William E. Friedrichs
University of Texas Health Science Center at San Antonio
37 Papers
547 Citations
William E. Friedrichs is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Gene expression & Virus. The author has an hindex of 25, co-authored 37 publications. Previous affiliations of William E. Friedrichs include University of Texas at Austin.
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Papers
Inhibition of mTOR activity restores tamoxifen response in breast cancer cells with aberrant Akt activity
Linda A. deGraffenried,William E. Friedrichs,Douglas H. Russell,Elissa J. Donzis,Amanda K. Middleton,Jessica M. Silva,Richard A. Roth,Manuel Hidalgo +7 more
TL;DR: It is found that MCF-7 breast cancer cell lines expressing a constitutively active Akt are able to proliferate under reduced estrogen conditions and are resistant to the growth inhibitory effects of tamoxifen, both in vitro as well as in vivo in xenograft models.
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NOX4 functions as a mitochondrial energetic sensor coupling cancer metabolic reprogramming to drug resistance.
Karthigayan Shanmugasundaram,Bijaya K. Nayak,William E. Friedrichs,Dharam Kaushik,Ronald Rodriguez,Karen Block +5 more
TL;DR: It is shown thatNOX4 regulates drug resistance in renal cancer carcinoma by regulating PKM2 and that NOX4 activity is allosterically activated by reduced mitochondrial ATP levels thus coupling energy metabolism to drug resistance.
Reduced PTEN expression in breast cancer cells confers susceptibility to inhibitors of the PI3 kinase/Akt pathway
Linda A. deGraffenried,Letitia C. Fulcher,William E. Friedrichs,Viktor Grünwald,Ratna B. Ray,Manuel Hidalgo +5 more
TL;DR: Inhibitors of mTOR, some of which are already in clinical development (CCI-779, an ester of rapamycin), have the potential to be effective in the treatment of breast cancer patients with PTEN-negative tumors and should be evaluated in this setting.
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NF-κB inhibition markedly enhances sensitivity of resistant breast cancer tumor cells to tamoxifen
Linda A. deGraffenried,B. Chandrasekar,William E. Friedrichs,Elissa J. Donzis,Jessica M. Silva,Manuel Hidalgo,James W. Freeman,Geoffrey R. Weiss +7 more
TL;DR: The present study found that co-treatment with the NF-kappa B inhibitor, parthenolide, or overexpression of I kappa B superrepressor restored tamoxifen sensitivity to the authors' refractory Akt MCF-7 cells, suggesting that activation of NF-Kappa B via the PI3K/Akt signaling pathway may be a significant mechanism for development of endocrine therapy resistance in breast cancer.
141
Expression and inflammatory regulation of haptoglobin gene in adipocytes
TL;DR: After inflammation had been induced in vivo, expression of the haptoglobin gene rose six-fold in adipose tissue, an increase compatible with that observed in the normal mouse liver.
133