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Chemical Compound Review

Honvan     [4-[(E)-4-(4- phosphonooxyphenyl)hex-3-en- 3...

Synonyms: fosfestrol, Desdp, Fosfestrolum, Phosphestrol, ST52-Asta, ...
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Disease relevance of diethylstilbestrol

  • Response differences between the strain and stock included the following: DES produced both pituitary tumors and mammary adenocarcinomas (MAC) in ACI rats only [1].
  • The altered mitogen response should be a stimulus for a detailed analysis of the immune system in women exposed to DES during fetal life, some of whom develop later in life clear cell adenocarcinoma of the uterine cervix and vagina [2].
  • The incidence of spontaneous and DES-induced cataracts in ER Delta 3 mice is 100%, yet these cataracts are absent from the wild-type mice [3].
  • Animals given a combination of DES and EE showed tubular hyperplasia but not interstitial lesions; this finding was of particular interest because hamsters given this combination of estrogens do not develop gross renal tumors [4].
  • Our data suggest that gene expression profiles of LNCaP human prostate cancer cells in response to PC-SPES are different from those found when diethylstilbestrol (DES), a synthetic estrogen, is used, suggesting that the estrogenic moieties within PC-SPES do not drive this expression signature [5].

Psychiatry related information on diethylstilbestrol

  • The presence of elevated hippocampal ER levels during the perinatal critical period and evidence of functional transformation to the DNA binding state following DES treatment in vivo or estrogen incubation in vitro suggests that the hippocampus is a potential substrate for estrogen-mediated organizational events [6].

High impact information on diethylstilbestrol

  • DES at 10(-7) M in the culture medium increased the number of sister chromatid exchanges (SCE); no further increases was obtained with higher concentrations of DES [7].
  • Female mice from three inbred strains (BALB/cCrgl, C3H/Crgl, and C57BL/Crgl) and one noninbred stock [RU:NCS (RU)] were treated perinatally with estradiol benzoate (EB), diethylstilbestrol (DES), or sesame oil and were killed on postnatal days 30--36 [8].
  • Neonatal DES treatment not only resulted in persistent changes in the cervicovaginal epithelium and in the hypothalamic-pituitary gland control system but also in the spleen lymphocyte mitogen response [2].
  • After 17 days of DES treatment, the increase in prolactin synthesis in the hyperplastic pituitaries was not as marked as that in the tumors [9].
  • However, while DES-induced pituitary growth exhibited quantitative, additive inheritance, the hemorrhagic phenotype exhibited recessive, epistatic inheritance [10].

Chemical compound and disease context of diethylstilbestrol


Biological context of diethylstilbestrol


Anatomical context of diethylstilbestrol

  • The testis weights of BALB/c mice remained normal during DES treatment, whereas those of the C3H decreased with time [19].
  • No significant differences were observed between the results obtained by the radioligand and enzyme immunoassay methods in the cytosol and nuclear fractions from the control and DES-treated tumors [20].
  • In contrast, the prostates of alphaERKO mice exhibited no response to neonatal DES either immediately after exposure or throughout life up to 18 months of age [21].
  • Uterus and liver served as positive and negative control tissues, respectively, for the effects of DES on IGF-I mRNA levels in OVX rats; mRNA levels were increased in uterus and decreased in liver after hormone treatment [22].
  • The oviducts from the DES-withdrawn chicks and from aged nonlaying hens showed marked atrophy [23].

Associations of diethylstilbestrol with other chemical compounds

  • Sprague-Dawley rats, resistant to estrogen-induced Leydig cell tumors, like C3H mice, also underwent testicular atrophy and lost LH receptors during DES treatment [19].
  • In a separate experiment, administration of progesterone with DES decreased the concentration of nuclear ER to less than one-half that observed after administration of DES alone, with proportional decreases in both cytosolic and nuclear PgR [20].
  • Sixteen previously untreated patients received DES (1 mg daily for 3 days) followed by FAC [5-fluorouracil (600 mg/m2): Adriamycin (50 mg/m2): Cytoxan (600 mg/m2)] i.v. on day 4 every 21 days [24].
  • In the nine patients submitted to surgery after three DES plus FAC courses, the average thymidine labeling index and primer-dependent alpha-DNA polymerase labeling index were 27.8 and 73% of the pretreatment values [24].
  • In spite of different structures and equilibrium parameters, E2, DES, and arachidonate are able to compete with each other for binding to the fetoprotein [25].

Gene context of diethylstilbestrol


Analytical, diagnostic and therapeutic context of diethylstilbestrol

  • Proliferative activity on tumor biopsies was evaluated immediately before and after treatment with DES, 24 h after chemotherapy and, in nine patients, at the time of radical surgery [24].
  • Use of an immunohistochemical method for the detection of ER in frozen sections indicated that the receptor was localized in the glandular epithelium in both control and DES-treated tumors [20].
  • Prepubertal ovariectomy of the prenatally DES-treated animals could only partially reverse the effects observed in the skeleton of the DES-treated animals [18].
  • The epithelial mitotic index was also 2-fold higher than control values 16-18 h after DES treatment [30].
  • Four types of coculture were set up as follows: 1) Control testis with control MD; 2) DES-treated testis with DES-treated MD; 3) Control testis with DES-treated MD; 4) DES-treated testis with control MD [31].


