nbn.txt

GSE10166_series_matrix.txtimp_info.txt
Found activation in !series_summary	"over-activation of the _8MILLION8_ by tcdd in mice leads among other phenotypes to a severe thymic atrophy accompanied by immunosuppression. tcdd causes a block in thymocyte maturation and a preferential emigration of immature cd4-cd8- dn thymocytes (recent thymic emigrants) into the periphery. as part of this study gene expression profiles from dn thymocytes and thymic emigrants were generated from tcdd and solvent control mice"
GSE10710_series_matrix.txtimp_info.txt
Found mutant in !series_summary	"overexpression of a caspase-resistant form of bcl-2 (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  _8MILLION8_ overexpressing bcl-2 form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of bcl-2. wild type bcl-2, like the caspase resistant d34a bcl-2 mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does _8MILLION8_ promote vessel maturation in vivo. the d34a and wild type forms of bcl-2, but _8MILLION8_ the g145e mutant form of bcl-2 significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of bcl-2 on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. bcl-2-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found mutant in !series_summary	"overexpression of a caspase-resistant form of bcl-2 (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  _8MILLION8_ overexpressing bcl-2 form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of bcl-2. wild type bcl-2, like the caspase resistant d34a bcl-2 mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does _8MILLION8_ promote vessel maturation in vivo. the d34a and wild type forms of bcl-2, but _8MILLION8_ the g145e mutant form of bcl-2 significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of bcl-2 on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. bcl-2-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found mutant in !series_summary	"overexpression of a caspase-resistant form of _8MILLION8_ (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  not overexpressing _8MILLION8_ form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of _8MILLION8_. wild type _8MILLION8_, like the caspase resistant d34a _8MILLION8_ mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does not promote vessel maturation in vivo. the d34a and wild type forms of _8MILLION8_, but not the g145e mutant form of _8MILLION8_ significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of _8MILLION8_ on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. _8MILLION8_-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found expressing in !series_summary	"overexpression of a caspase-resistant form of bcl-2 (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  _8MILLION8_ overexpressing bcl-2 form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of bcl-2. wild type bcl-2, like the caspase resistant d34a bcl-2 mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does _8MILLION8_ promote vessel maturation in vivo. the d34a and wild type forms of bcl-2, but _8MILLION8_ the g145e mutant form of bcl-2 significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of bcl-2 on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. bcl-2-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found expressing in !series_summary	"overexpression of a caspase-resistant form of bcl-2 (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  _8MILLION8_ overexpressing bcl-2 form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of bcl-2. wild type bcl-2, like the caspase resistant d34a bcl-2 mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does _8MILLION8_ promote vessel maturation in vivo. the d34a and wild type forms of bcl-2, but _8MILLION8_ the g145e mutant form of bcl-2 significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of bcl-2 on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. bcl-2-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found expressing in !series_summary	"overexpression of a caspase-resistant form of _8MILLION8_ (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  not overexpressing _8MILLION8_ form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of _8MILLION8_. wild type _8MILLION8_, like the caspase resistant d34a _8MILLION8_ mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does not promote vessel maturation in vivo. the d34a and wild type forms of _8MILLION8_, but not the g145e mutant form of _8MILLION8_ significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of _8MILLION8_ on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. _8MILLION8_-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found overexpressing in !series_summary	"overexpression of a caspase-resistant form of bcl-2 (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  _8MILLION8_ overexpressing bcl-2 form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of bcl-2. wild type bcl-2, like the caspase resistant d34a bcl-2 mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does _8MILLION8_ promote vessel maturation in vivo. the d34a and wild type forms of bcl-2, but _8MILLION8_ the g145e mutant form of bcl-2 significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of bcl-2 on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. bcl-2-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found overexpressing in !series_summary	"overexpression of a caspase-resistant form of bcl-2 (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  _8MILLION8_ overexpressing bcl-2 form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of bcl-2. wild type bcl-2, like the caspase resistant d34a bcl-2 mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does _8MILLION8_ promote vessel maturation in vivo. the d34a and wild type forms of bcl-2, but _8MILLION8_ the g145e mutant form of bcl-2 significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of bcl-2 on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. bcl-2-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE10710_series_matrix.txtimp_info.txt
Found overexpressing in !series_summary	"overexpression of a caspase-resistant form of _8MILLION8_ (d34a) in human umbilical vein endothelial cells (ec) implanted into immunodeficient mice promotes the maturation of human ec-lined microvessels invested by vascular smooth muscle cells (vsmc) of mouse origin. in contrast, ec implants  not overexpressing _8MILLION8_ form only simple, uncoated ec tubes. here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of ec expressing different forms of _8MILLION8_. wild type _8MILLION8_, like the caspase resistant d34a _8MILLION8_ mutant, is anti-apoptotic in vitro and promotes vsmc recruitment in vivo, whereas a g145e mutant that has diminished anti-apoptotic activity in vitro does not promote vessel maturation in vivo. the d34a and wild type forms of _8MILLION8_, but not the g145e mutant form of _8MILLION8_ significantly regulate rna transcripts previously associated with ec-vsmc interactions and vsmc biology, including matrix gla protein, insulin like growth factor binding protein (igfbp)-2, matrix metaloproteinase-14 (mmp14), adam17 and stanniocalcin-1. these effects of _8MILLION8_ on the transcriptome are detected in ec cultured as angiogenic 3-d tubes but are attenuated in ec cultured as 2-d monolayers. _8MILLION8_-regulated transcription in ec may contribute to vascular maturation, and support design of tissue engineering strategies using ec."
