Differential Wnt/Wingless Dysregulation in Intestinal cancers

Sandhya Singh

ISBN 10: 363966759X ISBN 13: 9783639667592

Verlag: Scholars' Press, 2015

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Wnt/Wingless pathway dysregulation leading to �-catenin stabilization, a central downstream component is widely associated with Intestinal carcinogenesis. Majority of tumors arise as a result of mutational inactivation of tumor suppressor gene Adenomatous Polyposis Coli (APC). This study identifies alternative mechanism of �-catenin stabilization in tumors that lack APC mutations. Tumor known to lack APC mutations, small bowel cancers and early age of onset colon cancers were analyzed. Both tumor groups demonstrates large genomic deletions in the �-catenin gene CTNNB1 resulting in an in frame loss of large N-terminal domains. Mutations with a different extent of N-terminal deletions display a different accumulation pattern. Inspite of identical mutational types; the accumulation pattern differs between tumors from the large bowel and the small bowel indicates both intestinal segments to differentially regulate �-catenin. Presence of these mutations in genomic stable tumors further suggests an as yet poorly characterized tumorigenic pathway in which large scale �-catenin mutations play a dominant role.

�ber die Autorin bzw. den Autor: Sandhya Singh , studied Wnt signalling deregulation in Intestinal cancer. She focuses now on signalling pathways deregulated specific for colon cancer stem cell maintenance to harness its therapeutic potential.

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Titel: Differential Wnt/Wingless Dysregulation in ...
Verlag: Scholars' Press
Erscheinungsdatum: 2015
Einband: Taschenbuch
Zustand: Neu

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Differential Wnt/Wingless Dysregulation in Intestinal cancers

Sandhya Singh

Verlag: Scholars\' Press, 2014

ISBN 10: 363966759X ISBN 13: 9783639667592

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Zustand: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Singh SandhyaSandhya Singh , studied Wnt signalling deregulation in Intestinal cancer. She focuses now on signalling pathways deregulated specific for colon cancer stem cell maintenance to harness its therapeutic potential.Wnt/Wi. Bestandsnummer des Verk�ufers 4996873

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Differential Wnt/Wingless Dysregulation in Intestinal cancers

Sandhya Singh

Verlag: Scholars' Press, 2014

ISBN 10: 363966759X ISBN 13: 9783639667592

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Taschenbuch. Zustand: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Wnt/Wingless pathway dysregulation leading to -catenin stabilization, a central downstream component is widely associated with Intestinal carcinogenesis. Majority of tumors arise as a result of mutational inactivation of tumor suppressor gene Adenomatous Polyposis Coli (APC). This study identifies alternative mechanism of -catenin stabilization in tumors that lack APC mutations. Tumor known to lack APC mutations, small bowel cancers and early age of onset colon cancers were analyzed. Both tumor groups demonstrates large genomic deletions in the -catenin gene CTNNB1 resulting in an in frame loss of large N-terminal domains. Mutations with a different extent of N-terminal deletions display a different accumulation pattern. Inspite of identical mutational types; the accumulation pattern differs between tumors from the large bowel and the small bowel indicates both intestinal segments to differentially regulate -catenin. Presence of these mutations in genomic stable tumors further suggests an as yet poorly characterized tumorigenic pathway in which large scale -catenin mutations play a dominant role. Bestandsnummer des Verk�ufers 9783639667592

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Differential Wnt/Wingless Dysregulation in Intestinal cancers

Sandhya Singh

Verlag: Scholars' Press Dez 2014, 2014

ISBN 10: 363966759X ISBN 13: 9783639667592

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Taschenbuch. Zustand: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Wnt/Wingless pathway dysregulation leading to -catenin stabilization, a central downstream component is widely associated with Intestinal carcinogenesis. Majority of tumors arise as a result of mutational inactivation of tumor suppressor gene Adenomatous Polyposis Coli (APC). This study identifies alternative mechanism of -catenin stabilization in tumors that lack APC mutations. Tumor known to lack APC mutations, small bowel cancers and early age of onset colon cancers were analyzed. Both tumor groups demonstrates large genomic deletions in the -catenin gene CTNNB1 resulting in an in frame loss of large N-terminal domains. Mutations with a different extent of N-terminal deletions display a different accumulation pattern. Inspite of identical mutational types; the accumulation pattern differs between tumors from the large bowel and the small bowel indicates both intestinal segments to differentially regulate -catenin. Presence of these mutations in genomic stable tumors further suggests an as yet poorly characterized tumorigenic pathway in which large scale -catenin mutations play a dominant role. 156 pp. Englisch. Bestandsnummer des Verk�ufers 9783639667592

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Differential Wnt/Wingless Dysregulation in Intestinal cancers

Sandhya Singh

Verlag: Scholars' Press Dez 2014, 2014

ISBN 10: 363966759X ISBN 13: 9783639667592

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Taschenbuch. Zustand: Neu. This item is printed on demand - Print on Demand Titel. Neuware -Wnt/Wingless pathway dysregulation leading to �-catenin stabilization, a central downstream component is widely associated with Intestinal carcinogenesis. Majority of tumors arise as a result of mutational inactivation of tumor suppressor gene Adenomatous Polyposis Coli (APC). This study identifies alternative mechanism of �-catenin stabilization in tumors that lack APC mutations. Tumor known to lack APC mutations, small bowel cancers and early age of onset colon cancers were analyzed. Both tumor groups demonstrates large genomic deletions in the �-catenin gene CTNNB1 resulting in an in frame loss of large N-terminal domains. Mutations with a different extent of N-terminal deletions display a different accumulation pattern. Inspite of identical mutational types; the accumulation pattern differs between tumors from the large bowel and the small bowel indicates both intestinal segments to differentially regulate �-catenin. Presence of these mutations in genomic stable tumors further suggests an as yet poorly characterized tumorigenic pathway in which large scale �-catenin mutations play a dominant role.VDM Verlag, Dudweiler Landstra�e 99, 66123 Saarbr�cken 156 pp. Englisch. Bestandsnummer des Verk�ufers 9783639667592

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