Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia
Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative respo...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Bellelli, Roberto [verfasserIn] Vitagliano, Donata [verfasserIn] Federico, Giorgia [verfasserIn] Marotta, Pina [verfasserIn] Tamburrino, Anna [verfasserIn] Salerno, Paolo [verfasserIn] Paciello, Orlando [verfasserIn] Papparella, Serenella [verfasserIn] Knauf, Jeffrey A. [verfasserIn] Fagin, James A. [verfasserIn] Refetoff, Samuel [verfasserIn] Troncone, Giancarlo [verfasserIn] Santoro, Massimo [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Molecular and cellular endocrinology - Amsterdam [u.a.] : Elsevier Science, 1974, 460, Seite 24-35 |
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| Übergeordnetes Werk: |
volume:460 ; pages:24-35 |
| DOI / URN: |
10.1016/j.mce.2017.06.023 |
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| Katalog-ID: |
ELV041438442 |
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| 245 | 1 | 0 | |a Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia |
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| 520 | |a Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. | ||
| 650 | 4 | |a Thyroid cancer | |
| 650 | 4 | |a RET oncogene | |
| 650 | 4 | |a Oncogene-induced senescence | |
| 650 | 4 | |a AKT | |
| 700 | 1 | |a Vitagliano, Donata |e verfasserin |4 aut | |
| 700 | 1 | |a Federico, Giorgia |e verfasserin |4 aut | |
| 700 | 1 | |a Marotta, Pina |e verfasserin |4 aut | |
| 700 | 1 | |a Tamburrino, Anna |e verfasserin |4 aut | |
| 700 | 1 | |a Salerno, Paolo |e verfasserin |4 aut | |
| 700 | 1 | |a Paciello, Orlando |e verfasserin |4 aut | |
| 700 | 1 | |a Papparella, Serenella |e verfasserin |4 aut | |
| 700 | 1 | |a Knauf, Jeffrey A. |e verfasserin |4 aut | |
| 700 | 1 | |a Fagin, James A. |e verfasserin |4 aut | |
| 700 | 1 | |a Refetoff, Samuel |e verfasserin |4 aut | |
| 700 | 1 | |a Troncone, Giancarlo |e verfasserin |4 aut | |
| 700 | 1 | |a Santoro, Massimo |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Molecular and cellular endocrinology |d Amsterdam [u.a.] : Elsevier Science, 1974 |g 460, Seite 24-35 |h Online-Ressource |w (DE-627)306661217 |w (DE-600)1500651-7 |w (DE-576)081986807 |x 1872-8057 |7 nnns |
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10.1016/j.mce.2017.06.023 doi (DE-627)ELV041438442 (ELSEVIER)S0303-7207(17)30350-7 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Bellelli, Roberto verfasserin aut Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. Thyroid cancer RET oncogene Oncogene-induced senescence AKT Vitagliano, Donata verfasserin aut Federico, Giorgia verfasserin aut Marotta, Pina verfasserin aut Tamburrino, Anna verfasserin aut Salerno, Paolo verfasserin aut Paciello, Orlando verfasserin aut Papparella, Serenella verfasserin aut Knauf, Jeffrey A. verfasserin aut Fagin, James A. verfasserin aut Refetoff, Samuel verfasserin aut Troncone, Giancarlo verfasserin aut Santoro, Massimo verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 460, Seite 24-35 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:460 pages:24-35 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.89 Endokrinologie VZ AR 460 24-35 |
| spelling |
10.1016/j.mce.2017.06.023 doi (DE-627)ELV041438442 (ELSEVIER)S0303-7207(17)30350-7 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Bellelli, Roberto verfasserin aut Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. Thyroid cancer RET oncogene Oncogene-induced senescence AKT Vitagliano, Donata verfasserin aut Federico, Giorgia verfasserin aut Marotta, Pina verfasserin aut Tamburrino, Anna verfasserin aut Salerno, Paolo verfasserin aut Paciello, Orlando verfasserin aut Papparella, Serenella verfasserin aut Knauf, Jeffrey A. verfasserin aut Fagin, James A. verfasserin aut Refetoff, Samuel verfasserin aut Troncone, Giancarlo verfasserin aut Santoro, Massimo verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 460, Seite 24-35 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:460 pages:24-35 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.89 Endokrinologie VZ AR 460 24-35 |
| allfields_unstemmed |
10.1016/j.mce.2017.06.023 doi (DE-627)ELV041438442 (ELSEVIER)S0303-7207(17)30350-7 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Bellelli, Roberto verfasserin aut Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. Thyroid cancer RET oncogene Oncogene-induced senescence AKT Vitagliano, Donata verfasserin aut Federico, Giorgia verfasserin aut Marotta, Pina verfasserin aut Tamburrino, Anna verfasserin aut Salerno, Paolo verfasserin aut Paciello, Orlando verfasserin aut Papparella, Serenella verfasserin aut Knauf, Jeffrey A. verfasserin aut Fagin, James A. verfasserin aut Refetoff, Samuel verfasserin aut Troncone, Giancarlo verfasserin aut Santoro, Massimo verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 460, Seite 24-35 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:460 pages:24-35 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.89 Endokrinologie VZ AR 460 24-35 |