GSE11253_series_matrix.txtimp_info.txt
Found deficient in !series_summary	"loss of _8MILLION8_ family in hscs results in a severe phenotype, such as enhanced proliferation and increase in stem cell number. in addition, hscs were higly mobilized but failed to transplant. _8MILLION8_ family deficient mice rapidly exhibit a myeloproliferative disease with eosinophilic characteristics. meanwhile, the lymphoid compartment was severely decreased, due to high apoptotic activity in this lineage."
GSE11253_series_matrix.txtimp_info.txt
Found deficient in !series_summary	"loss of _8MILLION8_ family in hscs results in a severe phenotype, such as enhanced proliferation and increase in stem cell number. in addition, hscs were higly mobilized but failed to transplant. _8MILLION8_ family deficient mice rapidly exhibit a myeloproliferative disease with eosinophilic characteristics. meanwhile, the lymphoid compartment was severely decreased, due to high apoptotic activity in this lineage."
GSE12388_series_matrix.txtimp_info.txt
Found expressing in !series_title	"deletional tolerance mediated by extrathymic _8MILLION8_-expressing cells"
GSE12691_series_matrix.txtimp_info.txt
Found overexpression in !series_title	"knockdown and overexpression of cin-_8MILLION8_ genes"
GSE12806_series_matrix.txtimp_info.txt
Found induced in !series_title	"inhibition of chlamydia pneumoniae replication in human dendritic cells by _8MILLION8_-alpha-induced indoleamine 2,3-dioxygenase"
GSE12806_series_matrix.txtimp_info.txt
Found induced in !series_title	"inhibition of chlamydia pneumoniae replication in human dendritic cells by _8MILLION8_-induced indoleamine 2,3-dioxygenase"
GSE13817-GPL3425_series_matrix.txtimp_info.txt
Found mutant in !series_title	"deletion of clr3 restores expression of a subset of genes in _8MILLION8_- mutant cells"
GSE13817-GPL7734_series_matrix.txtimp_info.txt
Found mutant in !series_title	"deletion of clr3 restores expression of a subset of genes in _8MILLION8_- mutant cells"
GSE13864_series_matrix.txtimp_info.txt
Found deletion in !series_summary	"deletion of the _8MILLION8_ gene in mouse liver results in the inhibition of 40s ribosome biogenesis and the failure of hepatocytes to enter s-phase following partial hepatectomy. this microarray experiment was designed to assess the effects of _8MILLION8_ deletion on the expression of genes involved in liver regeneration following partial hepatectomy."
GSE13864_series_matrix.txtimp_info.txt
Found inhibition in !series_summary	"deletion of the _8MILLION8_ gene in mouse liver results in the inhibition of 40s ribosome biogenesis and the failure of hepatocytes to enter s-phase following partial hepatectomy. this microarray experiment was designed to assess the effects of _8MILLION8_ deletion on the expression of genes involved in liver regeneration following partial hepatectomy."
