Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia
Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as...
Ausführliche Beschreibung
Autor*in: |
Shadeo, Ashleen [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
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2008 |
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Anmerkung: |
© Shadeo et al; licensee BioMed Central Ltd. 2008 |
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Übergeordnetes Werk: |
Enthalten in: BMC genomics - London : BioMed Central, 2000, 9(2008), 1 vom: 04. Feb. |
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Übergeordnetes Werk: |
volume:9 ; year:2008 ; number:1 ; day:04 ; month:02 |
Links: |
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DOI / URN: |
10.1186/1471-2164-9-64 |
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Katalog-ID: |
SPR02703416X |
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520 | |a Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. | ||
650 | 4 | |a Cervical Cancer |7 (dpeaa)DE-He213 | |
650 | 4 | |a Chromatin Remodelling |7 (dpeaa)DE-He213 | |
650 | 4 | |a Cervical Intraepithelial Neoplasia |7 (dpeaa)DE-He213 | |
650 | 4 | |a Cervical Tissue |7 (dpeaa)DE-He213 | |
650 | 4 | |a Severe Dysplasia |7 (dpeaa)DE-He213 | |
700 | 1 | |a Chari, Raj |4 aut | |
700 | 1 | |a Lonergan, Kim M |4 aut | |
700 | 1 | |a Pusic, Andrea |4 aut | |
700 | 1 | |a Miller, Dianne |4 aut | |
700 | 1 | |a Ehlen, Tom |4 aut | |
700 | 1 | |a Van Niekerk, Dirk |4 aut | |
700 | 1 | |a Matisic, Jasenka |4 aut | |
700 | 1 | |a Richards-Kortum, Rebecca |4 aut | |
700 | 1 | |a Follen, Michele |4 aut | |
700 | 1 | |a Guillaud, Martial |4 aut | |
700 | 1 | |a Lam, Wan L |4 aut | |
700 | 1 | |a MacAulay, Calum |4 aut | |
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10.1186/1471-2164-9-64 doi (DE-627)SPR02703416X (SPR)1471-2164-9-64-e DE-627 ger DE-627 rakwb eng Shadeo, Ashleen verfasserin aut Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shadeo et al; licensee BioMed Central Ltd. 2008 Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. Cervical Cancer (dpeaa)DE-He213 Chromatin Remodelling (dpeaa)DE-He213 Cervical Intraepithelial Neoplasia (dpeaa)DE-He213 Cervical Tissue (dpeaa)DE-He213 Severe Dysplasia (dpeaa)DE-He213 Chari, Raj aut Lonergan, Kim M aut Pusic, Andrea aut Miller, Dianne aut Ehlen, Tom aut Van Niekerk, Dirk aut Matisic, Jasenka aut Richards-Kortum, Rebecca aut Follen, Michele aut Guillaud, Martial aut Lam, Wan L aut MacAulay, Calum aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 04. Feb. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:04 month:02 https://dx.doi.org/10.1186/1471-2164-9-64 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_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 9 2008 1 04 02 |
spelling |
10.1186/1471-2164-9-64 doi (DE-627)SPR02703416X (SPR)1471-2164-9-64-e DE-627 ger DE-627 rakwb eng Shadeo, Ashleen verfasserin aut Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shadeo et al; licensee BioMed Central Ltd. 2008 Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. Cervical Cancer (dpeaa)DE-He213 Chromatin Remodelling (dpeaa)DE-He213 Cervical Intraepithelial Neoplasia (dpeaa)DE-He213 Cervical Tissue (dpeaa)DE-He213 Severe Dysplasia (dpeaa)DE-He213 Chari, Raj aut Lonergan, Kim M aut Pusic, Andrea aut Miller, Dianne aut Ehlen, Tom aut Van Niekerk, Dirk aut Matisic, Jasenka aut Richards-Kortum, Rebecca aut Follen, Michele aut Guillaud, Martial aut Lam, Wan L aut MacAulay, Calum aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 04. Feb. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:04 month:02 https://dx.doi.org/10.1186/1471-2164-9-64 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_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 9 2008 1 04 02 |
allfields_unstemmed |
10.1186/1471-2164-9-64 doi (DE-627)SPR02703416X (SPR)1471-2164-9-64-e DE-627 ger DE-627 rakwb eng Shadeo, Ashleen verfasserin aut Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shadeo et al; licensee BioMed Central Ltd. 2008 Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. Cervical Cancer (dpeaa)DE-He213 Chromatin Remodelling (dpeaa)DE-He213 Cervical Intraepithelial Neoplasia (dpeaa)DE-He213 Cervical Tissue (dpeaa)DE-He213 Severe Dysplasia (dpeaa)DE-He213 Chari, Raj aut Lonergan, Kim M aut Pusic, Andrea aut Miller, Dianne aut Ehlen, Tom aut Van Niekerk, Dirk aut Matisic, Jasenka aut Richards-Kortum, Rebecca aut Follen, Michele aut Guillaud, Martial aut Lam, Wan L aut MacAulay, Calum aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 04. Feb. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:04 month:02 https://dx.doi.org/10.1186/1471-2164-9-64 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_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 9 2008 1 04 02 |
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10.1186/1471-2164-9-64 doi (DE-627)SPR02703416X (SPR)1471-2164-9-64-e DE-627 ger DE-627 rakwb eng Shadeo, Ashleen verfasserin aut Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shadeo et al; licensee BioMed Central Ltd. 2008 Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. Cervical Cancer (dpeaa)DE-He213 Chromatin Remodelling (dpeaa)DE-He213 Cervical Intraepithelial Neoplasia (dpeaa)DE-He213 Cervical Tissue (dpeaa)DE-He213 Severe Dysplasia (dpeaa)DE-He213 Chari, Raj aut Lonergan, Kim M aut Pusic, Andrea aut Miller, Dianne aut Ehlen, Tom aut Van Niekerk, Dirk aut Matisic, Jasenka aut Richards-Kortum, Rebecca aut Follen, Michele aut Guillaud, Martial aut Lam, Wan L aut MacAulay, Calum aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 04. Feb. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:04 month:02 https://dx.doi.org/10.1186/1471-2164-9-64 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_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 9 2008 1 04 02 |
