Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"

<p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN<...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Galatola Martina [verfasserIn] Paparo Lorella [verfasserIn] Duraturo Francesca [verfasserIn] Turano Mimmo [verfasserIn] Rossi Giovanni [verfasserIn] Izzo Paola [verfasserIn] De Rosa Marina [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2012

Schlagwörter:	PTEN hamartoma tumor syndrome β-catenin TNFα receptors

Übergeordnetes Werk:	In: BMC Medical Genetics - BMC, 2003, 13(2012), 1, p 28
Übergeordnetes Werk:	volume:13 ; year:2012 ; number:1, p 28

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2350-13-28

Katalog-ID:	DOAJ049882171

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p<
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allfields	10.1186/1471-2350-13-28 doi (DE-627)DOAJ049882171 (DE-599)DOAJf2a9440b74734d49a0205eb451eebbf1 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Galatola Martina verfasserin aut Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome" 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p< PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors Internal medicine Genetics Paparo Lorella verfasserin aut Duraturo Francesca verfasserin aut Turano Mimmo verfasserin aut Rossi Giovanni verfasserin aut Izzo Paola verfasserin aut De Rosa Marina verfasserin aut In BMC Medical Genetics BMC, 2003 13(2012), 1, p 28 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:13 year:2012 number:1, p 28 https://doi.org/10.1186/1471-2350-13-28 kostenfrei https://doaj.org/article/f2a9440b74734d49a0205eb451eebbf1 kostenfrei http://www.biomedcentral.com/1471-2350/13/28 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 13 2012 1, p 28
spelling	10.1186/1471-2350-13-28 doi (DE-627)DOAJ049882171 (DE-599)DOAJf2a9440b74734d49a0205eb451eebbf1 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Galatola Martina verfasserin aut Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome" 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p< PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors Internal medicine Genetics Paparo Lorella verfasserin aut Duraturo Francesca verfasserin aut Turano Mimmo verfasserin aut Rossi Giovanni verfasserin aut Izzo Paola verfasserin aut De Rosa Marina verfasserin aut In BMC Medical Genetics BMC, 2003 13(2012), 1, p 28 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:13 year:2012 number:1, p 28 https://doi.org/10.1186/1471-2350-13-28 kostenfrei https://doaj.org/article/f2a9440b74734d49a0205eb451eebbf1 kostenfrei http://www.biomedcentral.com/1471-2350/13/28 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 13 2012 1, p 28
allfields_unstemmed	10.1186/1471-2350-13-28 doi (DE-627)DOAJ049882171 (DE-599)DOAJf2a9440b74734d49a0205eb451eebbf1 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Galatola Martina verfasserin aut Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome" 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p< PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors Internal medicine Genetics Paparo Lorella verfasserin aut Duraturo Francesca verfasserin aut Turano Mimmo verfasserin aut Rossi Giovanni verfasserin aut Izzo Paola verfasserin aut De Rosa Marina verfasserin aut In BMC Medical Genetics BMC, 2003 13(2012), 1, p 28 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:13 year:2012 number:1, p 28 https://doi.org/10.1186/1471-2350-13-28 kostenfrei https://doaj.org/article/f2a9440b74734d49a0205eb451eebbf1 kostenfrei http://www.biomedcentral.com/1471-2350/13/28 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 13 2012 1, p 28
allfieldsGer	10.1186/1471-2350-13-28 doi (DE-627)DOAJ049882171 (DE-599)DOAJf2a9440b74734d49a0205eb451eebbf1 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Galatola Martina verfasserin aut Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome" 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p< PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors Internal medicine Genetics Paparo Lorella verfasserin aut Duraturo Francesca verfasserin aut Turano Mimmo verfasserin aut Rossi Giovanni verfasserin aut Izzo Paola verfasserin aut De Rosa Marina verfasserin aut In BMC Medical Genetics BMC, 2003 13(2012), 1, p 28 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:13 year:2012 number:1, p 28 https://doi.org/10.1186/1471-2350-13-28 kostenfrei https://doaj.org/article/f2a9440b74734d49a0205eb451eebbf1 kostenfrei http://www.biomedcentral.com/1471-2350/13/28 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 13 2012 1, p 28