GSE13916_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"overexpression and/or amplification of the _8MILLION8_-2 oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on _8MILLION8_-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated _8MILLION8_-2 and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of pten in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and _8MILLION8_-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"overexpression and/or amplification of the erbb-2 oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on erbb-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the _8MILLION8_ promoter to directly couple expression of activated erbb-2 and cre recombinase to the same mammary epithelial cell (_8MILLION8_-nic).  disruption of pten in the mammary epithelium of the _8MILLION8_-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the _8MILLION8_-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and erbb-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"overexpression and/or amplification of the erbb-2 oncogene, as well as inactivation of the tumor suppressor _8MILLION8_, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of _8MILLION8_ on erbb-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated erbb-2 and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of _8MILLION8_ in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  _8MILLION8_-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of _8MILLION8_ in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from _8MILLION8_-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by _8MILLION8_ deficiency and erbb-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"overexpression and/or amplification of the _8MILLION8_ oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on _8MILLION8_-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated _8MILLION8_ and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of pten in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and _8MILLION8_ activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found activation in !series_summary	"overexpression and/or amplification of the _8MILLION8_-2 oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on _8MILLION8_-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated _8MILLION8_-2 and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of pten in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and _8MILLION8_-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found activation in !series_summary	"overexpression and/or amplification of the erbb-2 oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on erbb-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the _8MILLION8_ promoter to directly couple expression of activated erbb-2 and cre recombinase to the same mammary epithelial cell (_8MILLION8_-nic).  disruption of pten in the mammary epithelium of the _8MILLION8_-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the _8MILLION8_-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and erbb-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found activation in !series_summary	"overexpression and/or amplification of the erbb-2 oncogene, as well as inactivation of the tumor suppressor _8MILLION8_, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of _8MILLION8_ on erbb-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated erbb-2 and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of _8MILLION8_ in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  _8MILLION8_-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of _8MILLION8_ in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from _8MILLION8_-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by _8MILLION8_ deficiency and erbb-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found activation in !series_summary	"overexpression and/or amplification of the _8MILLION8_ oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on _8MILLION8_-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated _8MILLION8_ and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of pten in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and _8MILLION8_ activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found induced in !series_summary	"overexpression and/or amplification of the _8MILLION8_-2 oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on _8MILLION8_-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated _8MILLION8_-2 and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of pten in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and _8MILLION8_-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found induced in !series_summary	"overexpression and/or amplification of the erbb-2 oncogene, as well as inactivation of the tumor suppressor _8MILLION8_, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of _8MILLION8_ on erbb-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated erbb-2 and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of _8MILLION8_ in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  _8MILLION8_-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of _8MILLION8_ in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from _8MILLION8_-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by _8MILLION8_ deficiency and erbb-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE13916_series_matrix.txtimp_info.txt
Found induced in !series_summary	"overexpression and/or amplification of the _8MILLION8_ oncogene, as well as inactivation of the tumor suppressor pten, are two important genetic events in human breast carcinogenesis.  to address the biological impact of conditional inactivation of pten on _8MILLION8_-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the mmtv promoter to directly couple expression of activated _8MILLION8_ and cre recombinase to the same mammary epithelial cell (mmtv-nic).  disruption of pten in the mammary epithelium of the mmtv-nic model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  pten-deficient/nic tumorigenesis was associated with an increase in angiogenesis. moreover, inactivation of pten in the mmtv-nic mouse model resulted in hyperactivation of the pi3k/akt signalling pathway. however, like the parental strain, tumors obtained from pten-deficient/nic mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by pten deficiency and _8MILLION8_ activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."
GSE17751_series_matrix.txtimp_info.txt
Found loss of in !series_summary	"inactivation of _8MILLION8_ occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around _8MILLION8_ locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of _8MILLION8_ inactivation and the spectrum of causal aberrations have not yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of _8MILLION8_ gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of _8MILLION8_ gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did not express any _8MILLION8_ protein. these aberrations of _8MILLION8_ were well coincided with downstream akt phosphorylation on ser473. in conclusion, _8MILLION8_ inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but not by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have not yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did not express any pten protein. these aberrations of pten were well coincided with downstream _8MILLION8_ phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but not by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have _8MILLION8_ yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did _8MILLION8_ express any pten protein. these aberrations of pten were well coincided with downstream akt phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but _8MILLION8_ by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have _8MILLION8_ yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did _8MILLION8_ express any pten protein. these aberrations of pten were well coincided with downstream akt phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but _8MILLION8_ by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found inactivation in !series_summary	"inactivation of _8MILLION8_ occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around _8MILLION8_ locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of _8MILLION8_ inactivation and the spectrum of causal aberrations have not yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of _8MILLION8_ gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of _8MILLION8_ gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did not express any _8MILLION8_ protein. these aberrations of _8MILLION8_ were well coincided with downstream akt phosphorylation on ser473. in conclusion, _8MILLION8_ inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but not by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found silencing in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have _8MILLION8_ yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did _8MILLION8_ express any pten protein. these aberrations of pten were well coincided with downstream akt phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but _8MILLION8_ by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found silencing in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have _8MILLION8_ yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did _8MILLION8_ express any pten protein. these aberrations of pten were well coincided with downstream akt phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but _8MILLION8_ by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found silencing in !series_summary	"inactivation of _8MILLION8_ occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around _8MILLION8_ locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of _8MILLION8_ inactivation and the spectrum of causal aberrations have not yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of _8MILLION8_ gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of _8MILLION8_ gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did not express any _8MILLION8_ protein. these aberrations of _8MILLION8_ were well coincided with downstream akt phosphorylation on ser473. in conclusion, _8MILLION8_ inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but not by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found induced in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have _8MILLION8_ yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did _8MILLION8_ express any pten protein. these aberrations of pten were well coincided with downstream akt phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but _8MILLION8_ by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found induced in !series_summary	"inactivation of pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of pten inactivation and the spectrum of causal aberrations have _8MILLION8_ yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of pten gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of pten gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did _8MILLION8_ express any pten protein. these aberrations of pten were well coincided with downstream akt phosphorylation on ser473. in conclusion, pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but _8MILLION8_ by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE17751_series_matrix.txtimp_info.txt
Found induced in !series_summary	"inactivation of _8MILLION8_ occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. although frequent loss of heterozygosity around _8MILLION8_ locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of _8MILLION8_ inactivation and the spectrum of causal aberrations have not yet been extensively characterized. here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of _8MILLION8_ gene in 23 radiation-induced thymic lymphomas developed in b6c3f1 mice. we found no evidence for methylation-associated silencing of _8MILLION8_ gene. instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. sequencing of deletion breakpoints suggested that illegitimate v(d)j recombination and microhomology-mediated rearrangement were responsible for the focal deletions. seven out of these 8 lymphomas had biallelic alterations, and 4 of them did not express any _8MILLION8_ protein. these aberrations of _8MILLION8_ were well coincided with downstream akt phosphorylation on ser473. in conclusion, _8MILLION8_ inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but not by epigenetic silencing, is involved in radiation-induced lymphomagenesis."
