

hm1

• Allelic Composition: Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129S6/SvEvTac * 129S7/SvEvBrd

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

extended life span ( J:84989 )

• when mice are treated with flutamide compared with untreated homozygotes

premature death ( J:84989 )

• all mice die by 20 weeks of age

neoplasm

increased ovary tumor incidence ( J:84989 )

♀ • mice develop ovarian tumors with hemorrhage

♀ • mice treated with flutamide develop tumors with little evidence of gross hemorrhage

♀ • ovarian tumors contain undifferentiated or granulosa-like cells

increased testis tumor incidence ( J:84989 )

♂

growth/size/body

cachexia ( J:84989 )

homeostasis/metabolism

increased circulating estradiol level ( J:84989 )

decreased circulating follicle stimulating hormone level ( J:84989 )

• flutamide treated mice exhibit reduced follicle stimulating hormone levels in the serum compared with untreated homozygous mice

reproductive system

increased ovary tumor incidence ( J:84989 )

♀ • mice develop ovarian tumors with hemorrhage

♀ • mice treated with flutamide develop tumors with little evidence of gross hemorrhage

♀ • ovarian tumors contain undifferentiated or granulosa-like cells

increased testis tumor incidence ( J:84989 )

♂

endocrine/exocrine glands

increased ovary tumor incidence ( J:84989 )

♀ • mice develop ovarian tumors with hemorrhage

♀ • mice treated with flutamide develop tumors with little evidence of gross hemorrhage

♀ • ovarian tumors contain undifferentiated or granulosa-like cells

increased testis tumor incidence ( J:84989 )

♂

Genotype
MGI:2662287

hm2

• Allelic Composition: Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

Liver and stomach histology of Inha^tm1Bay/Inha^tm1Bay mice

neoplasm

increased adrenal gland tumor incidence ( J:20450 , J:125349 )

• derived from the adrenal cortex and observed in 99% of gonadectomized mice (J:20450)

• gonadectomy causes adrenal tumorigenesis which is dependent on the chronically elevated gonadotropin levels that result from this manipulation (J:125349)

• adrenal tumors originate in the subcapsular stem/progenitor zone of the adrenal cortex where upon gonadectomy cells express markers indistinguishable from tumorigenic granulose cells from the ovaries (J:125349)

• the 50% survival rate of female mice with gonadectomies is 22 weeks with all mice dying of extensive adrenal tumor burden (J:125349)

increased gonad tumor incidence ( J:3315 )

• gonadal stromal tumors, developing around 4 weeks of age with 100% penetrance in both males and females

increased ovary tumor incidence ( J:3315 , J:125349 )

♀ • ovarian tumors were either mixed or incompletely differentiated gonadal stromal tumors and either bilateral or unilateral (J:3315)

♀ • ovary tumors result from uncontrolled proliferation by granulosa cells (J:125349)

♀ • continuously expanding clusters of tumor cells in the ovary ablate normal ovarian architecture by 2 months of age (J:125349)

♀ • these tumorigenic granulosa cells contain high levels of phosphorylated Smad3 (J:125349)

increased testis tumor incidence ( J:125349 )

♂ • histological analysis indicates the presence of large, hemorrhagic tumors that lie adjacent to remnants of seminiferous tubules

♂ • testicular tumors result from uncontrolled proliferation of Sertoli cells

♂ • these tumorigenic Sertoli cells contain high levels of phosphorylated Smad3

cellular

increased Sertoli cell proliferation ( J:125349 )

♂ • massive proliferation of Sertoli cells progresses to testicular tumors by 2 months of age

digestive/alimentary system

abnormal stomach mucosa morphology ( J:20450 )

• mucosal atrophy in the glandular stomach

reproductive system

ovary hemorrhage ( J:3315 )

♀ • hemorrhaging evident at 7 to 16 weeks of age

increased Sertoli cell proliferation ( J:125349 )

♂ • massive proliferation of Sertoli cells progresses to testicular tumors by 2 months of age

abnormal ovarian follicle morphology ( J:3315 )

