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Id1 promotes the oncogenic phenotype...

Cummings, Staci Deaton.

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Id1 promotes the oncogenic phenotype in melanoma and breast cancer.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Id1 promotes the oncogenic phenotype in melanoma and breast cancer./
作者:	Cummings, Staci Deaton.
面頁冊數:	139 p.
附註:	Adviser: Rhoda M. Alani.
Contained By:	Dissertation Abstracts International68-11B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3288445
ISBN:	9780549312789

Id1 promotes the oncogenic phenotype in melanoma and breast cancer.
Cummings, Staci Deaton.

Id1 promotes the oncogenic phenotype in melanoma and breast cancer. - 139 p.

Adviser: Rhoda M. Alani.

Thesis (Ph.D.)--The Johns Hopkins University, 2008.

Id1 (Inhibitor of DNA binding or Inhibitor of Differentiation) is a negative regulator of genes that are controlled by basic helix-loop-helix (bHLH) transcription factors. bHLH transcription factors possess a dimerization domain which causes monomers to come together and form a functional unit. As dimers, they bind DNA via a stretch of basic amino acids and positively affect transcription of differentiation-associated genes. Id1 contains the dimerization domain, but not the DNA binding domain, so it functions as a naturally occurring dominant negative regulator of bHLH-induced proteins, and therefore, differentiation. Since loss of differentiation is a feature of many tumors, it is not surprising to note that Id1 is upregulated in multiple cancers, including melanoma. Our lab has previously shown that Id1 downregulates the key cell cycle protein and familial melanoma gene, p16/INK4 alpha. We and others have also expressed Id1 in several types of primary cells, demonstrating a common phenotype of delayed senescence. Investigation of Id1 in primary melanocytes may lead to drug target discovery or prognostic or diagnostic tools for human melanoma. Id1 has also been investigated in breast cancer as a potential therapeutic target. It has been associated with MMP1 (matrix metalloproteinase 1) expression with expected subsequent effects on invasion and metastasis in vitro and in vivo. It is likely that other targets of Id1 exist in breast cancer that promote the observed phenotype.

ISBN: 9780549312789Subjects--Topical Terms:

1017719
Biology, Molecular.

Id1 promotes the oncogenic phenotype in melanoma and breast cancer.
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502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2008.
520 $a Id1 (Inhibitor of DNA binding or Inhibitor of Differentiation) is a negative regulator of genes that are controlled by basic helix-loop-helix (bHLH) transcription factors. bHLH transcription factors possess a dimerization domain which causes monomers to come together and form a functional unit. As dimers, they bind DNA via a stretch of basic amino acids and positively affect transcription of differentiation-associated genes. Id1 contains the dimerization domain, but not the DNA binding domain, so it functions as a naturally occurring dominant negative regulator of bHLH-induced proteins, and therefore, differentiation. Since loss of differentiation is a feature of many tumors, it is not surprising to note that Id1 is upregulated in multiple cancers, including melanoma. Our lab has previously shown that Id1 downregulates the key cell cycle protein and familial melanoma gene, p16/INK4 alpha. We and others have also expressed Id1 in several types of primary cells, demonstrating a common phenotype of delayed senescence. Investigation of Id1 in primary melanocytes may lead to drug target discovery or prognostic or diagnostic tools for human melanoma. Id1 has also been investigated in breast cancer as a potential therapeutic target. It has been associated with MMP1 (matrix metalloproteinase 1) expression with expected subsequent effects on invasion and metastasis in vitro and in vivo. It is likely that other targets of Id1 exist in breast cancer that promote the observed phenotype.
520 $a The first focus of this thesis is to evaluate the function of Id1 in primary human melanocytes using a lentiviral expression system developed in our laboratory. Specific assessment of cell growth, migration, tumorigenicity, and senescence were evaluated in order to determine the function of Id1 in these cells. Delayed senescence in primary melanocytes expressing Id1 was observed with a concomitant decrease in p16/INK4alpha expression. In order to find targets of Id1 in these cells, a cDNA microarray study was performed, revealing cell cycle regulatory proteins associated with Id1 expression.
520 $a The second focus is to investigate the role of Id1 as a mediator of breast cancer metastasis to lung. Much evidence exists implicating Id1 in breast cancer invasion, growth, and metastasis. Recently, Id1 was identified as a member of a gene "signature" that promotes breast cancer metastasis to lung, initially found using mouse studies and verified using primary human tissues. Expression studies have revealed that Id1 expression affects levels of other genes in the signature, suggesting that Id1 may mediate this process. It was also found that Id1 confers a growth and migration advantage in the breast cancer line used for these studies.
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