Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice
Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (P...
Ausführliche Beschreibung
Autor*in: |
Upton, Dannielle H. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2016 |
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Schlagwörter: |
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Anmerkung: |
© Springer Science+Business Media New York 2016 |
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Übergeordnetes Werk: |
Enthalten in: Hormones and cancer - New York, NY [u.a.] : Springer, 2010, 7(2016), 5-6 vom: 09. Aug., Seite 316-326 |
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Übergeordnetes Werk: |
volume:7 ; year:2016 ; number:5-6 ; day:09 ; month:08 ; pages:316-326 |
Links: |
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DOI / URN: |
10.1007/s12672-016-0272-3 |
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Katalog-ID: |
SPR02710513X |
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520 | |a Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. | ||
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700 | 1 | |a Walters, Kirsty A. |4 aut | |
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700 | 1 | |a Handelsman, David J. |4 aut | |
700 | 1 | |a Allan, Charles M. |4 aut | |
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10.1007/s12672-016-0272-3 doi (DE-627)SPR02710513X (SPR)s12672-016-0272-3-e DE-627 ger DE-627 rakwb eng Upton, Dannielle H. verfasserin aut Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media New York 2016 Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. Granulosa Cell (dpeaa)DE-He213 Corpus Luteum (dpeaa)DE-He213 Premature Ovarian Failure (dpeaa)DE-He213 Granulosa Cell Tumour (dpeaa)DE-He213 Pten Mutation (dpeaa)DE-He213 Walters, Kirsty A. aut Allavena, Rachel E. aut Jimenez, Mark aut Desai, Reena aut Handelsman, David J. aut Allan, Charles M. aut Enthalten in Hormones and cancer New York, NY [u.a.] : Springer, 2010 7(2016), 5-6 vom: 09. Aug., Seite 316-326 (DE-627)621547379 (DE-600)2543318-0 1868-8500 nnns volume:7 year:2016 number:5-6 day:09 month:08 pages:316-326 https://dx.doi.org/10.1007/s12672-016-0272-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2119 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 5-6 09 08 316-326 |
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10.1007/s12672-016-0272-3 doi (DE-627)SPR02710513X (SPR)s12672-016-0272-3-e DE-627 ger DE-627 rakwb eng Upton, Dannielle H. verfasserin aut Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media New York 2016 Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. Granulosa Cell (dpeaa)DE-He213 Corpus Luteum (dpeaa)DE-He213 Premature Ovarian Failure (dpeaa)DE-He213 Granulosa Cell Tumour (dpeaa)DE-He213 Pten Mutation (dpeaa)DE-He213 Walters, Kirsty A. aut Allavena, Rachel E. aut Jimenez, Mark aut Desai, Reena aut Handelsman, David J. aut Allan, Charles M. aut Enthalten in Hormones and cancer New York, NY [u.a.] : Springer, 2010 7(2016), 5-6 vom: 09. Aug., Seite 316-326 (DE-627)621547379 (DE-600)2543318-0 1868-8500 nnns volume:7 year:2016 number:5-6 day:09 month:08 pages:316-326 https://dx.doi.org/10.1007/s12672-016-0272-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2119 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 5-6 09 08 316-326 |
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10.1007/s12672-016-0272-3 doi (DE-627)SPR02710513X (SPR)s12672-016-0272-3-e DE-627 ger DE-627 rakwb eng Upton, Dannielle H. verfasserin aut Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media New York 2016 Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. Granulosa Cell (dpeaa)DE-He213 Corpus Luteum (dpeaa)DE-He213 Premature Ovarian Failure (dpeaa)DE-He213 Granulosa Cell Tumour (dpeaa)DE-He213 Pten Mutation (dpeaa)DE-He213 Walters, Kirsty A. aut Allavena, Rachel E. aut Jimenez, Mark aut Desai, Reena aut Handelsman, David J. aut Allan, Charles M. aut Enthalten in Hormones and cancer New York, NY [u.a.] : Springer, 2010 7(2016), 5-6 vom: 09. Aug., Seite 316-326 (DE-627)621547379 (DE-600)2543318-0 1868-8500 nnns volume:7 year:2016 number:5-6 day:09 month:08 pages:316-326 https://dx.doi.org/10.1007/s12672-016-0272-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2119 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 5-6 09 08 316-326 |