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  2. Long-term effects of neonatal estrogen treatment on mitogen responsiveness of mouse spleen lymphocytes. Kalland, T., Strand, O., Forsberg, J.G. J. Natl. Cancer Inst. (1979) [Pubmed]
  3. An estrogen receptor repressor induces cataract formation in transgenic mice. Davis, V.L., Chan, C.C., Schoen, T.J., Couse, J.F., Chader, G.J., Korach, K.S. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
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  6. Transient elevation of estrogen receptors in the neonatal rat hippocampus. O'Keefe, J.A., Handa, R.J. Brain Res. Dev. Brain Res. (1990) [Pubmed]
  7. Estrogen effects on sister chromatid exchanges in mouse uterine cervical and kidney cells. Hillbertz-Nilsson, K., Forsberg, J.G. J. Natl. Cancer Inst. (1985) [Pubmed]
  8. Adenosis-like lesions and other cervicovaginal abnormalities in mice treated perinatally with estrogen. Plapinger, L., Bern, H.A. J. Natl. Cancer Inst. (1979) [Pubmed]
  9. Protein and RNA synthesis in pituitary tumors from F344 rats given implants of estrogen. Kaplan, S.E., De Nicola, A.F. J. Natl. Cancer Inst. (1976) [Pubmed]
  10. Genetic separation of tumor growth and hemorrhagic phenotypes in an estrogen-induced tumor. Wendell, D.L., Herman, A., Gorski, J. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
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  13. Transplacental estrogen responses in the fetal rat: increased uterine weight and ornithine decarboxylase activity. Harmon, J.R., Branham, W.S., Sheehan, D.M. Teratology (1989) [Pubmed]
  14. Effects of postnatal DES treatment on uterine growth, development, and estrogen receptor levels. Medlock, K.L., Sheehan, D.M., Nelson, C.J., Branham, W.S. J. Steroid Biochem. (1988) [Pubmed]
  15. Biochemical and molecular changes at the cellular level in response to exposure to environmental estrogen-like chemicals. Roy, D., Palangat, M., Chen, C.W., Thomas, R.D., Colerangle, J., Atkinson, A., Yan, Z.J. Journal of toxicology and environmental health. (1997) [Pubmed]
  16. Evidence that epithelial and mesenchymal estrogen receptor-alpha mediates effects of estrogen on prostatic epithelium. Risbridger, G., Wang, H., Young, P., Kurita, T., Wang, Y.Z., Lubahn, D., Gustafsson, J.A., Cunha, G., Wong, Y.Z. Dev. Biol. (2001) [Pubmed]
  17. Type-II estrogen binding sites in a lymphoblastoid cell line and growth-inhibitory effect of estrogen, anti-estrogen and bioflavonoids. Scambia, G., Ranelletti, F.O., Benedetti Panici, P., Piantelli, M., Rumi, C., Battaglia, F., Larocca, L.M., Capelli, A., Mancuso, S. Int. J. Cancer (1990) [Pubmed]
  18. Alterations of maternal estrogen levels during gestation affect the skeleton of female offspring. Migliaccio, S., Newbold, R.R., Bullock, B.C., Jefferson, W.J., Sutton, F.G., McLachlan, J.A., Korach, K.S. Endocrinology (1996) [Pubmed]
  19. Increase in testis luteinizing hormone receptor by estrogen in mice susceptible to Leydig cell tumors. Navickis, R.J., Shimkin, M.B., Hsueh, A.J. Cancer Res. (1981) [Pubmed]
  20. Regulation of estrogen and progestin receptor concentrations in an experimental rat prostatic carcinoma by estrogen, antiestrogen, and progesterone. Mobbs, B.G., Johnson, I.E., DeSombre, E.R., Toth, J., Hughes, A. Cancer Res. (1987) [Pubmed]
  21. Estrogen imprinting of the developing prostate gland is mediated through stromal estrogen receptor alpha: studies with alphaERKO and betaERKO mice. Prins, G.S., Birch, L., Couse, J.F., Choi, I., Katzenellenbogen, B., Korach, K.S. Cancer Res. (2001) [Pubmed]
  22. Mechanism of action of estrogen on intramembranous bone formation: regulation of osteoblast differentiation and activity. Turner, R.T., Backup, P., Sherman, P.J., Hill, E., Evans, G.L., Spelsberg, T.C. Endocrinology (1992) [Pubmed]
  23. Nonfunctioning progesterone receptors in the developed oviducts from estrogen-withdrawn immature chicks and in aged nonlaying hens. Boyd-Leinen, P.A., Fournier, D., Spelsberg, T.C. Endocrinology (1982) [Pubmed]
  24. Chemotherapy following estrogen-induced expansion of the growth fraction of human breast cancer. Conte, P.F., Fraschini, G., Alama, A., Nicolin, A., Corsaro, E., Canavese, G., Rosso, R., Drewinko, B. Cancer Res. (1985) [Pubmed]
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