scispace - formally typeset
B

Brett T. Marck

Researcher at Veterans Health Administration

Publications -  57
Citations -  3857

Brett T. Marck is an academic researcher from Veterans Health Administration. The author has contributed to research in topics: Prostate cancer & Testosterone. The author has an hindex of 26, co-authored 56 publications receiving 3510 citations. Previous affiliations of Brett T. Marck include Fred Hutchinson Cancer Research Center & United States Department of Veterans Affairs.

Papers
More filters
Journal ArticleDOI

Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants

TL;DR: It is indicated that abiraterone reduces CRPC growth via suppression of intratumoral androgens and that resistance to abIRaterone may occur through mechanisms that include upregulation of CYP17A1, and/or induction of AR and AR splice variants that confer ligand-independent AR transactivation.
Journal ArticleDOI

Multiple organ pathology, metabolic abnormalities and impaired homeostasis of reactive oxygen species in Epas1-/- mice

TL;DR: A rheostat role for HIF-2α is proposed that allows for the maintenance of ROS as well as mitochondrial homeostasis and avoids multiple-organ pathology, biochemical abnormalities and altered gene expression patterns in mice lacking this family member.
Journal ArticleDOI

Intratumoral de novo steroid synthesis activates androgen receptor in castration-resistant prostate cancer and is upregulated by treatment with CYP17A1 inhibitors.

TL;DR: It is reported that AR activity in castration-resistant VCaP tumor xenografts can be restored through CYP17A1-dependent de novo androgen synthesis, and that abiraterone treatment of these xenografteds imposes selective pressure for increased intratumoral expression of CYP 17A1, thereby generating a mechanism for development of resistance to CYP16A1 inhibitors.
Journal ArticleDOI

Dopamine production in the caudate putamen restores feeding in dopamine-deficient mice.

TL;DR: A fundamental difference exists between feeding for sustenance and the ability to prefer rewarding substances, and replacement of DA to either region restores preference for sucrose or a palatable diet without fully rescuing coordination or initiation of movement.
Journal ArticleDOI

Feeding behavior in dopamine-deficient mice

TL;DR: The feeding and locomotor responses of DA-deficient (DA-/-) mice to 3, 4-dihyroxy-L-phenylalanine (L-DOPA) were characterized to investigate the relationship between brain DA levels and these complex behaviors.