♀ • disruption of the follicular architecture by the gonadal tumors

increased ovary weight ( J:125349 )

♀ • ovaries weigh 100 times as much as littermate controls at 2 months of age

enlarged testis ( J:3315 )

♂ • testicular enlargement and hemorrhaging were evident at 5 weeks of age

increased testis weight ( J:125349 )

♂ • testis weight 3- to 5- fold more than normal testis by 2 months of age due to the large mass of testicular tumors

increased gonad tumor incidence ( J:3315 )

• gonadal stromal tumors, developing around 4 weeks of age with 100% penetrance in both males and females

increased ovary tumor incidence ( J:3315 , J:125349 )

♀ • ovarian tumors were either mixed or incompletely differentiated gonadal stromal tumors and either bilateral or unilateral (J:3315)

♀ • ovary tumors result from uncontrolled proliferation by granulosa cells (J:125349)

♀ • continuously expanding clusters of tumor cells in the ovary ablate normal ovarian architecture by 2 months of age (J:125349)

♀ • these tumorigenic granulosa cells contain high levels of phosphorylated Smad3 (J:125349)

increased testis tumor incidence ( J:125349 )

♂ • histological analysis indicates the presence of large, hemorrhagic tumors that lie adjacent to remnants of seminiferous tubules

♂ • testicular tumors result from uncontrolled proliferation of Sertoli cells

♂ • these tumorigenic Sertoli cells contain high levels of phosphorylated Smad3

abnormal spermatogenesis ( J:3315 )

♂ • although spermatogenesis was initially active and observed to be normal between 5 and 7 weeks of age, regression began with the enlargement of testcular tumors

female infertility ( J:3315 )

♀

male infertility ( J:3315 )

♂

homeostasis/metabolism

increased circulating follicle stimulating hormone level ( J:3315 )

• increased FSH levels in adolescent and older male and female mice

hematopoietic system

anemia ( J:20450 )

• developing between 7 and 12 weeks of age

• not observed in animals that had a gonadectomy prior to 6 weeks of age

pancytopenia ( J:20450 )

• observed in examined mice and believed to be contributing to the cachexia

growth/size/body

increased ovary weight ( J:125349 )

♀ • ovaries weigh 100 times as much as littermate controls at 2 months of age

decreased body weight ( J:20450 )

cachexia ( J:20450 )

• beginning after 6 to 7 weeks of age

• gonadectomy prior to 6 weeks of age prevented severe weight loss in both males and females

skeleton

kyphoscoliosis ( J:20450 )

• becoming severe as weight loss progresses

liver/biliary system

chronic liver inflammation ( J:20450 )

• foci of chronic lymphocytic inflammation

abnormal liver morphology ( J:20450 )

• uniformly micronodular

• liver abnormalities were observed in gonadectomized mice as well

diffuse hepatic necrosis ( J:20450 )

• necrosis around the central vein

immune system

chronic liver inflammation ( J:20450 )

• foci of chronic lymphocytic inflammation

endocrine/exocrine glands

ovary hemorrhage ( J:3315 )

♀ • hemorrhaging evident at 7 to 16 weeks of age

increased Sertoli cell proliferation ( J:125349 )

♂ • massive proliferation of Sertoli cells progresses to testicular tumors by 2 months of age

increased adrenal gland tumor incidence ( J:20450 , J:125349 )

• derived from the adrenal cortex and observed in 99% of gonadectomized mice (J:20450)

• gonadectomy causes adrenal tumorigenesis which is dependent on the chronically elevated gonadotropin levels that result from this manipulation (J:125349)

• adrenal tumors originate in the subcapsular stem/progenitor zone of the adrenal cortex where upon gonadectomy cells express markers indistinguishable from tumorigenic granulose cells from the ovaries (J:125349)

• the 50% survival rate of female mice with gonadectomies is 22 weeks with all mice dying of extensive adrenal tumor burden (J:125349)

abnormal ovarian follicle morphology ( J:3315 )