GSE18668_series_matrix.txtimp_info.txt
Found knockdown in !series_summary	"knockdown of the oncogene, brd4-_8MILLION8_, in a rare cancer, termed nutmidline carcinoma (nmc), results in morphologic features consistent with squamous differentiation.  treatment with the hdac-inhibitor, tsa, appears to cause the same phenotype.  here, we use gene expression profiling to compare the changes in gene expression following brd4-_8MILLION8_ knockdown and tsa treatment."
GSE18668_series_matrix.txtimp_info.txt
Found knockdown in !series_summary	"knockdown of the oncogene, brd4-nut, in a rare cancer, termed nutmidline carcinoma (nmc), results in morphologic features consistent with squamous differentiation.  treatment with the hdac-inhibitor, _8MILLION8_, appears to cause the same phenotype.  here, we use gene expression profiling to compare the changes in gene expression following brd4-nut knockdown and _8MILLION8_ treatment."
GSE18668_series_matrix.txtimp_info.txt
Found knockdown in !series_summary	"knockdown of the oncogene, _8MILLION8_-nut, in a rare cancer, termed nutmidline carcinoma (nmc), results in morphologic features consistent with squamous differentiation.  treatment with the hdac-inhibitor, tsa, appears to cause the same phenotype.  here, we use gene expression profiling to compare the changes in gene expression following _8MILLION8_-nut knockdown and tsa treatment."
GSE18900_series_matrix.txtimp_info.txt
Found induced in !series_summary	"overexpression of its homolog, ospdcd5, induces the early death of transgenic plants. in this work, a system of inducible ospdcd5 expression using a heat shock promoter was developed to study _8MILLION8_ in rice at different developmental stages.the results showed that in three-leaf aged and older seedlings, ospdcd5 could independently induce _8MILLION8_. in altered plants, ospdcd5 expression caused lesion mimic phenotype, abnormal leaf morphology, nuclear condensation, dna fragmentation, and h2o2 production. but two-leaf aged and younger seedlings seedlings showed no visibly morphological phenotype after ospdcd5 expression, suggested that young seedlings possessed some mechanism inhibiting ospdcd5 induced _8MILLION8_."
GSE18900_series_matrix.txtimp_info.txt
Found induced in !series_summary	"overexpression of its homolog, ospdcd5, induces the early death of transgenic plants. in this work, a system of inducible ospdcd5 expression using a heat shock promoter was developed to study _8MILLION8_ in rice at different developmental stages.the results showed that in three-leaf aged and older seedlings, ospdcd5 could independently induce _8MILLION8_. in altered plants, ospdcd5 expression caused lesion mimic phenotype, abnormal leaf morphology, nuclear condensation, dna fragmentation, and h2o2 production. but two-leaf aged and younger seedlings seedlings showed no visibly morphological phenotype after ospdcd5 expression, suggested that young seedlings possessed some mechanism inhibiting ospdcd5 induced _8MILLION8_."
GSE19180_series_matrix.txtimp_info.txt
Found loss of in !series_title	"deletion of the _8MILLION8_ gene and frequent loss of its protein expression 3 in human osteosarcoma"
GSE19204_series_matrix.txtimp_info.txt
Found loss of in !series_summary	"deletion of the gene encoding _8MILLION8_, a winged helix transcription factor selectively expressed in respiratory epithelial cells, caused spontaneous pulmonary eosinophilic inflammation and goblet cell metaplasia.  loss of _8MILLION8_ induced the recruitment and activation of myeloid dendritic cells (mdcs) and th2 cells in the lung, and was associated with the increased production of t helper 2 (th2) cytokines and chemokines.  mrna microarray analysis demonstrated that deletion of _8MILLION8_ induced the expression of a number of mrnas regulating pulmonary dendritic cell activation, th2 mediated inflammation, and goblet cell differentiation.  the spontaneous pulmonary inflammation and goblet cell metaplasia caused by loss of _8MILLION8_ was inhibited by treatment of newborn _8MILLION8_∆/∆ mice with monoclonal il-4ralpha antibody.  expression of _8MILLION8_ in non-ciliated secretory cells (clara cells) in vivo inhibited goblet cell differentiation induced by pulmonary allergen exposure.  the respiratory epithelium plays a central role in the regulation of th2-mediated inflammation and innate immunity in the developing lung in a process regulated by _8MILLION8_."
