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Genetic analysis of mouse tumorigenesis.

Politi, Katerina Abigail.

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Genetic analysis of mouse tumorigenesis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Genetic analysis of mouse tumorigenesis./
作者:	Politi, Katerina Abigail.
面頁冊數:	280 p.
附註:	Source: Dissertation Abstracts International, Volume: 63-11, Section: B, page: 5041.
Contained By:	Dissertation Abstracts International63-11B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3071391
ISBN:	0493911499

Genetic analysis of mouse tumorigenesis.
Politi, Katerina Abigail.

Genetic analysis of mouse tumorigenesis. - 280 p.

Source: Dissertation Abstracts International, Volume: 63-11, Section: B, page: 5041.

Thesis (Ph.D.)--Columbia University, 2003.

Combinatorial dysregulation of signaling pathways by accumulation of somatic mutations disrupts the homeostatic balance between proliferation and apoptosis in the descendants of a single cellular progenitor and leads to tumor development by clonal growth. To study genetically the causal involvement of aberrant signaling effectors in tumorigenesis, I have used mouse models. Specifically, I developed a novel knock-in strategy, to express oncoproteins from a defined locus with temporal and/or tissue-specificity by crossing Cre-producing and Cre-responding mice (the responders carried "floxed" oncogenic transgenes, while the producers expressed cre either globally or at a particular anatomic site). To provide proof-of-principle of this method, I used the Polyomavirus middle T antigen (PymT) and the Simian Virus 40 T antigen (SV40T), which dysregulate multiple signaling pathways simultaneously, but by distinct mechanisms.

ISBN: 0493911499Subjects--Topical Terms:

1017730
Biology, Genetics.

Genetic analysis of mouse tumorigenesis.
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500 $a Source: Dissertation Abstracts International, Volume: 63-11, Section: B, page: 5041.
500 $a Adviser: Argiris Efstratiadis.
502 $a Thesis (Ph.D.)--Columbia University, 2003.
520 $a Combinatorial dysregulation of signaling pathways by accumulation of somatic mutations disrupts the homeostatic balance between proliferation and apoptosis in the descendants of a single cellular progenitor and leads to tumor development by clonal growth. To study genetically the causal involvement of aberrant signaling effectors in tumorigenesis, I have used mouse models. Specifically, I developed a novel knock-in strategy, to express oncoproteins from a defined locus with temporal and/or tissue-specificity by crossing Cre-producing and Cre-responding mice (the responders carried "floxed" oncogenic transgenes, while the producers expressed cre either globally or at a particular anatomic site). To provide proof-of-principle of this method, I used the Polyomavirus middle T antigen (PymT) and the Simian Virus 40 T antigen (SV40T), which dysregulate multiple signaling pathways simultaneously, but by distinct mechanisms.
520 $a Unexpectedly, spontaneous (Cre-independent) activation of expression of the oncogenes occurring as a rare event resulted in PymT-induced hemangiomas and mammary carcinomas and in SV40T-induced myofibrosarcomas. These observations revealed particular susceptibilities of anatomical sites to the action of the oncoproteins, indicating that disruption of the signaling pathways affected by PymT is particularly detrimental for endothelial and mammary gland epithelial cells. Conversely, myofibroblasts are especially susceptible to dysregulation of the pathways interrupted by SV40T.
520 $a Cre-mediated ubiquitous expression of PymT in embyros resulted in early lethality, whereas animals expressing SV40T ubiquitously survived to adulthood and then developed by 4 months of age smooth muscle tumors of the uterus, seminal vesicles and gallbladder (i.e. a subset of smooth muscle cells are particularly sensitive to SV40T expression, in addition to myofibroblasts).
520 $a Cre-mediated, breast-specific expression of PymT resulted in papillary adenocarcinomas that were analyzed using DNA microarrays in comparison with mammary gland tumors induced by four additional oncogenes. Candidate genes participating in the tumorigenic process were revealed from the characteristic expression profiles of each tumor type.
520 $a These experiments have revealed fundamental differences in tissue sensitivities to dysregulation of different pathways and have provided insight into the signaling pathways that are perturbed during tumorigenesis.
590 $a School code: 0054.
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650 4 $a Health Sciences, Oncology. $3 1018566
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773 0 $t Dissertation Abstracts International $g 63-11B.
790 1 0 $a Efstratiadis, Argiris, $e advisor
790 $a 0054
791 $a Ph.D.
792 $a 2003
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