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At least 739 records · Page 41Linked to original sources
PubMed1986

Influence of age on induction of mammary tumors by diethylstilbestrol in C3H/HeN mice with low murine mammary tumor virus titer.

C3H/HeN female mice with low murine mammary tumor virus titer (MTV-) were fed diets containing a targeted concentration of 640 ppb diethylstilbestrol [(DES) CAS: 56-53-1; 4,4'-(1,2-diethyl-1,2-ethenediyl)bis-phenol]. Mice were started on DES at 3, 5, 7, or 9 weeks of age. Some continued on the diet throughout the rest of their life-spans, whereas others were killed as soon as they had been fed DES for 2, 4, 6, 8, 10, or 12 weeks. Controls were also examined throughout the study. Among mice killed early, the only observation significantly influenced by age at the start of DES treatment was the presence or absence of corpora lutea (CL). DES did not prevent CL from appearing in mice started on DES at 7 or 9 weeks of age, but it did prevent their appearance in about 25% of the mice started at 5 weeks and in up to 75% of the mice started at 3 weeks of age. In the life-span-exposure groups, CL either disappeared or were never formed in 88% or more of the mice, regardless of age at the start of treatment. Neoplastic or presumptive preneoplastic lesions apparently influenced by DES in the life-span-treatment groups included ovarian tubular adenomas; granulosa cell tumors and luteomas; pituitary cystoid degeneration, hyperplasia, and adenomas; uterine adenocarcinomas and cervical adenosis; mesotheliomas; and mammary hyperplastic alveolar nodules (HANs) and adenocarcinomas. Luteoma and granulosa cell tumor incidences were reduced by DES, regardless of age at the start of treatment. Influence of age at the start of treatment was minimal or not apparent for mesotheliomas, uterine adenocarcinomas, or pituitary adenomas; however, pituitary cystoid degeneration and hyperplasia and cervical adenosis occurred in higher frequency and/or with shorter duration of DES exposure the earlier that treatment was started. A delay in the start of DES treatment was associated with a remarkable delay in HAN and mammary adenocarcinoma development. This was especially apparent in young mice (3-7 wk old) in which a 2-week delay in treatment resulted in a 20-week delay in HAN or tumor onset. Age at the start of treatment was a major factor in susceptibility of C3H/HeN-MTV- female mice to DES-induced mammary tumorigenesis.

Adenocarcinoma↗
PubMed1986

[Endocrinological and clinico-pathologic study of granulosa-theca cell tumors of the ovary].

Nine granulosa-theca cell tumors (four pure theca cell tumors, one granulosa cell tumors, two granulosa-theca tumors and two juvenile granulosa-theca tumors) were studied endocrinologically and clinico-pathologically. The cases of juvenile granulosa-theca tumors developed precocious pseudopuberty. Three of seven other cases were re-feminized and four cases showed no hormonal manifestation clinically. The peripheral vein serum values of estradiol, progesterone, testosterone and prolactin were elevated in six of eight cases, three of four cases, four of six cases, and two of three cases, respectively. The concentration ratios between tumor harboring ovarian vein samples and peripheral vein (or opposite normal ovarian vein) samples was 2.7 to 16.9 for estrone, 8.8 to 28.6 for estradiol, 3.6 to 4.7 for progesterone, 1.6 to 6.6 for testosterone and 0.6 to 1.0 for prolactin. Estradiol was localized in both granulosa cells and theca cells, and testosterone was localized in granulosa cells in half of the cases and in theca cells in 60% of the cases. Also, testosterone was localized in all three cases in which luteinized theca cells were present. There were no cases with positive prolactin localization. These results are compatible with the concept that in granulosa-theca cell tumor, both granulosa and theca cells can produce a wide range of steroid hormones.

Aged↗
PubMed1987

[Realization of reproductive function and hormonally active ovarian tumors].

Reproductive function was studied in 438 women with practically all histotypes of hormone-producing tumors of the ovaries (141-theca cell, 97-granulosa cell, 14-mixed theca-granulosa cell, 11-masculinizing and 26-Brenner tumors). The said function was reduced in 141 reproductive patients (48.8%). It was shown that hormone producing tumors of the ovary do not cause reproductive function to decline. Conversely, it was infrequent or no births in the young age that could have been a factor of tumorigenesis.

Adenoma↗
PubMed1966

The nature and classification of ovarian neoplasms.

The classification of ovarian neoplasms on a histogenetic basis according to presentday concepts of development and structure of the ovary is considered. There are four histogenetic categories of primary ovarian tumours: neoplasms of germ cell origin, neoplasms of celomic (germinal) epithelium and its derivatives, neoplasms of specialized gonadal stroma (sex cords and mesenchyme), and neoplasms of non-specialized gonadal stromal and heterotopic elements. In patients of all ages, 70% of ovarian neoplasms were of celomic epithelial origin, 16% of germ-cell origin, 5% of specialized gonadal stromal origin, and 9% arose from the non-specialized stroma and heterotopic elements. Before 20 years of age, 59% of ovarian neoplasms were of germ cell origin and before puberty they accounted for 90% of all ovarian tumours. The different structural types of neoplasms within the four categories are described. Accurate classification of ovarian neoplasms on a histogenetic basis is stressed if proper treatment is to be given and intelligent assessment of end results is to be made.

Adenocarcinoma↗