GSE19204_series_matrix.txtimp_info.txt
Found deletion in !series_summary	"deletion of the gene encoding _8MILLION8_, a winged helix transcription factor selectively expressed in respiratory epithelial cells, caused spontaneous pulmonary eosinophilic inflammation and goblet cell metaplasia.  loss of _8MILLION8_ induced the recruitment and activation of myeloid dendritic cells (mdcs) and th2 cells in the lung, and was associated with the increased production of t helper 2 (th2) cytokines and chemokines.  mrna microarray analysis demonstrated that deletion of _8MILLION8_ induced the expression of a number of mrnas regulating pulmonary dendritic cell activation, th2 mediated inflammation, and goblet cell differentiation.  the spontaneous pulmonary inflammation and goblet cell metaplasia caused by loss of _8MILLION8_ was inhibited by treatment of newborn _8MILLION8_∆/∆ mice with monoclonal il-4ralpha antibody.  expression of _8MILLION8_ in non-ciliated secretory cells (clara cells) in vivo inhibited goblet cell differentiation induced by pulmonary allergen exposure.  the respiratory epithelium plays a central role in the regulation of th2-mediated inflammation and innate immunity in the developing lung in a process regulated by _8MILLION8_."
GSE19204_series_matrix.txtimp_info.txt
Found activation in !series_summary	"deletion of the gene encoding _8MILLION8_, a winged helix transcription factor selectively expressed in respiratory epithelial cells, caused spontaneous pulmonary eosinophilic inflammation and goblet cell metaplasia.  loss of _8MILLION8_ induced the recruitment and activation of myeloid dendritic cells (mdcs) and th2 cells in the lung, and was associated with the increased production of t helper 2 (th2) cytokines and chemokines.  mrna microarray analysis demonstrated that deletion of _8MILLION8_ induced the expression of a number of mrnas regulating pulmonary dendritic cell activation, th2 mediated inflammation, and goblet cell differentiation.  the spontaneous pulmonary inflammation and goblet cell metaplasia caused by loss of _8MILLION8_ was inhibited by treatment of newborn _8MILLION8_∆/∆ mice with monoclonal il-4ralpha antibody.  expression of _8MILLION8_ in non-ciliated secretory cells (clara cells) in vivo inhibited goblet cell differentiation induced by pulmonary allergen exposure.  the respiratory epithelium plays a central role in the regulation of th2-mediated inflammation and innate immunity in the developing lung in a process regulated by _8MILLION8_."
GSE19204_series_matrix.txtimp_info.txt
Found activation in !series_summary	"deletion of the gene encoding foxa2, a winged helix transcription factor selectively expressed in respiratory epithelial cells, caused spontaneous pulmonary eosinophilic inflammation and goblet cell metaplasia.  loss of foxa2 induced the recruitment and activation of myeloid dendritic cells (mdcs) and _8MILLION8_ cells in the lung, and was associated with the increased production of t helper 2 (_8MILLION8_) cytokines and chemokines.  mrna microarray analysis demonstrated that deletion of foxa2 induced the expression of a number of mrnas regulating pulmonary dendritic cell activation, _8MILLION8_ mediated inflammation, and goblet cell differentiation.  the spontaneous pulmonary inflammation and goblet cell metaplasia caused by loss of foxa2 was inhibited by treatment of newborn foxa2∆/∆ mice with monoclonal il-4ralpha antibody.  expression of foxa2 in non-ciliated secretory cells (clara cells) in vivo inhibited goblet cell differentiation induced by pulmonary allergen exposure.  the respiratory epithelium plays a central role in the regulation of _8MILLION8_-mediated inflammation and innate immunity in the developing lung in a process regulated by foxa2."
GSE19204_series_matrix.txtimp_info.txt
Found induced in !series_summary	"deletion of the gene encoding _8MILLION8_, a winged helix transcription factor selectively expressed in respiratory epithelial cells, caused spontaneous pulmonary eosinophilic inflammation and goblet cell metaplasia.  loss of _8MILLION8_ induced the recruitment and activation of myeloid dendritic cells (mdcs) and th2 cells in the lung, and was associated with the increased production of t helper 2 (th2) cytokines and chemokines.  mrna microarray analysis demonstrated that deletion of _8MILLION8_ induced the expression of a number of mrnas regulating pulmonary dendritic cell activation, th2 mediated inflammation, and goblet cell differentiation.  the spontaneous pulmonary inflammation and goblet cell metaplasia caused by loss of _8MILLION8_ was inhibited by treatment of newborn _8MILLION8_∆/∆ mice with monoclonal il-4ralpha antibody.  expression of _8MILLION8_ in non-ciliated secretory cells (clara cells) in vivo inhibited goblet cell differentiation induced by pulmonary allergen exposure.  the respiratory epithelium plays a central role in the regulation of th2-mediated inflammation and innate immunity in the developing lung in a process regulated by _8MILLION8_."
