Finding Synergistic Lipid Kinase and Mitotic Kinase Inhibitor Combination Treatments for Metastatic Breast Cancer

Loading...
Thumbnail Image

Authors

Al Ali, Nadia

Date

2024-01-17

Type

thesis

Language

eng

Keyword

Triple negative breast cancer , Inflammatory breast cancer , PI3K pathway , AURKA pathway , Alisertib , Buparlisib

Research Projects

Organizational Units

Journal Issue

Alternative Title

Abstract

Triple-negative breast cancer (TNBC) and Inflammatory breast cancer (IBC) are aggressive subtypes that lack targeted therapies options in most cases. The frequently activated phosphatidylinositol 3 kinase (PI3K) pathway in TNBC is a candidate but resistance to PI3K inhibitors has been observed. However, a recent functional genomics screen using PI3K inhibitor buparlisib in TNBC cells revealed a synthetic lethal interaction with Aurora kinase A (AURKA) gene. Here, I investigated if PI3K and AURKA inhibitors will act synergistically to eliminate TNBC cell growth and motility in culture models and halt progression in mouse tumor models. Testing dose responses of buparlisib and/or alisertib treatments in TNBC and IBC cell lines revealed synergistic effects that increased cytotoxicity in a dose dependent fashion by up to 10-fold change. The combination of buparlisib and alisertib were also better than monotherapies at reducing TNBC or IBC colony growth and cell migration rates. Combination treatments of IBC tumor-bearing mice with buparlisib and alisertib also reduced tumor growth and spontaneous lung metastases in vivo. Together, these results provide rationale for advancing targeted therapies comprised of PI3K and AURKA inhibitors to improve treatment options for TNBC and IBC.

Description

Citation

Publisher

License

Queen's University's Thesis/Dissertation Non-Exclusive License for Deposit to QSpace and Library and Archives Canada
ProQuest PhD and Master's Theses International Dissemination Agreement
Intellectual Property Guidelines at Queen's University
Copying and Preserving Your Thesis
This publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.
Attribution-NonCommercial-NoDerivatives 4.0 International

Journal

Volume

Issue

PubMed ID

External DOI

ISSN

EISSN