Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas

To explore mechanisms related to hormone resistance, three resistant variants of the MPA mouse breast cancer tumor model with low levels of progesterone receptor (PR) isoform A (PR-A)/high PR-B expression were developed by prolonged selective pressure with antiprogestins. The resistant phenotype of...

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Detalles Bibliográficos
Publicado: 2009
Materias:
AKT
ERK
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v116_n3_p449_Wargon
http://hdl.handle.net/20.500.12110/paper_01676806_v116_n3_p449_Wargon
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spelling paper:paper_01676806_v116_n3_p449_Wargon2023-06-08T15:16:41Z Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas Acquired hormone resistance AKT Antiprogestins Breast cancer De novo hormone resistance ERK Estrogen receptors Hormone resistance Metastasis Progesterone receptor isoforms Tumor regression estradiol estrogen receptor alpha lonaprisan mifepristone mitogen activated protein kinase 1 mitogen activated protein kinase 3 progesterone receptor A progesterone receptor B protein kinase B tamoxifen hormone antagonist isoprotein mifepristone mitogen activated protein kinase 1 mitogen activated protein kinase 3 progesterone receptor progesterone receptor A progesterone receptor B protein kinase B animal experiment animal model animal tissue article axillary lymph node breast cancer breast carcinoma cancer inhibition cancer resistance controlled study female lymph node metastasis metastasis potential mouse nonhuman priority journal tumor growth animal Bagg albino mouse cell proliferation drug resistance experimental neoplasm fluorescent antibody technique metabolism pathology survival rate Western blotting Animals Blotting, Western Cell Proliferation Drug Resistance, Neoplasm Female Fluorescent Antibody Technique Hormone Antagonists Lymphatic Metastasis Mammary Neoplasms, Experimental Mice Mice, Inbred BALB C Mifepristone Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Protein Isoforms Proto-Oncogene Proteins c-akt Receptors, Progesterone Survival Rate To explore mechanisms related to hormone resistance, three resistant variants of the MPA mouse breast cancer tumor model with low levels of progesterone receptor (PR) isoform A (PR-A)/high PR-B expression were developed by prolonged selective pressure with antiprogestins. The resistant phenotype of one tumor line was reversed spontaneously after several consecutive passages in syngeneic BALB/c mice or by 17-b-estradiol or tamoxifen treatment, and this reversion was significantly associated with an increase in PR-A expression. The responsive parental tumors disclosed low activation of ERK and high activation of AKT; resistant tumors on the other hand, showed the opposite, and this was associated with a higher metastatic potential, that did not revert. This study shows for the first time in vivo a relationship between PR isoform expression and antiprogestin responsiveness, demonstrating that, whereas acquired resistance may be reversed, changes in kinase activation and metastatic potential are unidirectional associated with tumor progression. © Springer Science+Business Media, LLC. 2008. 2009 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v116_n3_p449_Wargon http://hdl.handle.net/20.500.12110/paper_01676806_v116_n3_p449_Wargon
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Acquired hormone resistance
AKT
Antiprogestins
Breast cancer
De novo hormone resistance
ERK
Estrogen receptors
Hormone resistance
Metastasis
Progesterone receptor isoforms
Tumor regression
estradiol
estrogen receptor alpha
lonaprisan
mifepristone
mitogen activated protein kinase 1
mitogen activated protein kinase 3
progesterone receptor A
progesterone receptor B
protein kinase B
tamoxifen
hormone antagonist
isoprotein
mifepristone
mitogen activated protein kinase 1
mitogen activated protein kinase 3
progesterone receptor
progesterone receptor A
progesterone receptor B
protein kinase B
animal experiment
animal model
animal tissue
article
axillary lymph node
breast cancer
breast carcinoma
cancer inhibition
cancer resistance
controlled study
female
lymph node metastasis
metastasis potential
mouse
nonhuman
priority journal
tumor growth
animal
Bagg albino mouse
cell proliferation
drug resistance
experimental neoplasm
fluorescent antibody technique
metabolism
pathology
survival rate
Western blotting
Animals
Blotting, Western
Cell Proliferation
Drug Resistance, Neoplasm
Female
Fluorescent Antibody Technique
Hormone Antagonists
Lymphatic Metastasis
Mammary Neoplasms, Experimental
Mice
Mice, Inbred BALB C