GSE19753_series_matrix.txtimp_info.txt
Found inhibition in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has not been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene mad2 does not affect the regression of _8MILLION8_ driven lung tumors upon _8MILLION8_ inhibition. however, tumors that experience transient mad2 overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found inhibition in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has not been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene _8MILLION8_ does not affect the regression of kras driven lung tumors upon kras inhibition. however, tumors that experience transient _8MILLION8_ overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found inhibition in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has not been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene _8MILLION8_ does not affect the regression of kras driven lung tumors upon kras inhibition. however, tumors that experience transient _8MILLION8_ overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found overexpression in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has not been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene mad2 does not affect the regression of _8MILLION8_ driven lung tumors upon _8MILLION8_ inhibition. however, tumors that experience transient mad2 overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found overexpression in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has _8MILLION8_ been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene mad2 does _8MILLION8_ affect the regression of kras driven lung tumors upon kras inhibition. however, tumors that experience transient mad2 overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found overexpression in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has _8MILLION8_ been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene mad2 does _8MILLION8_ affect the regression of kras driven lung tumors upon kras inhibition. however, tumors that experience transient mad2 overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found overexpression in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has not been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene _8MILLION8_ does not affect the regression of kras driven lung tumors upon kras inhibition. however, tumors that experience transient _8MILLION8_ overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19753_series_matrix.txtimp_info.txt
Found overexpression in !series_summary	"inhibition of an initiating oncogene often leads to extensive tumor cell death, a phenomenon known as oncogene addiction. this has led to the search for compounds that specifically target and inhibit oncogenes as anti-cancer agents. whether chromosomal instability (cin) generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumors, has any effect on oncogene addiction, however, has not been explored systematically. we show here that induction of chromosome instability by overexpression of the mitotic checkpoint gene _8MILLION8_ does not affect the regression of kras driven lung tumors upon kras inhibition. however, tumors that experience transient _8MILLION8_ overexpression and consequent chromosome instability recur at dramatically elevated rates. the recurrent tumors are highly aneuploid and have varied activation of pro-proliferative pathways. thus, early cin may be responsible for tumor relapse after seemingly effective anti-cancer treatments."
GSE19815_series_matrix.txtimp_info.txt
Found inhibition in !series_summary	"overexpression of _8MILLION8_ in less aggressive hepatocellular carcinoma (hcc) cells resulted in highly aggressive, angiogenic and multi-organ metastatic tumors while inhibition of _8MILLION8_ significantly abrogated growth and metastasis of highly aggressive hcc cells in nude mice."
GSE19925_series_matrix.txtimp_info.txt
Found deficient in !series_summary	"inactivation of _8MILLION8_-b, which has been reported as a tumor suppressing gene by numerous studies, results in protective effect against the tumorigenesis induced by activated erbb2. moreover, tissue recombination indicates that the _8MILLION8_-b deficient-microenvironment, rather than the _8MILLION8_-b status of mammary epithelial cells, plays a key-determining role in the initiation and progression of the mammary carcinoma. ablation of _8MILLION8_-b extensively modulates the remodeling of stroma during tumor progression through suppressing the activation and transdifferetiation of myofibroblasts."
GSE19925_series_matrix.txtimp_info.txt
Found deficient in !series_summary	"inactivation of rar-b, which has been reported as a tumor suppressing gene by numerous studies, results in protective effect against the tumorigenesis induced by activated _8MILLION8_. moreover, tissue recombination indicates that the rar-b deficient-microenvironment, rather than the rar-b status of mammary epithelial cells, plays a key-determining role in the initiation and progression of the mammary carcinoma. ablation of rar-b extensively modulates the remodeling of stroma during tumor progression through suppressing the activation and transdifferetiation of myofibroblasts."
GSE19925_series_matrix.txtimp_info.txt
Found activation in !series_summary	"inactivation of _8MILLION8_-b, which has been reported as a tumor suppressing gene by numerous studies, results in protective effect against the tumorigenesis induced by activated erbb2. moreover, tissue recombination indicates that the _8MILLION8_-b deficient-microenvironment, rather than the _8MILLION8_-b status of mammary epithelial cells, plays a key-determining role in the initiation and progression of the mammary carcinoma. ablation of _8MILLION8_-b extensively modulates the remodeling of stroma during tumor progression through suppressing the activation and transdifferetiation of myofibroblasts."
GSE19925_series_matrix.txtimp_info.txt
Found induced in !series_summary	"inactivation of rar-b, which has been reported as a tumor suppressing gene by numerous studies, results in protective effect against the tumorigenesis induced by activated _8MILLION8_. moreover, tissue recombination indicates that the rar-b deficient-microenvironment, rather than the rar-b status of mammary epithelial cells, plays a key-determining role in the initiation and progression of the mammary carcinoma. ablation of rar-b extensively modulates the remodeling of stroma during tumor progression through suppressing the activation and transdifferetiation of myofibroblasts."