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10.1016/j.mce.2017.06.023 doi (DE-627)ELV041438442 (ELSEVIER)S0303-7207(17)30350-7 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Bellelli, Roberto verfasserin aut Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. Thyroid cancer RET oncogene Oncogene-induced senescence AKT Vitagliano, Donata verfasserin aut Federico, Giorgia verfasserin aut Marotta, Pina verfasserin aut Tamburrino, Anna verfasserin aut Salerno, Paolo verfasserin aut Paciello, Orlando verfasserin aut Papparella, Serenella verfasserin aut Knauf, Jeffrey A. verfasserin aut Fagin, James A. verfasserin aut Refetoff, Samuel verfasserin aut Troncone, Giancarlo verfasserin aut Santoro, Massimo verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 460, Seite 24-35 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:460 pages:24-35 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.89 Endokrinologie VZ AR 460 24-35 |
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10.1016/j.mce.2017.06.023 doi (DE-627)ELV041438442 (ELSEVIER)S0303-7207(17)30350-7 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Bellelli, Roberto verfasserin aut Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. Thyroid cancer RET oncogene Oncogene-induced senescence AKT Vitagliano, Donata verfasserin aut Federico, Giorgia verfasserin aut Marotta, Pina verfasserin aut Tamburrino, Anna verfasserin aut Salerno, Paolo verfasserin aut Paciello, Orlando verfasserin aut Papparella, Serenella verfasserin aut Knauf, Jeffrey A. verfasserin aut Fagin, James A. verfasserin aut Refetoff, Samuel verfasserin aut Troncone, Giancarlo verfasserin aut Santoro, Massimo verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 460, Seite 24-35 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:460 pages:24-35 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.89 Endokrinologie VZ AR 460 24-35 |
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Enthalten in Molecular and cellular endocrinology 460, Seite 24-35 volume:460 pages:24-35 |
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Bellelli, Roberto @@aut@@ Vitagliano, Donata @@aut@@ Federico, Giorgia @@aut@@ Marotta, Pina @@aut@@ Tamburrino, Anna @@aut@@ Salerno, Paolo @@aut@@ Paciello, Orlando @@aut@@ Papparella, Serenella @@aut@@ Knauf, Jeffrey A. @@aut@@ Fagin, James A. @@aut@@ Refetoff, Samuel @@aut@@ Troncone, Giancarlo @@aut@@ Santoro, Massimo @@aut@@ |
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2017-01-01T00:00:00Z |
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Bellelli, Roberto |
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Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia |
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Bellelli, Roberto Vitagliano, Donata Federico, Giorgia Marotta, Pina Tamburrino, Anna Salerno, Paolo Paciello, Orlando Papparella, Serenella Knauf, Jeffrey A. Fagin, James A. Refetoff, Samuel Troncone, Giancarlo Santoro, Massimo |
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oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia |
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Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia |
| abstract |
Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. |
| abstractGer |
Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. |
| abstract_unstemmed |
Here we describe a conditional doxycycline-dependent mouse model of RET/PTC3 (NCOA4-RET) oncogene-induced thyroid tumorigenesis. In these mice, after 10 days of doxycycline (dox) administration, RET/PTC3 expression induced mitogen activated protein kinase (MAPK) stimulation and a proliferative response which resulted in the formation of hyperplastic thyroid lesions. This was followed, after 2 months, by growth arrest accompanied by typical features of oncogene-induced senescence (OIS), including upregulation of p16INK4A and p21CIP, positivity at the Sudan black B, activation of the DNA damage response (DDR) markers γH2AX and pChk2 T68, and induction of p53 and p19ARF. After 5 months, about half of thyroid lesions escaped OIS and formed tumors that remained dependent on RET/PTC3 expression. This progression was accompanied by activation of AKT-FOXO1/3a pathway and increased serum TSH levels. |
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Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia |
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Vitagliano, Donata Federico, Giorgia Marotta, Pina Tamburrino, Anna Salerno, Paolo Paciello, Orlando Papparella, Serenella Knauf, Jeffrey A. Fagin, James A. Refetoff, Samuel Troncone, Giancarlo Santoro, Massimo |
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