Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model

Medroxyprogesterone acetate (MPA)-induced mammary carcinomas express high levels of estrogen (ER) and progesterone receptors (PR) and when transplanted in syngeneic mice they show a progestin-dependent (PD) growth pattern. By successive transplantation, progestin-independent (PI) variants were gener...

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Autores principales:	Fabris, V.T., Benavides, F., Conti, C., Merani, S., Lanari, C.
Formato:	JOUR
Materias:	estrogen receptor gestagen medroxyprogesterone acetate progesterone receptor aneuploidy animal cell animal model animal tissue article breast cancer cancer growth cancer transplantation chromosomal instability chromosome 16 chromosome 3 chromosome 4 chromosome 6 chromosome 7 chromosome mutation chromosome number chromosome translocation controlled study cytogenetics diploidy female gene mutation hormone response mouse mouse strain nonhuman point mutation priority journal single strand conformation polymorphism tetraploidy triploidy tumor X chromosome Aneuploidy Animals Chromosome Banding Female Genes, p53 In Situ Hybridization, Fluorescence Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Neoplasms, Hormone-Dependent Point Mutation Tryptophan Murinae
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_01654608_v161_n2_p130_Fabris
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	todo:paper_01654608_v161_n2_p130_Fabris
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spelling	todo:paper_01654608_v161_n2_p130_Fabris2023-10-03T15:02:55Z Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model Fabris, V.T. Benavides, F. Conti, C. Merani, S. Lanari, C. estrogen receptor gestagen medroxyprogesterone acetate progesterone receptor aneuploidy animal cell animal model animal tissue article breast cancer cancer growth cancer transplantation chromosomal instability chromosome 16 chromosome 3 chromosome 4 chromosome 6 chromosome 7 chromosome mutation chromosome number chromosome translocation controlled study cytogenetics diploidy female gene mutation hormone response mouse mouse strain nonhuman point mutation priority journal single strand conformation polymorphism tetraploidy triploidy tumor X chromosome Aneuploidy Animals Chromosome Banding Female Genes, p53 In Situ Hybridization, Fluorescence Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Neoplasms, Hormone-Dependent Point Mutation Tryptophan Murinae Medroxyprogesterone acetate (MPA)-induced mammary carcinomas express high levels of estrogen (ER) and progesterone receptors (PR) and when transplanted in syngeneic mice they show a progestin-dependent (PD) growth pattern. By successive transplantation, progestin-independent (PI) variants were generated and showed a different response to antihormone therapy. A diploid chromosome number (2n = 40) was found in three of five PD tumors, with numbers in the triploid to tetraploid range in the other two. Some PI tumors were diploid, but most were aneuploid (8 of 12 tumors). The most frequent alterations found in PD and PI tumors were gains of chromosomes 3, 4, and 6 and losses of chromosomes 16 and X. Chromosomes 4 and 7 were involved in translocations in three of the four tumor families studied. single-strand conformation polymorphism analysis revealed a point mutation on the Trp53 gene in one of the PD tumors; this showed a stable diploid karyotype, suggesting that mutated Trp53 is not uniquely involved in chromosome instability. We have shown that hormone independence may be acquired without changes in ploidy, suggesting that the increase in ploidy is favored by successive transplantation. In our model, diploid tumors responded to hormone treatment but aneuploid tumors were either responsive or not. © 2005 Elsevier Inc. All rights reserved. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_01654608_v161_n2_p130_Fabris
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	estrogen receptor gestagen medroxyprogesterone acetate progesterone receptor aneuploidy animal cell animal model animal tissue article breast cancer cancer growth cancer transplantation chromosomal instability chromosome 16 chromosome 3 chromosome 4 chromosome 6 chromosome 7 chromosome mutation chromosome number chromosome translocation controlled study cytogenetics diploidy female gene mutation hormone response mouse mouse strain nonhuman point mutation priority journal single strand conformation polymorphism tetraploidy triploidy tumor X chromosome Aneuploidy Animals Chromosome Banding Female Genes, p53 In Situ Hybridization, Fluorescence Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Neoplasms, Hormone-Dependent Point Mutation Tryptophan Murinae
