Reversal of estrogen-resistance in murine mammary adenocarcinomas
From mouse mammary progestin-dependent (PD) adenocarcinomas induced with medroxyprogesterone acetate (MPA) we developed several in vivo lines that are maintained by subcutaneous syngeneic passages in MPA-treated mice and express estrogen (ER) and progesterone receptors (PR). Although most lines rema...
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1999
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v54_n2_p93_Montecchia http://hdl.handle.net/20.500.12110/paper_01676806_v54_n2_p93_Montecchia |
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paper:paper_01676806_v54_n2_p93_Montecchia2023-06-08T15:16:43Z Reversal of estrogen-resistance in murine mammary adenocarcinomas Estrogens Hormone independence Hormone resistance Mammary adenocarcinomas Mice Reversibility estradiol estrogen estrogen receptor gestagen hormone receptor medroxyprogesterone acetate progesterone receptor silastic animal experiment animal model article breast adenocarcinoma drug resistance estrogen therapy estrus cycle hormone resistance ligand binding mouse nonhuman priority journal protein expression receptor density receptor down regulation tumor regression Adenocarcinoma Animals Antineoplastic Agents, Hormonal Cell Division Drug Implants Drug Resistance, Neoplasm Estradiol Female Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Progestins Receptors, Estrogen Receptors, Progesterone From mouse mammary progestin-dependent (PD) adenocarcinomas induced with medroxyprogesterone acetate (MPA) we developed several in vivo lines that are maintained by subcutaneous syngeneic passages in MPA-treated mice and express estrogen (ER) and progesterone receptors (PR). Although most lines remained PD, with time some progestin-independent (PI) variants arose. Both PD and PI tumors regress with estrogen treatment although estrogen-resistant variants may also arise. The object of this paper was to investigate the reversibility of estrogen-resistance and its possible relation with hormone receptor down-regulation. Tumor regression was induced in a progestin-independent tumor line (BET) by treatment with a 5 mg 17β-estradiol (E2) silastic pellet. One of the tumors started to grow disclosing an estrogen-resistant pattern of growth. This tumor line (BET-R) was transplanted into E2-treated and untreated animals (n = 4-6), selecting for the next passage tumors growing in treated animals. Seven new sublines were obtained at different passages by selecting for the next passage the tumors that had grown in untreated mice (BET-Ra-BET-Rg), until no tumors grew in E2-treated mice. ER and PR were measured by a ligand-binding, dextran-coated charcoal method using a single saturating point. From the seven sublines initiated, the first four proved to be reversible after 3-6 generation transplantation and the last three did not revert. A difference in PR expression between BET and BET-R (p < 0.05) was registered, but it did not correlate with the specific hormone behavior since two reverted lines had a pattern similar to that of BET and the other two were similar to BET-R. The expression of PR was higher in E2-treated mice (p < 0.05) and highly variable in the parental line. This led us to study the expression of PR at different stages of the estrous cycle. Higher levels of PR were observed in proestrous, estrous, and metestrous (p < 0.05) than in diestrous, and undetectable levels were found in ovariectomized mice. No differences in ER expression were detected during the estrous cycle. It can be concluded that under certain experimental conditions, estrogen-resistance is a reversible phenomenon. The experimental manipulation of hormone resistance may help develop strategies to modify the response to anti-hormones in humans. 1999 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v54_n2_p93_Montecchia http://hdl.handle.net/20.500.12110/paper_01676806_v54_n2_p93_Montecchia |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Estrogens Hormone independence Hormone resistance Mammary adenocarcinomas Mice Reversibility estradiol estrogen estrogen receptor gestagen hormone receptor medroxyprogesterone acetate progesterone receptor silastic animal experiment animal model article breast adenocarcinoma drug resistance estrogen therapy estrus cycle hormone resistance ligand binding mouse nonhuman priority journal protein expression receptor density receptor down regulation tumor regression Adenocarcinoma Animals Antineoplastic Agents, Hormonal Cell Division Drug Implants Drug Resistance, Neoplasm Estradiol Female Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Progestins Receptors, Estrogen Receptors, Progesterone |
