Joseph A. Wawrzyniak

TL;DR: One of the major functions of C-MYC overexpression in melanoma progression is to continuous suppress BRAFV600E- or NRASQ61R-dependent senescence programs, which agrees with the generally higher rates of activating mutations in BRAF than NRAS gene in human cutaneous melanomas.

TL;DR: It is demonstrated that Klf9 independently causes increased ROS levels in various types of cultured cells and in mouse tissues and is required for pathogenesis of bleomycin-induced pulmonary fibrosis in mice and identified as a ubiquitous regulator of oxidative stress and lung injury.

TL;DR: It is reported that this non-thermal plasma torch kills melanoma cells growing in soft agar, suggesting that the plasma torch is capable of inducing melanoma cell death in 3D settings and demonstrating that the presence of gap junctions may increase the area of cell death, likely due to the "bystander effect" of passing apoptotic signals between cells.

TL;DR: KLF9 is identified as a novel and potentially clinically relevant transcriptional regulator of drug-induced apoptosis in MM cells and knockdown impaired NOXA up-regulation and apoptosis caused by bortezomib, LBH589, or a combination of theses drugs.

TL;DR: GMPR is identified as a melanoma invasion suppressor and a link between guanosine metabolism and Rho-GTPase-dependent melanoma cell invasion is established and demonstrated that GMPR partially depletes intracellular GTP pools.