♀ • disruption of the follicular architecture by the gonadal tumors

increased ovary weight ( J:125349 )

♀ • ovaries weigh 100 times as much as littermate controls at 2 months of age

increased ovary tumor incidence ( J:3315 , J:125349 )

♀ • ovarian tumors were either mixed or incompletely differentiated gonadal stromal tumors and either bilateral or unilateral (J:3315)

♀ • ovary tumors result from uncontrolled proliferation by granulosa cells (J:125349)

♀ • continuously expanding clusters of tumor cells in the ovary ablate normal ovarian architecture by 2 months of age (J:125349)

♀ • these tumorigenic granulosa cells contain high levels of phosphorylated Smad3 (J:125349)

enlarged testis ( J:3315 )

♂ • testicular enlargement and hemorrhaging were evident at 5 weeks of age

increased testis weight ( J:125349 )

♂ • testis weight 3- to 5- fold more than normal testis by 2 months of age due to the large mass of testicular tumors

increased testis tumor incidence ( J:125349 )

♂ • histological analysis indicates the presence of large, hemorrhagic tumors that lie adjacent to remnants of seminiferous tubules

♂ • testicular tumors result from uncontrolled proliferation of Sertoli cells

♂ • these tumorigenic Sertoli cells contain high levels of phosphorylated Smad3

cardiovascular system

ovary hemorrhage ( J:3315 )

♀ • hemorrhaging evident at 7 to 16 weeks of age

Genotype
MGI:4418901

cx3

• Allelic Composition: Esr1^tm1Ksk/Esr1^tm1Ksk; Esr2^tm1Unc/Esr2^tm1Unc; Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd

mortality/aging

premature death ( J:84989 )

• most female mice die between 4 and 6 weeks of age and all die by 9 weeks of age

• male mice survival 19 weeks

reproductive system

decreased male germ cell number ( J:84989 )

♂ • male germ cells are depleted and degenerated

abnormal ovary morphology ( J:84989 )

♀ • tubule-like structures resembling Sertoli-like cells are found adjacent to tumor unlike in wild-type mice

increased ovary tumor incidence ( J:84989 )

♀ • mice develop aggressive bilateral ovarian tumors with hemorrhagic foci

♀ • tumors contain granulosa-like cells

abnormal seminiferous tubule morphology ( J:84989 )

♂ • tubule lumens are filled with Sertoli cells unlike in wild-type mice

dilated seminiferous tubule ( J:84989 )

♂

increased testis tumor incidence ( J:84989 )

♂ • mice develop testicular tumors formed of granulosa-like cells with numerous sites of hemorrhage

♂ • mice fail to develop early Sertoli cells unlike in Esr1^tm1Ksk Inha^tm1Bay or Esr2^tm1Unc Inha^tm1Bay double homozygotes

neoplasm

increased ovary tumor incidence ( J:84989 )

♀ • mice develop aggressive bilateral ovarian tumors with hemorrhagic foci

♀ • tumors contain granulosa-like cells

increased testis tumor incidence ( J:84989 )

♂ • mice develop testicular tumors formed of granulosa-like cells with numerous sites of hemorrhage

♂ • mice fail to develop early Sertoli cells unlike in Esr1^tm1Ksk Inha^tm1Bay or Esr2^tm1Unc Inha^tm1Bay double homozygotes

growth/size/body

decreased body weight ( J:84989 )

• compared with Esr1^tm1Ksk and Esr2^tm1Unc single homozygotes

cachexia ( J:84989 )

• at 26 weeks

increased body weight ( J:84989 )

• compared to in Inha^tm1Bay

homeostasis/metabolism

decreased circulating follicle stimulating hormone level ( J:84989 )

endocrine/exocrine glands

abnormal ovary morphology ( J:84989 )

♀ • tubule-like structures resembling Sertoli-like cells are found adjacent to tumor unlike in wild-type mice

increased ovary tumor incidence ( J:84989 )

