scispace - formally typeset
L

Luke Whitesell

Researcher at Massachusetts Institute of Technology

Publications -  75
Citations -  8817

Luke Whitesell is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: HSF1 & Drug resistance. The author has an hindex of 36, co-authored 75 publications receiving 7756 citations. Previous affiliations of Luke Whitesell include University of Arizona & University of Toronto.

Papers
More filters
Journal ArticleDOI

Fitness trade-offs restrict the evolution of resistance to amphotericin B.

TL;DR: The rarity of clinical drug resistance to the antifungal amphotericin B is explained by the extreme costs that resistance mutations impose upon stress responses and virulence factors.
Journal ArticleDOI

Inhibiting the transcription factor HSF1 as an anticancer strategy.

TL;DR: It is likely that within the next 5 years usable inhibitors of HSF1 will be identified and in early pre-clinical evaluation, suggesting a therapeutic role forHSF1 inhibitors.

Fitness Trade-offs Restrict the Evolution of Resistance to Amphotericin B

TL;DR: In this article, the authors used whole genome sequencing of rare AmB-resistant clinical isolates as well as laboratory-evolved strains to identify and investigate mutations that confer AmB resistance in vitro.
Journal ArticleDOI

Using the heat-shock response to discover anticancer compounds that target protein homeostasis.

TL;DR: The findings reveal that diverse organisms elaborate structurally complex thiol-reactive metabolites that act on the stress responses of heterologous organisms including humans, and define a robust approach for discovering candidate compounds that target the malignant phenotype by disrupting protein homeostasis.
Journal ArticleDOI

Loss of tumor suppressor NF1 activates HSF1 to promote carcinogenesis

TL;DR: A surprising biological consequence of NF1 deficiency is activation of HSF1 and ensuing addiction to this master regulator of the heat shock response, which engages an evolutionarily conserved cellular survival mechanism that ultimately impairs survival of the whole organism by facilitating carcinogenesis.