| spellingShingle |
Estrogens Hormone independence Hormone resistance Mammary adenocarcinomas Mice Reversibility estradiol estrogen estrogen receptor gestagen hormone receptor medroxyprogesterone acetate progesterone receptor silastic animal experiment animal model article breast adenocarcinoma drug resistance estrogen therapy estrus cycle hormone resistance ligand binding mouse nonhuman priority journal protein expression receptor density receptor down regulation tumor regression Adenocarcinoma Animals Antineoplastic Agents, Hormonal Cell Division Drug Implants Drug Resistance, Neoplasm Estradiol Female Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Progestins Receptors, Estrogen Receptors, Progesterone Reversal of estrogen-resistance in murine mammary adenocarcinomas |
| topic_facet |
Estrogens Hormone independence Hormone resistance Mammary adenocarcinomas Mice Reversibility estradiol estrogen estrogen receptor gestagen hormone receptor medroxyprogesterone acetate progesterone receptor silastic animal experiment animal model article breast adenocarcinoma drug resistance estrogen therapy estrus cycle hormone resistance ligand binding mouse nonhuman priority journal protein expression receptor density receptor down regulation tumor regression Adenocarcinoma Animals Antineoplastic Agents, Hormonal Cell Division Drug Implants Drug Resistance, Neoplasm Estradiol Female Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Progestins Receptors, Estrogen Receptors, Progesterone |
| description |
From mouse mammary progestin-dependent (PD) adenocarcinomas induced with medroxyprogesterone acetate (MPA) we developed several in vivo lines that are maintained by subcutaneous syngeneic passages in MPA-treated mice and express estrogen (ER) and progesterone receptors (PR). Although most lines remained PD, with time some progestin-independent (PI) variants arose. Both PD and PI tumors regress with estrogen treatment although estrogen-resistant variants may also arise. The object of this paper was to investigate the reversibility of estrogen-resistance and its possible relation with hormone receptor down-regulation. Tumor regression was induced in a progestin-independent tumor line (BET) by treatment with a 5 mg 17β-estradiol (E2) silastic pellet. One of the tumors started to grow disclosing an estrogen-resistant pattern of growth. This tumor line (BET-R) was transplanted into E2-treated and untreated animals (n = 4-6), selecting for the next passage tumors growing in treated animals. Seven new sublines were obtained at different passages by selecting for the next passage the tumors that had grown in untreated mice (BET-Ra-BET-Rg), until no tumors grew in E2-treated mice. ER and PR were measured by a ligand-binding, dextran-coated charcoal method using a single saturating point. From the seven sublines initiated, the first four proved to be reversible after 3-6 generation transplantation and the last three did not revert. A difference in PR expression between BET and BET-R (p < 0.05) was registered, but it did not correlate with the specific hormone behavior since two reverted lines had a pattern similar to that of BET and the other two were similar to BET-R. The expression of PR was higher in E2-treated mice (p < 0.05) and highly variable in the parental line. This led us to study the expression of PR at different stages of the estrous cycle. Higher levels of PR were observed in proestrous, estrous, and metestrous (p < 0.05) than in diestrous, and undetectable levels were found in ovariectomized mice. No differences in ER expression were detected during the estrous cycle. It can be concluded that under certain experimental conditions, estrogen-resistance is a reversible phenomenon. The experimental manipulation of hormone resistance may help develop strategies to modify the response to anti-hormones in humans. |
| title |
Reversal of estrogen-resistance in murine mammary adenocarcinomas |
| title_short |
Reversal of estrogen-resistance in murine mammary adenocarcinomas |
| title_full |
Reversal of estrogen-resistance in murine mammary adenocarcinomas |
| title_fullStr |
Reversal of estrogen-resistance in murine mammary adenocarcinomas |
| title_full_unstemmed |
Reversal of estrogen-resistance in murine mammary adenocarcinomas |
| title_sort |
reversal of estrogen-resistance in murine mammary adenocarcinomas |
| publishDate |
1999 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v54_n2_p93_Montecchia http://hdl.handle.net/20.500.12110/paper_01676806_v54_n2_p93_Montecchia |
| _version_ |
1768543365366808576 |