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Exploring the mechanism of constitut...

Bailey, Shannon Terrell.

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Exploring the mechanism of constitutive nuclear factor kappa B activation in breast cancer cells.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Exploring the mechanism of constitutive nuclear factor kappa B activation in breast cancer cells./
作者:	Bailey, Shannon Terrell.
面頁冊數:	134 p.
附註:	Adviser: Sankar Ghosh.
Contained By:	Dissertation Abstracts International67-04B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3214171
ISBN:	9780542651175

Exploring the mechanism of constitutive nuclear factor kappa B activation in breast cancer cells.
Bailey, Shannon Terrell.

Exploring the mechanism of constitutive nuclear factor kappa B activation in breast cancer cells. - 134 p.

Adviser: Sankar Ghosh.

Thesis (Ph.D.)--Yale University, 2006.

Nuclear factor kappa B (NF-kappaB) is a family of inducible transcription factors that participates in a number of important biological processes including inflammation, leukocyte development, differentiation, and apoptosis. Activation of (NF-kappaB) leads to the expression of numerous genes, including those involved in cellular proliferation and survival. Constitutive activation of (NF-kappaB) has been correlated with various solid and hematological carcinomas. This aberrant activation is thought to be responsible for the continued expression of genes that promote cell survival, growth, and thus, inchoateness. In the mammary gland, (NF-kappaB) plays a normal physiological role in the epithelial ducts where it participates in proliferation and anti-apoptosis during involution, and abnormal (NF-kappaB) activity has been linked to development of mammary cancer. Although some tumors may result from various genetic lesions such as mutations, amplifications, and translocations of (NF-kappaB) components, the mechanism behind the generation of constitutive (NF-kappaB) activity in other cancers is unknown.

ISBN: 9780542651175Subjects--Topical Terms:

1017686
Biology, Cell.

Exploring the mechanism of constitutive nuclear factor kappa B activation in breast cancer cells.
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245 1 0 $a Exploring the mechanism of constitutive nuclear factor kappa B activation in breast cancer cells.
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520 $a Nuclear factor kappa B (NF-kappaB) is a family of inducible transcription factors that participates in a number of important biological processes including inflammation, leukocyte development, differentiation, and apoptosis. Activation of (NF-kappaB) leads to the expression of numerous genes, including those involved in cellular proliferation and survival. Constitutive activation of (NF-kappaB) has been correlated with various solid and hematological carcinomas. This aberrant activation is thought to be responsible for the continued expression of genes that promote cell survival, growth, and thus, inchoateness. In the mammary gland, (NF-kappaB) plays a normal physiological role in the epithelial ducts where it participates in proliferation and anti-apoptosis during involution, and abnormal (NF-kappaB) activity has been linked to development of mammary cancer. Although some tumors may result from various genetic lesions such as mutations, amplifications, and translocations of (NF-kappaB) components, the mechanism behind the generation of constitutive (NF-kappaB) activity in other cancers is unknown.
520 $a Activation of (NF-kappaB) occurs through at least two different pathways known as the 'classical' and 'alternative' pathways, and both pathways proceed though subunits of the IKK complex. To begin to elucidate the mechanism by which NF-kappaB is constitutively activated in breast cancer cells in vivo, we examined human mammary epithelial tumor cell lines to characterize their NF-kappaB activity using a number of different approaches. We found that NF-kappaB is highly active in estrogen receptor negative mammary epithelial cell lines, which also demonstrate an enhanced level of NF-kappaB2/p100 processing, resulting in increased amounts of p52 containing NF-kappaB transcriptional complexes. However, contributing to this activity is the "classical" Toll/IL-1 mediated signaling pathway, which is likely the result of activation by NF-kappaB regulated secreted factors in an apparent positive feedback loop. The primary signal that initiates this activation cascade may be DNA damage. We found that the DNA damage mediator BRCA1 interacts with the alternative pathway components NIK and NF-kappaB2/p100 and ultimately leads to the production of p52.
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