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Molecular Origins of Heterogeneity i...

Inde, Zintis R.

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Molecular Origins of Heterogeneity in Cancer Cell Death.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Molecular Origins of Heterogeneity in Cancer Cell Death./
作者:	Inde, Zintis R.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
面頁冊數:	143 p.
附註:	Source: Dissertations Abstracts International, Volume: 82-02, Section: B.
Contained By:	Dissertations Abstracts International82-02B.
標題:	Cellular biology. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28103910
ISBN:	9798662510562

Molecular Origins of Heterogeneity in Cancer Cell Death.
Inde, Zintis R.

Molecular Origins of Heterogeneity in Cancer Cell Death. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 143 p.

Source: Dissertations Abstracts International, Volume: 82-02, Section: B.

Thesis (Ph.D.)--Stanford University, 2020.

This item must not be sold to any third party vendors.

Anti-cancer drugs and other lethal agents can induce heterogeneous cell death responses in a population of cancer cells, a phenomenon referred to as fractional killing (FK). FK arises from a wide variety of molecular mechanisms, the study of which has been limited by inadequate tools for quantifying and studying cell death. We have developed and validated methods to quantify FK in a high-throughput manner. Here, I use this approach to investigate FK induced by inhibitors of mitogen activated protein kinase kinase (MEK) 1/2. I show that Bcl-2 family members play a critical role in executing cell death upon MEK inhibition, and that among pro-survival Bcl-2 family members, MCL1 (and not BCL-xL) is an important determinant of FK. I show that JNK activity modulates MEK inhibitor-induced death via effects on MCL1. These effects are consistent across some, but not all cell lines, suggesting that generalizable molecular models of FK are rare. These studies lay the foundation for quantitative high-throughput analyses of FK.

ISBN: 9798662510562Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Fractional killing

Molecular Origins of Heterogeneity in Cancer Cell Death.
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506 $a This item must not be sold to any third party vendors.
520 $a Anti-cancer drugs and other lethal agents can induce heterogeneous cell death responses in a population of cancer cells, a phenomenon referred to as fractional killing (FK). FK arises from a wide variety of molecular mechanisms, the study of which has been limited by inadequate tools for quantifying and studying cell death. We have developed and validated methods to quantify FK in a high-throughput manner. Here, I use this approach to investigate FK induced by inhibitors of mitogen activated protein kinase kinase (MEK) 1/2. I show that Bcl-2 family members play a critical role in executing cell death upon MEK inhibition, and that among pro-survival Bcl-2 family members, MCL1 (and not BCL-xL) is an important determinant of FK. I show that JNK activity modulates MEK inhibitor-induced death via effects on MCL1. These effects are consistent across some, but not all cell lines, suggesting that generalizable molecular models of FK are rare. These studies lay the foundation for quantitative high-throughput analyses of FK.
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