♀ • mice develop aggressive bilateral ovarian tumors with hemorrhagic foci

♀ • tumors contain granulosa-like cells

abnormal seminiferous tubule morphology ( J:84989 )

♂ • tubule lumens are filled with Sertoli cells unlike in wild-type mice

dilated seminiferous tubule ( J:84989 )

♂

increased testis tumor incidence ( J:84989 )

♂ • mice develop testicular tumors formed of granulosa-like cells with numerous sites of hemorrhage

♂ • mice fail to develop early Sertoli cells unlike in Esr1^tm1Ksk Inha^tm1Bay or Esr2^tm1Unc Inha^tm1Bay double homozygotes

cellular

decreased male germ cell number ( J:84989 )

♂ • male germ cells are depleted and degenerated

Genotype
MGI:4418903

cx4

• Allelic Composition: Esr1^tm1Ksk/Esr1^tm1Ksk; Esr2^tm1Unc/Esr2^tm1Unc; Inha^tm1Bay/Inha⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd

reproductive system

abnormal ovary morphology ( J:84989 )

♀ • ovaries develop tubule-like structures unlike in wild-type mice

increased ovary tumor incidence ( J:84989 )

♀ • in one mouse

neoplasm

increased ovary tumor incidence ( J:84989 )

♀ • in one mouse

endocrine/exocrine glands

abnormal ovary morphology ( J:84989 )

♀ • ovaries develop tubule-like structures unlike in wild-type mice

increased ovary tumor incidence ( J:84989 )

♀ • in one mouse

Genotype
MGI:4418905

cx5

• Allelic Composition: Esr1^tm1Ksk/Esr1^tm1Ksk; Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd

mortality/aging

premature death ( J:84989 )

• male mice exhibit reduced survival compared with Esr1^tm1Ksk homozygotes that is similar to in Inha^tm1Bay homozygotes

• female mice exhibit reduced survival compared with Esr1^tm1Ksk or Inha^tm1Bay homozygotes

neoplasm

increased ovary tumor incidence ( J:84989 )

♀ • tumors are larger than in Inha^tm1Bay homozygotes

♀ • tumors contain tubule-like follicle-like structures

increased testis tumor incidence ( J:84989 )

♂ • tumor cells contain diffuse granulosa-like cells

growth/size/body

decreased body weight ( J:84989 )

• in female mice compared with Esr1^tm1Ksk homozygotes, Inha^tm1Bay homozygotes, and wild-type mice

cachexia ( J:84989 )

• mice develop rapid cancer-associated wasting unlike wild-type mice that is more severe than in Inha^tm1Bay homozygotes

homeostasis/metabolism

increased circulating estradiol level ( J:84989 )

decreased circulating follicle stimulating hormone level ( J:84989 )

• in terminal mice compared with Inha^tm1Bay homozygotes

decreased circulating luteinizing hormone level ( J:84989 )

• in terminal mice compared with Inha^tm1Bay homozygotes

digestive/alimentary system

abnormal stomach mucosa morphology ( J:84989 )

• terminal mice exhibit mucosal atrophy in the stomach unlike in wild-type mice

abnormal stomach glandular epithelium morphology ( J:84989 )

• terminal mice exhibit depletion of parietal cells in the glandular stomach unlike in wild-type mice

immune system

liver inflammation ( J:84989 )

liver/biliary system

liver inflammation ( J:84989 )

abnormal hepatocyte morphology ( J:84989 )

• hepatocytes in terminal mice are darkened irregularly shaped and round surrounding the central vein unlike in wild-type mice

hepatic necrosis ( J:84989 )

• in terminal mice

skeleton

kyphoscoliosis ( J:84989 )

• in terminal mice

endocrine/exocrine glands

increased ovary tumor incidence ( J:84989 )

♀ • tumors are larger than in Inha^tm1Bay homozygotes

♀ • tumors contain tubule-like follicle-like structures

increased testis tumor incidence ( J:84989 )

