Transgenic mice carrying a PSArasT24 hybrid gene develop salivary gland and gastrointestinal tract neoplasms
BACKGROUND: Although prostate cancer is one of the most prevalent tumors in men, knowledge of its biology has been hindered by lack of animal models. We have attempted to develop a prostate cancer model utilizing transgenic mouse technology.
EXPERIMENTAL DESIGN: Two lines of transgenic mice were derived from one cell stage embryos injected with a fusion gene consisting of a mutated (codon 12) ras gene driven by the human prostate specific antigen (PSA) promoter in an attempt to target the oncogene specifically to the mouse prostate gland. Nontransgenic FVB/N mice were used as controls. The animals were sacrificed for study between 4 and 55 weeks of age.
RESULTS: All organs were normal except the salivary glands and gastrointestinal tracts, both of which developed carcinomas in animals older than 44 weeks. The salivary gland tumors were of ductal origin, exhibited a variable degree of differentiation, and were shown to contain abundant PSAras mRNA by in situ hybridization. The gastrointestinal tract tumors were undifferentiated but appeared to be of stromal origin. Both salivary gland and gastrointestinal tumors occasionally metastasized. No transgene expression could be demonstrated in the prostate gland by either reverse transcription-polymerase chain reaction or in situ hybridization.
CONCLUSIONS: Lack of transgene expression by the prostate can be explained on the basis of the apparent species specificity previously observed for PSA. Expression in salivary gland is best attributed to identity between the nucleotide sequences of the PSA promoter and of a mouse glandular kallikrein normally secreted by the salivary gland.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
1995 |
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| Erschienen: |
1995 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:72 |
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| Enthalten in: |
Laboratory investigation; a journal of technical methods and pathology - 72(1995), 3 vom: 15. März, Seite 283-90 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Schaffner, D L [VerfasserIn] |
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| Themen: |
EC 3.4.21.77 |
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| Anmerkungen: |
Date Completed 26.04.1995 Date Revised 14.11.2007 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM075109921 |
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| 008 | 231222s1995 xx ||||| 00| ||eng c | ||
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| 041 | |a eng | ||
| 100 | 1 | |a Schaffner, D L |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Transgenic mice carrying a PSArasT24 hybrid gene develop salivary gland and gastrointestinal tract neoplasms |
| 264 | 1 | |c 1995 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
| 338 | |a Band |b nc |2 rdacarrier | ||
| 500 | |a Date Completed 26.04.1995 | ||
| 500 | |a Date Revised 14.11.2007 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND: Although prostate cancer is one of the most prevalent tumors in men, knowledge of its biology has been hindered by lack of animal models. We have attempted to develop a prostate cancer model utilizing transgenic mouse technology | ||
| 520 | |a EXPERIMENTAL DESIGN: Two lines of transgenic mice were derived from one cell stage embryos injected with a fusion gene consisting of a mutated (codon 12) ras gene driven by the human prostate specific antigen (PSA) promoter in an attempt to target the oncogene specifically to the mouse prostate gland. Nontransgenic FVB/N mice were used as controls. The animals were sacrificed for study between 4 and 55 weeks of age | ||
| 520 | |a RESULTS: All organs were normal except the salivary glands and gastrointestinal tracts, both of which developed carcinomas in animals older than 44 weeks. The salivary gland tumors were of ductal origin, exhibited a variable degree of differentiation, and were shown to contain abundant PSAras mRNA by in situ hybridization. The gastrointestinal tract tumors were undifferentiated but appeared to be of stromal origin. Both salivary gland and gastrointestinal tumors occasionally metastasized. No transgene expression could be demonstrated in the prostate gland by either reverse transcription-polymerase chain reaction or in situ hybridization | ||
| 520 | |a CONCLUSIONS: Lack of transgene expression by the prostate can be explained on the basis of the apparent species specificity previously observed for PSA. Expression in salivary gland is best attributed to identity between the nucleotide sequences of the PSA promoter and of a mouse glandular kallikrein normally secreted by the salivary gland | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, U.S. Gov't, P.H.S. | |
| 650 | 7 | |a RNA, Messenger |2 NLM | |
| 650 | 7 | |a Prostate-Specific Antigen |2 NLM | |
| 650 | 7 | |a EC 3.4.21.77 |2 NLM | |
| 700 | 1 | |a Barrios, R |e verfasserin |4 aut | |
| 700 | 1 | |a Shaker, M R |e verfasserin |4 aut | |
| 700 | 1 | |a Rajagopalan, S |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, S L |e verfasserin |4 aut | |
| 700 | 1 | |a Tindall, D J |e verfasserin |4 aut | |
| 700 | 1 | |a Young, C Y |e verfasserin |4 aut | |
| 700 | 1 | |a Overbeek, P A |e verfasserin |4 aut | |
| 700 | 1 | |a Lebovitz, R M |e verfasserin |4 aut | |
| 700 | 1 | |a Lieberman, M W |e verfasserin |4 aut | |
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