scispace - formally typeset
A

Alexandra S. Bause

Researcher at Harvard University

Publications -  9
Citations -  2066

Alexandra S. Bause is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer cell & Oxidative stress. The author has an hindex of 8, co-authored 9 publications receiving 1787 citations. Previous affiliations of Alexandra S. Bause include University of Arizona.

Papers
More filters
Journal ArticleDOI

Pancreatic cancers require autophagy for tumor growth

TL;DR: Inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on Autophagy.
Journal ArticleDOI

SIRT3 regulation of mitochondrial oxidative stress

TL;DR: The mitochondrial sirtuin, SIRT3, is emerging as a pivotal regulator of oxidative stress by deacetylation of substrates involved in both ROS production and detoxification.
Journal ArticleDOI

The cinnamon-derived Michael acceptor cinnamic aldehyde impairs melanoma cell proliferation, invasiveness, and tumor growth

TL;DR: It is demonstrated that the cinnamon-derived dietary Michael acceptor trans-cinnamic aldehyde (CA) impairs melanoma cell proliferation and tumor growth and supports a previously unrecognized role of CA as a dietary Michael acceptanceor with potential anti-cancer activity.
Journal ArticleDOI

The cinnamon-derived dietary factor cinnamic aldehyde activates the Nrf2-dependent antioxidant response in human epithelial colon cells.

TL;DR: Data demonstrate that the cinnamon-derived food factor CA is a potent activator of the Nrf2-orchestrated antioxidant response in cultured human epithelial colon cells, suggesting that CA may represent an underappreciated chemopreventive dietary factor targeting colorectal carcinogenesis.
Journal ArticleDOI

HDAC6 and SIRT2 Regulate the Acetylation State and Oncogenic Activity of Mutant K-RAS

TL;DR: The results suggest that therapeutic targeting of HDAC6 and/or SIRT2 may represent a new way to treat cancers expressing mutant forms of K-RAS and suggest that altering K- RAS acetylation is a feasible approach to limiting tumorigenic potential.