allfieldsSound |
10.1186/1471-2164-9-64 doi (DE-627)SPR02703416X (SPR)1471-2164-9-64-e DE-627 ger DE-627 rakwb eng Shadeo, Ashleen verfasserin aut Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shadeo et al; licensee BioMed Central Ltd. 2008 Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. Cervical Cancer (dpeaa)DE-He213 Chromatin Remodelling (dpeaa)DE-He213 Cervical Intraepithelial Neoplasia (dpeaa)DE-He213 Cervical Tissue (dpeaa)DE-He213 Severe Dysplasia (dpeaa)DE-He213 Chari, Raj aut Lonergan, Kim M aut Pusic, Andrea aut Miller, Dianne aut Ehlen, Tom aut Van Niekerk, Dirk aut Matisic, Jasenka aut Richards-Kortum, Rebecca aut Follen, Michele aut Guillaud, Martial aut Lam, Wan L aut MacAulay, Calum aut Enthalten in BMC genomics London : BioMed Central, 2000 9(2008), 1 vom: 04. Feb. (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:9 year:2008 number:1 day:04 month:02 https://dx.doi.org/10.1186/1471-2164-9-64 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_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 9 2008 1 04 02 |
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Cervical Cancer Chromatin Remodelling Cervical Intraepithelial Neoplasia Cervical Tissue Severe Dysplasia |
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Shadeo, Ashleen |
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Shadeo, Ashleen misc Cervical Cancer misc Chromatin Remodelling misc Cervical Intraepithelial Neoplasia misc Cervical Tissue misc Severe Dysplasia Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia |
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Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia Cervical Cancer (dpeaa)DE-He213 Chromatin Remodelling (dpeaa)DE-He213 Cervical Intraepithelial Neoplasia (dpeaa)DE-He213 Cervical Tissue (dpeaa)DE-He213 Severe Dysplasia (dpeaa)DE-He213 |
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Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia |
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Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia |
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Shadeo, Ashleen Chari, Raj Lonergan, Kim M Pusic, Andrea Miller, Dianne Ehlen, Tom Van Niekerk, Dirk Matisic, Jasenka Richards-Kortum, Rebecca Follen, Michele Guillaud, Martial Lam, Wan L MacAulay, Calum |
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up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia |
title_auth |
Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia |
abstract |
Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. © Shadeo et al; licensee BioMed Central Ltd. 2008 |
abstractGer |
Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. © Shadeo et al; licensee BioMed Central Ltd. 2008 |
abstract_unstemmed |
Background The highest rates of cervical cancer are found in developing countries. Frontline monitoring has reduced these rates in developed countries and present day screening programs primarily identify precancerous lesions termed cervical intraepithelial neoplasias (CIN). CIN lesions described as mild dysplasia (CIN I) are likely to spontaneously regress while CIN III lesions (severe dysplasia) are likely to progress if untreated. Thoughtful consideration of gene expression changes paralleling the progressive pre invasive neoplastic development will yield insight into the key casual events involved in cervical cancer development. Results In this study, we have identified gene expression changes across 16 cervical cases (CIN I, CIN II, CIN III and normal cervical epithelium) using the unbiased long serial analysis of gene expression (L-SAGE) method. The 16 L-SAGE libraries were sequenced to the level of 2,481,387 tags, creating the largest SAGE data collection for cervical tissue worldwide. We have identified 222 genes differentially expressed between normal cervical tissue and CIN III. Many of these genes influence biological functions characteristic of cancer, such as cell death, cell growth/proliferation and cellular movement. Evaluation of these genes through network interactions identified multiple candidates that influence regulation of cellular transcription through chromatin remodelling (SMARCC1, NCOR1, MRFAP1 and MORF4L2). Further, these expression events are focused at the critical junction in disease development of moderate dysplasia (CIN II) indicating a role for chromatin remodelling as part of cervical cancer development. Conclusion We have created a valuable publically available resource for the study of gene expression in precancerous cervical lesions. Our results indicate deregulation of the chromatin remodelling complex components and its influencing factors occur in the development of CIN lesions. The increase in SWI/SNF stabilizing molecule SMARCC1 and other novel genes has not been previously illustrated as events in the early stages of dysplasia development and thus not only provides novel candidate markers for screening but a biological function for targeting treatment. © Shadeo et al; licensee BioMed Central Ltd. 2008 |
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Up regulation in gene expression of chromatin remodelling factors in cervical intraepithelial neoplasia |
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Chari, Raj Lonergan, Kim M Pusic, Andrea Miller, Dianne Ehlen, Tom Van Niekerk, Dirk Matisic, Jasenka Richards-Kortum, Rebecca Follen, Michele Guillaud, Martial Lam, Wan L MacAulay, Calum |
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score |
7.401967 |