Serum levels of human placental lactogen and pregnancy-specific β1-glycoprotein in breast cancer

Monteiro, J C; Biswas, S.; Al-Awqati, M A; Greening, W P; McKinna, J A; Neville, A. Munro

doi:10.1038/bjc.1982.193

Cited by 10 publications

(6 citation statements)

References 13 publications

(17 reference statements)

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“…The most widely accepted explanation for pregnancy protection against mammary cancer is that the protective effect is attributable to the pregnancy-induced differentiation of the target structures, terminal-end buds, and terminal ducts for carcinogenesis, thus reducing the target cells for carcinogenesis (24). The other explanation for pregnancy protection against mammary cancer is that pregnancy primes the maternal immune system against pregnancy-related antigens which are expressed during the growth of mammary tumors (25)(26)(27)(28). Furthermore, the splenocytes of parous rats have significantly higher cytotoxic activity against mammary tumor cells when compared with virgin controls (29).…”

mentioning

confidence: 99%

Short-term exposure to pregnancy levels of estrogen prevents mammary carcinogenesis

Lakshmanaswamy

Guzman

Yang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

109

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It is well established that pregnancy early in life reduces the risk of breast cancer in women and that this effect is universal. This phenomenon of parity protection against mammary cancer is also observed in rodents. Earlier studies have demonstrated that shortterm administration of estradiol (E) in combination with progesterone mimics the protective effect of parity in rats. In this study, the lowest effective E dosage for preventing mammary cancer was determined. Rats were injected with N-methyl-N-nitrosourea at 7 weeks of age; 2 weeks later, the rats were subjected to sustained treatment with 20 g, 100 g, 200 g, or 30 mg of E in silastic capsules for 3 weeks. Treatments with 100 g, 200 g, and 30 mg of E resulted in serum levels of E equivalent to those of pregnancy and were highly effective in preventing mammary cancer. E treatment (20 g) did not result in pregnancy levels of E and was not effective in reducing the mammary cancer incidence. In another set of experiments, we determined the effect of different durations of E with or without progesterone treatments on mammary carcinogenesis. These experiments indicate that a period as short as one-third the period of gestation is sufficient to induce protection against mammary carcinogenesis. The pioneering aspect of our study in contrast to long-term estrogen exposure, which is thought to increase the risk of breast cancer, is that short-term sustained treatments with pregnancy levels of E can induce protection against frank mammary cancer. B reast cancer is the most common cancer among women worldwide. The incidence of breast cancer in the United States for the year 2000 was estimated to be Ϸ184,200 new cases (1). The epidemiological evidence provides strong support for the concept that environmental, hormonal, and genetic factors affect the risk for development of breast cancer (2-6). Among the various recognized reproductive risk factors are age at menarche, age at first pregnancy, and age at menopause, all of which seem to suggest that endogenous ovarian steroids may profoundly affect the process of carcinogenesis (3,6,7).Various studies reveal that nulliparous women have a higher risk of breast cancer compared with women who have undergone single or multiple pregnancies early in life (8-10). The protective effect of pregnancy is universal, and pregnancy is the only normal physiological condition that consistently prevents breast cancers in all ethnic backgrounds in all countries without known adverse effects (8-10). The phenomenon of parity protection against mammary carcinogenesis is also observed in rats and mice. Moon (11) demonstrated that parous rats exposed to chemical carcinogens developed fewer cancers compared with virgin rats. Earlier Marchant (12) and very recently Medina and Smith (13) have demonstrated that pregnancy provides protection against mammary carcinogenesis in mouse models. Shortterm administration with ovarian steroids [estrogens and progesterone (P)] or human chorionic gonadotropins either before or after carcinogen treatment dec...

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mentioning

confidence: 99%

Short-term exposure to pregnancy levels of estrogen prevents mammary carcinogenesis

Lakshmanaswamy

Guzman

Yang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

109

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“…One possible explanation that might account for the tumor-inhibitory effect by the splenocytes from parous rats is that these cells were already primed to the tumor-related antigen(s) during pregnancy, as fetoplacental tissue produces some antigens in common with the tumor itself. Such common antigens have been reported to be produced by both fetus and/or placenta and also by breast tumor [1,10,14,15,20]. It is not unlikely that such common oncofetal antigens may prove immunogenic to the host.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of mammary tumorigenesis in virgin rats by adoptive transfer of splenocytes from parous donors

Chakravarty¹,

Sinha²

1991

Cancer Immunol Immunother

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Splenocytes from parous rats have been previously found to have cytotoxic activity against mammary tumor cells in vitro. Experiments were carried out to determine if this pregnancy-induced cytotoxic nature of the splenocytes is inherent and transferable. Splenocytes from parous rats wer adoptively transferred to a group of virgin rats. Another group of age-matched, virgin rats received splenocytes from virgin donors in a similar way. After a period of rest, at the age of 55 days, the rats belonging to both of the groups, received 7,12-dimethylbenz(a)anthracene (DMBA) intragastrically. A third group of untreated virgin rats were also given the chemical carcinogen the same way as above and were considered as intact controls. The rats were monitored for development and growth of mammary tumor from 60 days of DMBA administration. After 4 months of DMBA administration the rats were sacrificed and mammary glands were examined for tumors. Mammary glands with no visible tumors were taken for whole mount preparation, to be examined for microscopic lesions. The results showed that 33 of 41 intact control rats, developed tumor and 27 of the 34 rats that received spleen cells from virgin rats developed tumors. Of the rats that received spleen cells from parous rats, only 18 out of 37 rats developed tumors, indicating an inhibition of tumor induction in these rats. Growth rate of the tumors in this group was also slower than in the control groups.

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“…Entirely negative results have been reported in large series of cases of ovarian (Monteiro et al, 1983) and breast cancer (Monteiro et al, 1982). High levels have been found, together with hCG, in a case of ovarian dysgerminoma (Kofler and Spona, 1971).…”

Section: (D) Other Factors Which May Affect Hpl Levelsmentioning

confidence: 93%

Hormones of the Placenta: hCG and hPL

Butt¹,

Chard²,

Iles³

1994

Marshall’s Physiology of Reproduction

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Serum levels of human placental lactogen and pregnancy-specific β1-glycoprotein in breast cancer

Cited by 10 publications

References 13 publications

Short-term exposure to pregnancy levels of estrogen prevents mammary carcinogenesis

Short-term exposure to pregnancy levels of estrogen prevents mammary carcinogenesis

Inhibition of mammary tumorigenesis in virgin rats by adoptive transfer of splenocytes from parous donors

Hormones of the Placenta: hCG and hPL

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