Analysis Tools
neoplasm
|
• 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)
• derived from the adrenal cortex and observed in 99% of gonadectomized mice
(J:20450)
|
|
• gonadal stromal tumors, developing around 4 weeks of age with 100% penetrance in both males and females
|
 |
• 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)
• ovarian tumors were either mixed or incompletely differentiated gonadal stromal tumors and either bilateral or unilateral
(J:3315)
|
 |
• 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
|
|
• massive proliferation of Sertoli cells progresses to testicular tumors by 2 months of age
|
digestive/alimentary system
|
• mucosal atrophy in the glandular stomach
|
reproductive system
|
|
• hemorrhaging evident at 7 to 16 weeks of age
|
|
|
• massive proliferation of Sertoli cells progresses to testicular tumors by 2 months of age
|
|
|
• disruption of the follicular architecture by the gonadal tumors
|
|
|
• ovaries weigh 100 times as much as littermate controls at 2 months of age
|
|
|
• testicular enlargement and hemorrhaging were evident at 5 weeks of age
|
|
|
• testis weight 3- to 5- fold more than normal testis by 2 months of age due to the large mass of testicular tumors
|
|
• gonadal stromal tumors, developing around 4 weeks of age with 100% penetrance in both males and females
|
|
|
• 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)
• ovarian tumors were either mixed or incompletely differentiated gonadal stromal tumors and either bilateral or unilateral
(J:3315)
|
|
|
• 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
|
|
|
• 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
|
homeostasis/metabolism
|
• increased FSH levels in adolescent and older male and female mice
|
hematopoietic system
|
• 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
|
|
• ovaries weigh 100 times as much as littermate controls at 2 months of age
|
|
• 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
|
• becoming severe as weight loss progresses
|
liver/biliary system
|
• foci of chronic lymphocytic inflammation
|
|
• uniformly micronodular
• liver abnormalities were observed in gonadectomized mice as well
|
|
• necrosis around the central vein
|
immune system
|
• foci of chronic lymphocytic inflammation
|
endocrine/exocrine glands
|
|
• hemorrhaging evident at 7 to 16 weeks of age
|
|
|
• massive proliferation of Sertoli cells progresses to testicular tumors by 2 months of age
|
|
• 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)
• derived from the adrenal cortex and observed in 99% of gonadectomized mice
(J:20450)
|
|
|
• disruption of the follicular architecture by the gonadal tumors
|
|
|
• ovaries weigh 100 times as much as littermate controls at 2 months of age
|
|
|
• 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)
• ovarian tumors were either mixed or incompletely differentiated gonadal stromal tumors and either bilateral or unilateral
(J:3315)
|
|
|
• testicular enlargement and hemorrhaging were evident at 5 weeks of age
|
|
|
• testis weight 3- to 5- fold more than normal testis by 2 months of age due to the large mass of testicular tumors
|
|
|
• 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
|
|
• hemorrhaging evident at 7 to 16 weeks of age
|
