Origin and progression of pregnancy-dependent mammary tumors induced by new mouse mammary tumor virus variants
In order to study mechanisms of progression of mouse mammary tumor virus (MMTV)-induced pregnancy-dependent mammary lesions, we removed and serially transplanted 17 small tumors detected in MMTV-infected pregnant females. This gave rise to the same number of 'in vivo' tumor lines. Hormone-...
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| Veröffentlicht in: | Breast cancer research and treatment 2002-10, Vol.75 (3), p.191-202 |
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| creator | Buggiano, Valeria Levy, Carolina Schere Gattelli, Albana Cirio, María Cecilia Marfil, Mariana Nepomnaschy, Irene Piazzon, Isabel Helguero, Luisa Vanzulli, Silvia Kordon, Edith C |
| description | In order to study mechanisms of progression of mouse mammary tumor virus (MMTV)-induced pregnancy-dependent mammary lesions, we removed and serially transplanted 17 small tumors detected in MMTV-infected pregnant females. This gave rise to the same number of 'in vivo' tumor lines. Hormone-dependency of the passages was determined by comparing tumor development in multiparous versus virgin hosts. We found that the first passages of most of these lesions (11/17) required pregnancy to grow. However, all these tumor lines lost their hormone-dependence through successive passages. The original pregnancy-dependent lesions were mostly multiclonal and showed high levels of estrogen and progesterone receptors. Alternatively, pregnancy-independent tumors arose as clonal dominant populations exhibiting a lower hormone receptor content. Our data show that the progression of hormone-dependent MMTV-induced mammary tumors is an irreversible process associated with the appearance of additional MMTV insertional events as well as alterations in the composition of the tumor cell population. |
| doi_str_mv | 10.1023/A:1019932516887 |
| format | Article |
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This gave rise to the same number of 'in vivo' tumor lines. Hormone-dependency of the passages was determined by comparing tumor development in multiparous versus virgin hosts. We found that the first passages of most of these lesions (11/17) required pregnancy to grow. However, all these tumor lines lost their hormone-dependence through successive passages. The original pregnancy-dependent lesions were mostly multiclonal and showed high levels of estrogen and progesterone receptors. Alternatively, pregnancy-independent tumors arose as clonal dominant populations exhibiting a lower hormone receptor content. Our data show that the progression of hormone-dependent MMTV-induced mammary tumors is an irreversible process associated with the appearance of additional MMTV insertional events as well as alterations in the composition of the tumor cell population.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1023/A:1019932516887</identifier><identifier>PMID: 12353808</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Animals ; Breast cancer ; Cancer research ; Cancer therapies ; Disease Progression ; DNA, Neoplasm - metabolism ; Estrogens - metabolism ; Female ; Mammary Neoplasms, Experimental - metabolism ; Mammary Neoplasms, Experimental - pathology ; Mammary Neoplasms, Experimental - virology ; Mammary Tumor Virus, Mouse - pathogenicity ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Neoplasms, Hormone-Dependent - metabolism ; Neoplasms, Hormone-Dependent - pathology ; Neoplasms, Hormone-Dependent - virology ; Pregnancy ; Pregnancy, Animal ; Progesterone - metabolism ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - metabolism</subject><ispartof>Breast cancer research and treatment, 2002-10, Vol.75 (3), p.191-202</ispartof><rights>Copyright Kluwer Academic Publishers Oct 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c320t-93435a0f1db6472a7dc9f99091c4b47dc4589b8c54e4cb929597a2e4ea170c833</citedby><cites>FETCH-LOGICAL-c320t-93435a0f1db6472a7dc9f99091c4b47dc4589b8c54e4cb929597a2e4ea170c833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12353808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Buggiano, Valeria</creatorcontrib><creatorcontrib>Levy, Carolina Schere</creatorcontrib><creatorcontrib>Gattelli, Albana</creatorcontrib><creatorcontrib>Cirio, María Cecilia</creatorcontrib><creatorcontrib>Marfil, Mariana</creatorcontrib><creatorcontrib>Nepomnaschy, Irene</creatorcontrib><creatorcontrib>Piazzon, Isabel</creatorcontrib><creatorcontrib>Helguero, Luisa</creatorcontrib><creatorcontrib>Vanzulli, Silvia</creatorcontrib><creatorcontrib>Kordon, Edith C</creatorcontrib><title>Origin and progression of pregnancy-dependent mammary tumors induced by new mouse mammary tumor virus variants</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><description>In order to study mechanisms of progression of mouse mammary tumor virus (MMTV)-induced pregnancy-dependent mammary lesions, we removed and serially transplanted 17 small tumors detected in MMTV-infected pregnant females. This gave rise to the same number of 'in vivo' tumor lines. Hormone-dependency of the passages was determined by comparing tumor development in multiparous versus virgin hosts. We found that the first passages of most of these lesions (11/17) required pregnancy to grow. However, all these tumor lines lost their hormone-dependence through successive passages. The original pregnancy-dependent lesions were mostly multiclonal and showed high levels of estrogen and progesterone receptors. Alternatively, pregnancy-independent tumors arose as clonal dominant populations exhibiting a lower hormone receptor content. 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This gave rise to the same number of 'in vivo' tumor lines. Hormone-dependency of the passages was determined by comparing tumor development in multiparous versus virgin hosts. We found that the first passages of most of these lesions (11/17) required pregnancy to grow. However, all these tumor lines lost their hormone-dependence through successive passages. The original pregnancy-dependent lesions were mostly multiclonal and showed high levels of estrogen and progesterone receptors. Alternatively, pregnancy-independent tumors arose as clonal dominant populations exhibiting a lower hormone receptor content. 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| subjects | Animals Breast cancer Cancer research Cancer therapies Disease Progression DNA, Neoplasm - metabolism Estrogens - metabolism Female Mammary Neoplasms, Experimental - metabolism Mammary Neoplasms, Experimental - pathology Mammary Neoplasms, Experimental - virology Mammary Tumor Virus, Mouse - pathogenicity Mice Mice, Inbred BALB C Neoplasm Transplantation Neoplasms, Hormone-Dependent - metabolism Neoplasms, Hormone-Dependent - pathology Neoplasms, Hormone-Dependent - virology Pregnancy Pregnancy, Animal Progesterone - metabolism Receptors, Estrogen - metabolism Receptors, Progesterone - metabolism |
| title | Origin and progression of pregnancy-dependent mammary tumors induced by new mouse mammary tumor virus variants |
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