spellingShingle	estrogen receptor gestagen medroxyprogesterone acetate progesterone receptor aneuploidy animal cell animal model animal tissue article breast cancer cancer growth cancer transplantation chromosomal instability chromosome 16 chromosome 3 chromosome 4 chromosome 6 chromosome 7 chromosome mutation chromosome number chromosome translocation controlled study cytogenetics diploidy female gene mutation hormone response mouse mouse strain nonhuman point mutation priority journal single strand conformation polymorphism tetraploidy triploidy tumor X chromosome Aneuploidy Animals Chromosome Banding Female Genes, p53 In Situ Hybridization, Fluorescence Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Neoplasms, Hormone-Dependent Point Mutation Tryptophan Murinae Fabris, V.T. Benavides, F. Conti, C. Merani, S. Lanari, C. Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
topic_facet	estrogen receptor gestagen medroxyprogesterone acetate progesterone receptor aneuploidy animal cell animal model animal tissue article breast cancer cancer growth cancer transplantation chromosomal instability chromosome 16 chromosome 3 chromosome 4 chromosome 6 chromosome 7 chromosome mutation chromosome number chromosome translocation controlled study cytogenetics diploidy female gene mutation hormone response mouse mouse strain nonhuman point mutation priority journal single strand conformation polymorphism tetraploidy triploidy tumor X chromosome Aneuploidy Animals Chromosome Banding Female Genes, p53 In Situ Hybridization, Fluorescence Mammary Neoplasms, Experimental Medroxyprogesterone 17-Acetate Mice Mice, Inbred BALB C Neoplasms, Hormone-Dependent Point Mutation Tryptophan Murinae
description	Medroxyprogesterone acetate (MPA)-induced mammary carcinomas express high levels of estrogen (ER) and progesterone receptors (PR) and when transplanted in syngeneic mice they show a progestin-dependent (PD) growth pattern. By successive transplantation, progestin-independent (PI) variants were generated and showed a different response to antihormone therapy. A diploid chromosome number (2n = 40) was found in three of five PD tumors, with numbers in the triploid to tetraploid range in the other two. Some PI tumors were diploid, but most were aneuploid (8 of 12 tumors). The most frequent alterations found in PD and PI tumors were gains of chromosomes 3, 4, and 6 and losses of chromosomes 16 and X. Chromosomes 4 and 7 were involved in translocations in three of the four tumor families studied. single-strand conformation polymorphism analysis revealed a point mutation on the Trp53 gene in one of the PD tumors; this showed a stable diploid karyotype, suggesting that mutated Trp53 is not uniquely involved in chromosome instability. We have shown that hormone independence may be acquired without changes in ploidy, suggesting that the increase in ploidy is favored by successive transplantation. In our model, diploid tumors responded to hormone treatment but aneuploid tumors were either responsive or not. © 2005 Elsevier Inc. All rights reserved.
format	JOUR
author	Fabris, V.T. Benavides, F. Conti, C. Merani, S. Lanari, C.
author_facet	Fabris, V.T. Benavides, F. Conti, C. Merani, S. Lanari, C.
author_sort	Fabris, V.T.
title	Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
title_short	Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
title_full	Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
title_fullStr	Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
title_full_unstemmed	Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
title_sort	cytogenetic findings, trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model
url	http://hdl.handle.net/20.500.12110/paper_01654608_v161_n2_p130_Fabris
work_keys_str_mv	AT fabrisvt cytogeneticfindingstrp53mutationsandhormoneresponsivenessinamedroxyprogesteroneacetateinducedmurinebreastcancermodel AT benavidesf cytogeneticfindingstrp53mutationsandhormoneresponsivenessinamedroxyprogesteroneacetateinducedmurinebreastcancermodel AT contic cytogeneticfindingstrp53mutationsandhormoneresponsivenessinamedroxyprogesteroneacetateinducedmurinebreastcancermodel AT meranis cytogeneticfindingstrp53mutationsandhormoneresponsivenessinamedroxyprogesteroneacetateinducedmurinebreastcancermodel AT lanaric cytogeneticfindingstrp53mutationsandhormoneresponsivenessinamedroxyprogesteroneacetateinducedmurinebreastcancermodel
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Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model

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