♂ • tumor cells contain diffuse granulosa-like cells

reproductive system

increased ovary tumor incidence ( J:84989 )

♀ • tumors are larger than in Inha^tm1Bay homozygotes

♀ • tumors contain tubule-like follicle-like structures

increased testis tumor incidence ( J:84989 )

♂ • tumor cells contain diffuse granulosa-like cells

Genotype
MGI:4418907

cx6

• Allelic Composition: Esr2^tm1Unc/Esr2^tm1Unc; Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac * 129S7/SvEvBrd

mortality/aging

premature death ( J:84989 )

• all mice die by 20 weeks of age similar to Inha^tm1Bay homozygotes

neoplasm

increased ovary tumor incidence ( J:84989 )

♀ • similar to Inha^tm1Bay homozygotes

increased testis tumor incidence ( J:84989 )

♂ • similar to Inha^tm1Bay homozygotes

digestive/alimentary system

abnormal stomach morphology ( J:84989 )

• mice develop hallmarks of disease progression that are similar to in Inha^tm1Bay homozygotes

growth/size/body

cachexia ( J:84989 )

• similar to Inha^tm1Bay homozygotes

liver/biliary system

abnormal liver morphology ( J:84989 )

• mice develop hallmarks of disease progression that are similar to in Inha^tm1Bay homozygotes

endocrine/exocrine glands

increased ovary tumor incidence ( J:84989 )

♀ • similar to Inha^tm1Bay homozygotes

increased testis tumor incidence ( J:84989 )

♂ • similar to Inha^tm1Bay homozygotes

reproductive system

increased ovary tumor incidence ( J:84989 )

♀ • similar to Inha^tm1Bay homozygotes

increased testis tumor incidence ( J:84989 )

♂ • similar to Inha^tm1Bay homozygotes

Genotype
MGI:3790431

cx7

• Allelic Composition: Inha^tm1Bay/Inha^tm1Bay; Smad3^tm1Par/Smad3^tm1Par
• Genetic Background: involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/Sv * C57BL/6

endocrine/exocrine glands

abnormal ovarian folliculogenesis ( J:125349 )

♀ • oocytes are surrounded by small follicles although follicular development is arrested in a similar manner to mice homozygous for just the Smad3^tm1Par allele

increased ovary tumor incidence ( J:125349 )

♀ • the rapid ovarian tumorigenesis associated with Inha^tm1Bay homozygotes is greatly attenuated when on a Smad3^tm1Par background

♀ • tumorigenesis still occurs as demonstrated by a mass of expansive stromal tissue commonly found on the periphery of the ovary

increased Sertoli cell number ( J:125349 )

♂ • some focal Sertoli cell hyperplasia is present in the testes of two month old mice though no tumors are observed

reproductive system

abnormal ovarian folliculogenesis ( J:125349 )

♀ • oocytes are surrounded by small follicles although follicular development is arrested in a similar manner to mice homozygous for just the Smad3^tm1Par allele

increased ovary tumor incidence ( J:125349 )

♀ • the rapid ovarian tumorigenesis associated with Inha^tm1Bay homozygotes is greatly attenuated when on a Smad3^tm1Par background

♀ • tumorigenesis still occurs as demonstrated by a mass of expansive stromal tissue commonly found on the periphery of the ovary

increased Sertoli cell number ( J:125349 )

♂ • some focal Sertoli cell hyperplasia is present in the testes of two month old mice though no tumors are observed

neoplasm

increased ovary tumor incidence ( J:125349 )

♀ • the rapid ovarian tumorigenesis associated with Inha^tm1Bay homozygotes is greatly attenuated when on a Smad3^tm1Par background

♀ • tumorigenesis still occurs as demonstrated by a mass of expansive stromal tissue commonly found on the periphery of the ovary

Genotype
MGI:3790432

cx8

• Allelic Composition: Inha^tm1Bay/Inha^tm1Bay; Smad3^tm1Par/Smad3⁺
• Genetic Background: involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/Sv * C57BL/6

neoplasm

increased adrenal gland tumor incidence ( J:125349 )