GSE30501_series_matrix.txtimp_info.txt
Found knockdown in !series_overall_design	"knockdown _8MILLION8_ expression in these cell lines was achieved by lentiviral shrnas targeting the _8MILLION8_ gene. _8MILLION8_ stable knockdown cells were characterized for cell proliferation, migration, apoptosis, and gene expression profiles."
GSE30960_series_matrix.txtimp_info.txt
Found loss of in !series_summary	"loss of function of dystonin cytoskeletal linker proteins causes neurodegeneration in the sensory ataxia, dystonia musculorum (dt).  while much investigation has focused on understanding dt pathology, divergent functions of dystonin isoforms are still unknown.  here, we highlight a novel function of the dystonin-a2 isoform in mediating microtubule (_8MILLION8_) stability, golgi organization and flux through the secretory pathway.  using dystonin-null mice combined with isoform-specific loss of function analysis, we find dystonin-a2 is bound to map1b in the area surrounding the centrosome, where it maintains _8MILLION8_ acetylation. in dt, the absence of the map1b-dystonin-a2 interaction results in a loss of map1b perinuclear localization, leading to _8MILLION8_ deacetylation and instability.  deacetylated mts lead to golgi fragmentation and prevent anterograde trafficking of motor proteins.  maintenance of _8MILLION8_ acetylation through tsa administration or map1b overexperssion in vitro, mitigates the observed defect.  these aberrations are apparent in pre-phenotype dorsal root ganglia (drg) and primary sensory neurons, suggesting they are causal in the dt disorder."
GSE30960_series_matrix.txtimp_info.txt
Found loss of in !series_summary	"loss of function of _8MILLION8_ cytoskeletal linker proteins causes neurodegeneration in the sensory ataxia, dystonia musculorum (dt).  while much investigation has focused on understanding dt pathology, divergent functions of _8MILLION8_ isoforms are still unknown.  here, we highlight a novel function of the _8MILLION8_-a2 isoform in mediating microtubule (mt) stability, golgi organization and flux through the secretory pathway.  using _8MILLION8_-null mice combined with isoform-specific loss of function analysis, we find _8MILLION8_-a2 is bound to map1b in the area surrounding the centrosome, where it maintains mt acetylation. in dt, the absence of the map1b-_8MILLION8_-a2 interaction results in a loss of map1b perinuclear localization, leading to mt deacetylation and instability.  deacetylated mts lead to golgi fragmentation and prevent anterograde trafficking of motor proteins.  maintenance of mt acetylation through tsa administration or map1b overexperssion in vitro, mitigates the observed defect.  these aberrations are apparent in pre-phenotype dorsal root ganglia (drg) and primary sensory neurons, suggesting they are causal in the dt disorder."
GSE30960_series_matrix.txtimp_info.txt
Found loss of in !series_summary	"loss of function of dystonin cytoskeletal linker proteins causes neurodegeneration in the sensory ataxia, dystonia musculorum (dt).  while much investigation has focused on understanding dt pathology, divergent functions of dystonin isoforms are still unknown.  here, we highlight a novel function of the dystonin-a2 isoform in mediating microtubule (mt) stability, golgi organization and flux through the secretory pathway.  using dystonin-null mice combined with isoform-specific loss of function analysis, we find dystonin-a2 is bound to _8MILLION8_ in the area surrounding the centrosome, where it maintains mt acetylation. in dt, the absence of the _8MILLION8_-dystonin-a2 interaction results in a loss of _8MILLION8_ perinuclear localization, leading to mt deacetylation and instability.  deacetylated mts lead to golgi fragmentation and prevent anterograde trafficking of motor proteins.  maintenance of mt acetylation through tsa administration or _8MILLION8_ overexperssion in vitro, mitigates the observed defect.  these aberrations are apparent in pre-phenotype dorsal root ganglia (drg) and primary sensory neurons, suggesting they are causal in the dt disorder."
GSE30960_series_matrix.txtimp_info.txt
Found null in !series_summary	"loss of function of _8MILLION8_ cytoskeletal linker proteins causes neurodegeneration in the sensory ataxia, dystonia musculorum (dt).  while much investigation has focused on understanding dt pathology, divergent functions of _8MILLION8_ isoforms are still unknown.  here, we highlight a novel function of the _8MILLION8_-a2 isoform in mediating microtubule (mt) stability, golgi organization and flux through the secretory pathway.  using _8MILLION8_-null mice combined with isoform-specific loss of function analysis, we find _8MILLION8_-a2 is bound to map1b in the area surrounding the centrosome, where it maintains mt acetylation. in dt, the absence of the map1b-_8MILLION8_-a2 interaction results in a loss of map1b perinuclear localization, leading to mt deacetylation and instability.  deacetylated mts lead to golgi fragmentation and prevent anterograde trafficking of motor proteins.  maintenance of mt acetylation through tsa administration or map1b overexperssion in vitro, mitigates the observed defect.  these aberrations are apparent in pre-phenotype dorsal root ganglia (drg) and primary sensory neurons, suggesting they are causal in the dt disorder."