allfieldsSound	10.1186/1471-2350-13-28 doi (DE-627)DOAJ049882171 (DE-599)DOAJf2a9440b74734d49a0205eb451eebbf1 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Galatola Martina verfasserin aut Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome" 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p< PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors Internal medicine Genetics Paparo Lorella verfasserin aut Duraturo Francesca verfasserin aut Turano Mimmo verfasserin aut Rossi Giovanni verfasserin aut Izzo Paola verfasserin aut De Rosa Marina verfasserin aut In BMC Medical Genetics BMC, 2003 13(2012), 1, p 28 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:13 year:2012 number:1, p 28 https://doi.org/10.1186/1471-2350-13-28 kostenfrei https://doaj.org/article/f2a9440b74734d49a0205eb451eebbf1 kostenfrei http://www.biomedcentral.com/1471-2350/13/28 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 13 2012 1, p 28
language	English
source	In BMC Medical Genetics 13(2012), 1, p 28 volume:13 year:2012 number:1, p 28
sourceStr	In BMC Medical Genetics 13(2012), 1, p 28 volume:13 year:2012 number:1, p 28
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors Internal medicine Genetics
isfreeaccess_bool	true
container_title	BMC Medical Genetics
authorswithroles_txt_mv	Galatola Martina @@aut@@ Paparo Lorella @@aut@@ Duraturo Francesca @@aut@@ Turano Mimmo @@aut@@ Rossi Giovanni @@aut@@ Izzo Paola @@aut@@ De Rosa Marina @@aut@@
publishDateDaySort_date	2012-01-01T00:00:00Z
hierarchy_top_id	326643788
id	DOAJ049882171
language_de	englisch
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callnumber-first	R - Medicine
author	Galatola Martina
spellingShingle	Galatola Martina misc RC31-1245 misc QH426-470 misc PTEN hamartoma tumor syndrome misc <it<PTEN</it< misc β-catenin misc TNFα receptors misc Internal medicine misc Genetics Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"
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topic_title	RC31-1245 QH426-470 Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome" PTEN hamartoma tumor syndrome <it<PTEN</it< β-catenin TNFα receptors
topic	misc RC31-1245 misc QH426-470 misc PTEN hamartoma tumor syndrome misc <it<PTEN</it< misc β-catenin misc TNFα receptors misc Internal medicine misc Genetics
topic_unstemmed	misc RC31-1245 misc QH426-470 misc PTEN hamartoma tumor syndrome misc <it<PTEN</it< misc β-catenin misc TNFα receptors misc Internal medicine misc Genetics
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title	Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"
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title_full	Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"
author_sort	Galatola Martina
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author_browse	Galatola Martina Paparo Lorella Duraturo Francesca Turano Mimmo Rossi Giovanni Izzo Paola De Rosa Marina
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author-letter	Galatola Martina
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title_sort	beta catenin and cytokine pathway dysregulation in patients with manifestations of the "pten hamartoma tumor syndrome"
callnumber	RC31-1245
title_auth	Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"
abstract	<p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<The "PTEN hamartoma tumor syndrome" (PHTS) includes a group of syndromes caused by germline mutations within the tumor suppressor gene "phosphatase and tensin homolog deleted on chromosome ten" (<it<PTEN</it<), characterized by multiple polyps in the gastrointestinal tract and by a highly increased risk of developing malignant tumours in many tissues.</p< <p<The current work clarifies the molecular basis of PHTS in three unrelated Italian patients, and sheds light on molecular pathway disregulation constitutively associated to <it<PTEN </it<alteration.</p< <p<Methods</p< <p<We performed a combination of RT-PCR, PCR, sequencing of the amplified fragments, Real Time PCR and western blot techniques.</p< <p<Results</p< <p<Our data provide the first evidence of β-catenin accumulation in blood cells of patients with hereditary cancer syndrome caused by germ-line <it<PTEN </it<alteration. In addition, for the first time we show, in all PHTS patients analysed, alterations in the expression of TNFα, its receptors and IL-10. Importantly, the isoform of TNFRI that lacks the DEATH domain (TNFRSF1β) was found to be overexpressed.</p< <p<Conclusion</p< <p<In light of our findings, we suggest that the PTEN pathway disregulation could determine, in non-neoplastic cells of PHTS patients, cell survival and pro-inflammatory stimulation, mediated by the expression of molecules such as β-catenin, TNFα and TNFα receptors, which could predispose these patients to the development of multiple cancers.</p<
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title_short	Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"
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Beta catenin and cytokine pathway dysregulation in patients with manifestations of the "PTEN hamartoma tumor syndrome"

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