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Original Research

Open Access

Assessment of ER-α and ER-β expression levels in malicious tumors of the uterine corpus


  • A. Popiela1,*,
  • W. Baranowski2
  • G. Popiela3
  • M. Slomczynska4
  • M. Manowiec1
  • M. Gabrys1

12nd Department of Gynaecology and Obstetrics, Department of Gynaecology, Wroclaw Medical University, Wroclaw, Poland

2Department of Gynaeculogy, Military, Medical Institute, Warsaw, Poland

3Department of Ophthalmology, Wroclaw Medical University, Wroclaw, Poland

4Laboratory of Endocrinology and Tissue Culture, Department of Animal Physiology, Jagiellonian University, Krakow, Poland

DOI: 10.12892/ejgo200502170 Vol.26,Issue 2,March 2005 pp.170-174

Published: 10 March 2005

*Corresponding Author(s): A. Popiela E-mail:

Abstract

Purpose: The purpose of this article is to present an assessment of the expression levels of estrogen receptors ER-alpha and ER-beta in malicious tumors of the uterine corpus.

Material and methods: Estrogen receptor expression levels were tested using semiquantitative immunohistochemical methods. Paraffin-embedded sections of tissue from the corpus of the uterus from 171 patients were used in the research.

Results: Analysis of the relation between ER-beta expression levels and the clinical grade of disease (based on FIGO classification) showed that these parameters are significantly related: p = 0.0099. There were no statistically significant relations between ER-alpha expression levels in tumors or clinical stages of tumors based on the FIGO criteria. The presence of high estrogen receptor beta expression levels is often accompanied by a low estrogen receptor alpha expression level and such arrangements allow the overt biological function of a dominant receptor.

Conclusion: The differences in tissue distribution of both estrogen receptors could indicate their different biological roles.

Cite and Share

A. Popiela,W. Baranowski,G. Popiela,M. Slomczynska,M. Manowiec,M. Gabrys. Assessment of ER-α and ER-β expression levels in malicious tumors of the uterine corpus. European Journal of Gynaecological Oncology. 2005. 26(2);170-174.

References

[1] Baranowski W.: "Zagrozenia nowotworowe narzadu plciowego w okresie menopauzalnym". In: Jakowicki J.A., Klimakterium "Hormonalna terapia zastepcza". Poradnik terapeutyczny BiFolium, 2001, 103.

[2] Dockerty M.B., Lovelady S.B., Foust G.T. Jr.: “Carcinoma of corpus uteri in young women". Am. J. Obstet. Gynecol., 1951, 61, 147.

[3] Woodruff J.D., Pickar J.H.: "Incidence of endometrial hyperplasia in postmenopausal women taking conjugated estrogens (Premarin) with medroxyprogesterone acetate or conjugated estrogens alone" Am. J. Obstet. Gynecol., 1994, 170, 1213.

[4] Roy D., Liher J.G.: "Estrogen DNA damage and mutations". Mutations Research - Fundamental and Molecular Mechanisms of Mutagenesis, 1999, 424, 107.

[5] Service R.F.: "New role for estrogen in cancer". Science, 1998, 279, 1631.

[6] Cavalieri E.L: "Molecular origin of cancer: Catechol estrogen -3,4 quinones as endogenous tumor initiators". Proc. Natl. Acad. Sci. USA, 1997, 94, 10937.

[7] Zhu B.T, Conney A.H.: "Functional role of estrogen metabolism in target cells review and perspectives". Carcinogenesis, 1998, 19, 1.

[8] Monks T.J., Hanzlik R.P., Cohen G.M.: "Quinone chemistry and toxicity". Toxicol. Appl. Pharmacol., 1992, 112, 2.

[9] Beato M., Klug J.: "Steroid hormone receptors: an update". Hum Reprod., 2000, 6, 225.

[10] Spencer T.E., Jenster G., Burcin M.M.: "Steroid receptor coacllvator-1 is a histone acetyltransferase". Nature, 1997, 389, 194.

[11] Webb P., Lopez G.N., Uht R.M., Kushner P.J.: "Tamoxifen activation of the estrogen receptor/ AP-I pathway: potential origin for the cell specific estrogen like effects of antiestrogens". Mal Endocrinol., 1995, 9, 443.

[12] Peach B., Webb P., Kuiper G.: "Differential ligand activation of estrogen receptors ERa and ERP at APl sites". Science, 1997, 277, 1508.

[13] Kuiper G.G., Carlsson B., Grandien K: "Comparison of the ligand binding specificity and transcript tissue distribution of estrogen receptors a and P"- Endocrinology, 1997, 138, 863.

[14] lwao K., Miyoshi Y., Egawa Ch.: "Quantitative analysis of estrogen receptor- a and p messenger RNA expression in breast carcinoma by real-time polymerase chain reaction". Am. Cancer Soc., 2000, 8, 1732.

[15] Johnston S.D., Liu X., Zuo F: "Estrogen - related receptor a 1 functionally binds as a monomer to extended half-site sequences including ones contained within estrogen-response elements" Mot. Endocrinol., 1997, 11, 342.

[16] Pffefer U., Fecarotta E., Castagnetta L.: "Alternative splicing of the estrogen receptor primary transcript normally occurs in estrogen receptor positive tissues and ce11 lines". J. Steroid Biochem., 1996, 56, 99.

[17] Rey J.M., Pu」ol P., Dechaud H.: "Expression of estrogen receptor-alfa splicing variants and estrogen receptor beta in endometrium of infertile patients". Mot. Hum. Reprod., 1998, 7, 641.

[18] Popiela A., Baranowski W., Slomczynska M., Panszczyk M., Gabrys M.: "Estimation of estrogen receptor alfa and beta izoform expression in endometrial cancer". Gynecol. Endocrinol., 2002, 16 (suppl. 1).

[19] Kern S.E.: "Progressive genetic abnormalities in human neoplasia". In: Mendelson J., Howley P.M., Israel M.A., Liotta LA "The molecular basis of cancer". W.B. Saunders Company, 2001, 41, 70.

[20] Popiela A.: "Stezenie 5-metylo-2'deoksycytydyny w genomyowym DNA a ekspresja wybranych receptorow steroidowych w stanach przedrakowych i rakach trzonu macicy". Praca hab山tacyjna w toku. Postgraduate research project (in press).

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