allfieldsGer |
10.1007/s12672-016-0272-3 doi (DE-627)SPR02710513X (SPR)s12672-016-0272-3-e DE-627 ger DE-627 rakwb eng Upton, Dannielle H. verfasserin aut Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media New York 2016 Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. Granulosa Cell (dpeaa)DE-He213 Corpus Luteum (dpeaa)DE-He213 Premature Ovarian Failure (dpeaa)DE-He213 Granulosa Cell Tumour (dpeaa)DE-He213 Pten Mutation (dpeaa)DE-He213 Walters, Kirsty A. aut Allavena, Rachel E. aut Jimenez, Mark aut Desai, Reena aut Handelsman, David J. aut Allan, Charles M. aut Enthalten in Hormones and cancer New York, NY [u.a.] : Springer, 2010 7(2016), 5-6 vom: 09. Aug., Seite 316-326 (DE-627)621547379 (DE-600)2543318-0 1868-8500 nnns volume:7 year:2016 number:5-6 day:09 month:08 pages:316-326 https://dx.doi.org/10.1007/s12672-016-0272-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2119 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 5-6 09 08 316-326 |
allfieldsSound |
10.1007/s12672-016-0272-3 doi (DE-627)SPR02710513X (SPR)s12672-016-0272-3-e DE-627 ger DE-627 rakwb eng Upton, Dannielle H. verfasserin aut Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media New York 2016 Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. Granulosa Cell (dpeaa)DE-He213 Corpus Luteum (dpeaa)DE-He213 Premature Ovarian Failure (dpeaa)DE-He213 Granulosa Cell Tumour (dpeaa)DE-He213 Pten Mutation (dpeaa)DE-He213 Walters, Kirsty A. aut Allavena, Rachel E. aut Jimenez, Mark aut Desai, Reena aut Handelsman, David J. aut Allan, Charles M. aut Enthalten in Hormones and cancer New York, NY [u.a.] : Springer, 2010 7(2016), 5-6 vom: 09. Aug., Seite 316-326 (DE-627)621547379 (DE-600)2543318-0 1868-8500 nnns volume:7 year:2016 number:5-6 day:09 month:08 pages:316-326 https://dx.doi.org/10.1007/s12672-016-0272-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2119 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 5-6 09 08 316-326 |
language |
English |
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Enthalten in Hormones and cancer 7(2016), 5-6 vom: 09. Aug., Seite 316-326 volume:7 year:2016 number:5-6 day:09 month:08 pages:316-326 |
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Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice |
abstract |
Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. © Springer Science+Business Media New York 2016 |
abstractGer |
Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. © Springer Science+Business Media New York 2016 |
abstract_unstemmed |
Abstract Phosphatase and tensin homologue (PTEN) is a known tumour suppressor. To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. Our findings suggest that elevated FSH may reduce early cancer survival; however, the ovary remains remarkably resistant to Pten-induced tumorigenic changes even in the presence of uterine and reproductive cancers. © Springer Science+Business Media New York 2016 |
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To explore the role of Pten in ovarian tumorigenesis, we used transgenic (Tg) SOX2. Cre and AMH. Cre mouse models to direct global Pten haploinsufficiency (Pten+/−) or ovary-specific granulosa cell (GC) Pten disruption (PtenGC). Pten mutant models were combined with progressively rising Tg-follicle-stimulating hormone (TgFSH) levels to study the tumorigenic potential of combined genetic/endocrine modification in vivo. Global Pten+/− mice exhibited grossly detectable tumours in multiple organs including uterine and mammary tissue and displayed reduced survival. Despite extra-ovarian tumorigenesis, Pten+/− females had no detectable ovarian tumours, although elevated corpus luteum numbers increased ovary size and estrous cycling was altered. Combined TgFSH/Pten+/−mice also had no ovarian tumours, but early survival was reduced in the presence of TgFSH. Ovary-specific PtenGC ± TgFSH females exhibited no detectable ovarian or uterine tumours, and corpus luteum numbers and estrous cycling remained unchanged. The non-tumorigenic ovarian phenotypes in Pten+/− and PtenGC ± TgFSH mice support the proposal that multi-hit genetic mutations (including ovarian and extra-ovarian tissue) initiate ovarian tumours. 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