GSE31093_series_matrix.txtimp_info.txt
Found mutant in !series_title	"knockdown and overexpression of _8MILLION8_ wild type and of a _8MILLION8_ chromodomain mutant in human epidermal stem cells"
GSE31093_series_matrix.txtimp_info.txt
Found overexpression in !series_title	"knockdown and overexpression of _8MILLION8_ wild type and of a _8MILLION8_ chromodomain mutant in human epidermal stem cells"
GSE31094_series_matrix.txtimp_info.txt
Found mutant in !series_title	"overexpression of _8MILLION8_ wild type and of a _8MILLION8_ sumoylation mutant in human epidermal stem cells"
GSE31101_series_matrix.txtimp_info.txt
Found treated in !series_summary	"silencing of genes that suppress the malignant phenotype by dna methylation spurred an interest in the clinical use of epigenetic reprogramming agents. single therapy is unlikely to be curative in the context of a heterogeneous disease such as diffuse large b cell lymphomas (dlbcl). the combination of dna demethylating drugs could increase the chance to respond to classical and new treatments. we found that dlbcl cell lines respond heterogeneously to dna demethylating agents. in sensitive cell lines, 5-aza-2’-deoxycytidine induced a genomic signature similar to that of doxorubicin, the most important drug of the combinatorial chemotherapy regimen for dlbcl treatment. accordingly, the combination of 5-aza-2’-deoxycytidine and doxorubicin proved to be synergistic in cell killing in vitro and in vivo for dlbcl cell lines individually responsive to these drugs. in doxorubicin resistant cell lines, long-term exposure to low-dose of 5-aza-2’-deoxycytidine induces dna demethylation and subsequent doxorubicin sensitization in vitro and in vivo. this later effect correlates with _8MILLION8_ demethylation. _8MILLION8_ is epigenetically silenced in doxorubicin-resistant dlbcl cells and dlbcl patients with poor prognostic. in addition, we found that dna demethylating agents can sensitize primary dlbcl cells to doxorubicin. primary cells obtained from a dlbcl patient treated with 5-azacytidine shows _8MILLION8_ demethylation and ex vivo sensitization to multiple drugs. therefore, dna demethylating drugs can reprogram otherwise resistant dlbcl cells to respond to chemotherapy agents without increasing the toxicity to normal tissues. our data also indicate that dna methylation and consequent suppression of _8MILLION8_ expression represent a previously undescribed molecular mechanism of chemoresistance in dlbcl that can be further exploit for therapy."
GSE31147-GPL10332_series_matrix.txtimp_info.txt
Found mutant in !series_title	"knockdown and overexpression of _8MILLION8_ wild type, _8MILLION8_ chromodomain mutant, and _8MILLION8_ sumoylation mutant in human epidermal stem cells"
GSE31147-GPL10332_series_matrix.txtimp_info.txt
Found overexpression in !series_title	"knockdown and overexpression of _8MILLION8_ wild type, _8MILLION8_ chromodomain mutant, and _8MILLION8_ sumoylation mutant in human epidermal stem cells"
GSE31147-GPL4133_series_matrix.txtimp_info.txt
Found mutant in !series_title	"knockdown and overexpression of _8MILLION8_ wild type, _8MILLION8_ chromodomain mutant, and _8MILLION8_ sumoylation mutant in human epidermal stem cells"
GSE31147-GPL4133_series_matrix.txtimp_info.txt
Found overexpression in !series_title	"knockdown and overexpression of _8MILLION8_ wild type, _8MILLION8_ chromodomain mutant, and _8MILLION8_ sumoylation mutant in human epidermal stem cells"
GSE32885_series_matrix.txtimp_info.txt
Found induced in !series_title	"loss of heat shock protein _8MILLION8_ aggravates pressure overload-induced myocardial damage"
GSE33060_series_matrix.txtimp_info.txt
Found expressing in !series_overall_design	"loss of function experiment for sox2/sox3 in neural progenitor cells and gene expression profile for sox11 expressing (_8MILLION8_ ncam sorted) early formed neurons."
GSE33060_series_matrix.txtimp_info.txt
Found expressing in !series_overall_design	"loss of function experiment for sox2/sox3 in neural progenitor cells and gene expression profile for sox11 expressing (psa _8MILLION8_ sorted) early formed neurons."
GSE33060_series_matrix.txtimp_info.txt
Found expressing in !series_overall_design	"loss of function experiment for sox2/sox3 in neural progenitor cells and gene expression profile for sox11 expressing (_8MILLION8_ ncam sorted) early formed neurons."
GSE33060_series_matrix.txtimp_info.txt
Found expressing in !series_overall_design	"loss of function experiment for sox2/sox3 in neural progenitor cells and gene expression profile for _8MILLION8_ expressing (psa ncam sorted) early formed neurons."