• gonadectomy causes adrenal tumorigenesis which is dependent on the chronically elevated gonadotropin levels that result from this manipulation

• the 50% survival rate of female mice with gonadectomies is 37.5 weeks with all mice dying of extensive adrenal tumor burden

• this survival rate is significantly longer than in mice that are homozygote for Inha^tm1Bay but which have two wild-type alleles for Smad3

increased ovary tumor incidence ( J:125349 )

♀ • tumor mass is 50% less than in mice homozygote for Inha^tm1Bay but which have two wild-type alleles for Smad3

reproductive system

increased ovary tumor incidence ( J:125349 )

♀ • tumor mass is 50% less than in mice homozygote for Inha^tm1Bay but which have two wild-type alleles for Smad3

endocrine/exocrine glands

increased adrenal gland tumor incidence ( J:125349 )

• gonadectomy causes adrenal tumorigenesis which is dependent on the chronically elevated gonadotropin levels that result from this manipulation

• the 50% survival rate of female mice with gonadectomies is 37.5 weeks with all mice dying of extensive adrenal tumor burden

• this survival rate is significantly longer than in mice that are homozygote for Inha^tm1Bay but which have two wild-type alleles for Smad3

increased ovary tumor incidence ( J:125349 )

♀ • tumor mass is 50% less than in mice homozygote for Inha^tm1Bay but which have two wild-type alleles for Smad3

Genotype
MGI:3042187

cx9

• Allelic Composition: Amhr2^tm1Bhr/Amhr2^tm1Bhr; Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd

neoplasm

increased tumor incidence ( J:36027 )

• multifocal Sertoli/granulosa cell tumors

increased granulosa cell tumor incidence ( J:36027 )

• multifocal granulosa cell tumors

increased testis tumor incidence ( J:36027 )

• testicular tumors, larger than those observed in Inha-deficient mice

increased Leydig cell tumor incidence ( J:36027 )

• Leydig cell neoplasia

reproductive system

increased granulosa cell tumor incidence ( J:36027 )

• multifocal granulosa cell tumors

increased testis tumor incidence ( J:36027 )

• testicular tumors, larger than those observed in Inha-deficient mice

increased Leydig cell tumor incidence ( J:36027 )

• Leydig cell neoplasia

dilated uterus ( J:36027 )

• the uteri observed in male pseudohermaphrodites were dilated and fluid-filled

male pseudohermaphroditism ( J:36027 )

secondary sex reversal ( J:36027 )

endocrine/exocrine glands

increased granulosa cell tumor incidence ( J:36027 )

• multifocal granulosa cell tumors

increased testis tumor incidence ( J:36027 )

• testicular tumors, larger than those observed in Inha-deficient mice

increased Leydig cell tumor incidence ( J:36027 )

• Leydig cell neoplasia

Genotype
MGI:3042188

cx10

• Allelic Composition: Amhr2^tm1Bhr/Amhr2^tm1Bhr; Inha^tm1Bay/Inha⁺
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

neoplasm

increased testis tumor incidence ( J:36027 )

• unilateral stromal tumors observed in the testes of some mice at 6 to 7 months of age

reproductive system

increased testis tumor incidence ( J:36027 )

• unilateral stromal tumors observed in the testes of some mice at 6 to 7 months of age

male pseudohermaphroditism ( J:36027 )

secondary sex reversal ( J:36027 )

endocrine/exocrine glands

increased testis tumor incidence ( J:36027 )

• unilateral stromal tumors observed in the testes of some mice at 6 to 7 months of age

Genotype
MGI:2662292

cx11

• Allelic Composition: Gnrh1^hpg/Gnrh1^hpg; Inha^tm1Bay/Inha^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6 * HPG/Bm

normal phenotype

no abnormal phenotype detected ( J:83261 )

• mice survive past 1 year of age, do not exhibit cachexia, and do not develop either gonadal or adrenal tumors