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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2005
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01654608_v161_n2_p130_Fabris http://hdl.handle.net/20.500.12110/paper_01654608_v161_n2_p130_Fabris |
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paper:paper_01654608_v161_n2_p130_Fabris2023-06-08T15:14:53Z Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model 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. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01654608_v161_n2_p130_Fabris 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 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. |
| 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 |
| publishDate |
2005 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01654608_v161_n2_p130_Fabris http://hdl.handle.net/20.500.12110/paper_01654608_v161_n2_p130_Fabris |
| _version_ |
1768545045225406464 |