Showing papers in "Journal of the National Cancer Institute in 1972"

Menopause and breast cancer risk.

Abstract: Age at menopause and type of menopause from hospital records of breast cancer patients were compared with similar information reported by a national probability sample of women. The national sample comprised 3581 women who responded to the 1960-1962 National Health Examination Survey. The cancer series consisted of 3887 patients selected from those reported to the Connecticut Cancer Registry between 1950 and 1959. No substantial bias was identified when the validity of the comparison and the effect of the relatively large number of breast cancer patients whose menopause histories were deficient were evaluated. Overall surgically induced menopause was associated with a reduction in breast cancer risk to about 60% of that experienced by women having natural menopause induced before age 35 but induction up to age 50 was protective. There was little effect in the 10 years following the surgical procedure but substantial reduction occurred in all subsequent periods. Among women with menopause induced before age 35 breast cancer risk stayed as low as 1/3 that expected 30 and more years later. Relative risk of breast cancer increased with age at natural menopause. Women with natural menopause at age 55 or older had twice the breast cancer risk experienced by those whose menopause occurred before age 45. The relative risk of breast cancer associated with late natural menopause was greatest after age 70.(AUTHORS MODIFIED)

Herpes-Type Virus Particles in Tissue Culture of Kaposi's Sarcoma From Different Geographic Regions

Abstract: Typical herpes-type virus particles were observed in 5 of 8 selected tissue culture lines derived from different cases of Kaposi's sarcoma from 2 equatorial African regions, Congo and Uganda. Common and different traits of cellular morphology related to viral involvement were found. In one line, morphologic aspects and preliminary immunologic characterization suggested a virus resembling cytomegalovirus. The other 4 cases presented one important trait in common: The appearance of viruses (at an early stage in lines 13, 16, 19) in undifferentiated cells that resembled fibroblastoid or macrophage elements.-J Natl Cancer Inst 49: 1509-1526, 1972.

Relation of Prolactin and Estrogen to Mammary Tumorigenesis in the Rat

Abstract: In rats estrogen and prolactin are the 2 most important hormones involved in development and growth of mammary tumors. Both are controlled by the pituitary gland and hypothalamous. Ovariectomy or hypophysectomy can inhibit development of mammary tumors or can cause regression. Growth of established mammary tumors can be increased by doses of estrogen estrogen with progesterone or prolactin. Estrogen increases prolactin and growth hormone secretion by the pituitary but has no effect on tumorigenesis in the absence of the pituitary. However prolactin or prolactin with growth hormone together may promote mammary tumor development in the absence of ovaries. In an experiment to study the effects of different doses of estrogen on mammary cancer de velopment and growth in ovariectomized rats tumors were induced with 5 mg of 712-dimethylbenz (a) anthracene (DMBA) at 52 days of age. Test animals received estradiol benzoate (EB) every other day for 150 days by sc injection; controls were given only the corn oil solvent. Mammary cancers developed in all 18 controls with an average latency period of 59 days. No cancers developed in ovariectomized rats who did not receive DMBA. Greatest tumor incidence (17 of 19) occurred in rats given 2 mcg EB. Average latency was 73 days. Regression occurred in 8% of mammary tumors in intact controls but in 20% of ovariectomized rats given .2 and 2.0 mcg EB. Regression rate was 39% in ovariectomized rats given 20 mcg EB. At 150 days ovariectomized rats not treated with EB showed reduced prolactin levels; those with .2 mcg EB showed a small inc rease; the highest doses (up to 2 mcg) produced increases ranging from 11.5 to 12-fold. In rats given 2 mcg EB fewer cancers followed and the latency period was longer than in intact controls. In another experiment a large dose of estrogen given 3 months after DMBA prevented tumor growth while prolactin alone increased mammary tumor growth about 190%. EB alone completely suppressed growth of tumors whereas EB with prolactin restored growth to that of controls. Large doses of estrogen may block binding of prolactin to receptor sites or otherwise prevent prolactin from acting on tumor cells. Changes in hypothalamic function may give rise to spontaneous mammary tumors by increasing prolactin secretion especially in old female rats. Whether this applies to humans is undetermined.