Abstract A24: Hypoxia signaling pathway plays a role in ovarian cancer chemoresistance.

Noelle L. Cutter; Tyler Walther; Liam Gallagher; Robert Lucito; Kazimierz Wrzeszczynski

doi:10.1158/1557-3265.OVCA15-A24

Abstract A24: Hypoxia signaling pathway plays a role in ovarian cancer chemoresistance.

Noelle L. Cutter, Tyler Walther, Liam Gallagher, Robert Lucito, Kazimierz Wrzeszczynski

Biology, Chemistry, Environmental Studies

Research & Scholarship: Contribution to conference › Abstract

Original language	American English
DOIs	https://doi.org/10.1158/1557-3265.OVCA15-A24
State	Published - Jan 15 2016

Disciplines

Biology
Oncology
Immunology and Infectious Disease

Access to Document

10.1158/1557-3265.OVCA15-A24

Cite this

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title = "Abstract A24: Hypoxia signaling pathway plays a role in ovarian cancer chemoresistance.",

author = "Cutter, \{Noelle L.\} and Tyler Walther and Liam Gallagher and Robert Lucito and Kazimierz Wrzeszczynski",

note = "Abstracts: AACR Special Conference: Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; October 17-20, 2015; Orlando, FL Epithelial ovarian cancer (EOC) is the leading cause of gynecologic cancer mortality worldwide. These cancers are highly heterogeneous and while chemotherapy is the preferred treatment many patients are intrinsically resistant or quickly develop resistance.",

year = "2016",

month = jan,

day = "15",

doi = "10.1158/1557-3265.OVCA15-A24",

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T1 - Abstract A24: Hypoxia signaling pathway plays a role in ovarian cancer chemoresistance.

AU - Cutter, Noelle L.

AU - Walther, Tyler

AU - Gallagher, Liam

AU - Lucito, Robert

AU - Wrzeszczynski, Kazimierz

N1 - Abstracts: AACR Special Conference: Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; October 17-20, 2015; Orlando, FL Epithelial ovarian cancer (EOC) is the leading cause of gynecologic cancer mortality worldwide. These cancers are highly heterogeneous and while chemotherapy is the preferred treatment many patients are intrinsically resistant or quickly develop resistance.

PY - 2016/1/15

Y1 - 2016/1/15

U2 - 10.1158/1557-3265.OVCA15-A24

DO - 10.1158/1557-3265.OVCA15-A24

M3 - Abstract

ER -