Mifepristone
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Protein Isoforms
Proto-Oncogene Proteins c-akt
Receptors, Progesterone
Survival Rate
spellingShingle Acquired hormone resistance
AKT
Antiprogestins
Breast cancer
De novo hormone resistance
ERK
Estrogen receptors
Hormone resistance
Metastasis
Progesterone receptor isoforms
Tumor regression
estradiol
estrogen receptor alpha
lonaprisan
mifepristone
mitogen activated protein kinase 1
mitogen activated protein kinase 3
progesterone receptor A
progesterone receptor B
protein kinase B
tamoxifen
hormone antagonist
isoprotein
mifepristone
mitogen activated protein kinase 1
mitogen activated protein kinase 3
progesterone receptor
progesterone receptor A
progesterone receptor B
protein kinase B
animal experiment
animal model
animal tissue
article
axillary lymph node
breast cancer
breast carcinoma
cancer inhibition
cancer resistance
controlled study
female
lymph node metastasis
metastasis potential
mouse
nonhuman
priority journal
tumor growth
animal
Bagg albino mouse
cell proliferation
drug resistance
experimental neoplasm
fluorescent antibody technique
metabolism
pathology
survival rate
Western blotting
Animals
Blotting, Western
Cell Proliferation
Drug Resistance, Neoplasm
Female
Fluorescent Antibody Technique
Hormone Antagonists
Lymphatic Metastasis
Mammary Neoplasms, Experimental
Mice
Mice, Inbred BALB C
Mifepristone
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Protein Isoforms
Proto-Oncogene Proteins c-akt
Receptors, Progesterone
Survival Rate
Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
topic_facet Acquired hormone resistance
AKT
Antiprogestins
Breast cancer
De novo hormone resistance
ERK
Estrogen receptors
Hormone resistance
Metastasis
Progesterone receptor isoforms
Tumor regression
estradiol
estrogen receptor alpha
lonaprisan
mifepristone
mitogen activated protein kinase 1
mitogen activated protein kinase 3
progesterone receptor A
progesterone receptor B
protein kinase B
tamoxifen
hormone antagonist
isoprotein
mifepristone
mitogen activated protein kinase 1
mitogen activated protein kinase 3
progesterone receptor
progesterone receptor A
progesterone receptor B
protein kinase B
animal experiment
animal model
animal tissue
article
axillary lymph node
breast cancer
breast carcinoma
cancer inhibition
cancer resistance
controlled study
female
lymph node metastasis
metastasis potential
mouse
nonhuman
priority journal
tumor growth
animal
Bagg albino mouse
cell proliferation
drug resistance
experimental neoplasm
fluorescent antibody technique
metabolism
pathology
survival rate
Western blotting
Animals
Blotting, Western
Cell Proliferation
Drug Resistance, Neoplasm
Female
Fluorescent Antibody Technique
Hormone Antagonists
Lymphatic Metastasis
Mammary Neoplasms, Experimental
Mice
Mice, Inbred BALB C
Mifepristone
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Protein Isoforms
Proto-Oncogene Proteins c-akt
Receptors, Progesterone
Survival Rate
description To explore mechanisms related to hormone resistance, three resistant variants of the MPA mouse breast cancer tumor model with low levels of progesterone receptor (PR) isoform A (PR-A)/high PR-B expression were developed by prolonged selective pressure with antiprogestins. The resistant phenotype of one tumor line was reversed spontaneously after several consecutive passages in syngeneic BALB/c mice or by 17-b-estradiol or tamoxifen treatment, and this reversion was significantly associated with an increase in PR-A expression. The responsive parental tumors disclosed low activation of ERK and high activation of AKT; resistant tumors on the other hand, showed the opposite, and this was associated with a higher metastatic potential, that did not revert. This study shows for the first time in vivo a relationship between PR isoform expression and antiprogestin responsiveness, demonstrating that, whereas acquired resistance may be reversed, changes in kinase activation and metastatic potential are unidirectional associated with tumor progression. © Springer Science+Business Media, LLC. 2008.
title Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
title_short Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
title_full Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
title_fullStr Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
title_full_unstemmed Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
title_sort reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
publishDate 2009
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v116_n3_p449_Wargon
http://hdl.handle.net/20.500.12110/paper_01676806_v116_n3_p449_Wargon
_version_ 1768546249138503680