The goal of our study was to determine current melanoma reporting methods available to dermatologists and dermatopathologists and quantify changes in reporting methods from 2012 to 2014. A cross-sectional study design was utilized consisting of website perusal of reporting procedures, followed up by telephone and email inquiry of reporting methods from every state cancer registry. This study was conducted over a six-month period from February to August 2014. A previous similar survey was conducted in 2012 over the same time frame and results were compared. Kansas state cancer registry provided no data. As of August 2014, 96% of 49 state cancer registries had electronic methods available to all designated reporters. Seven (14%) states required an electronic-only method of reporting melanoma cases. Eighty-six percent allowed hard copy pathology report submission. Compared to the 2012 survey, 2 additional states were found to have initiated electronic reporting methods by 2014. In conclusion, a variety of methods exist for reporting diagnosed melanoma cases. Although most state cancer registries were equipped for electronic transmission of cases for mandated reporters, a number of states were ill-equipped for electronic submission from outpatient dermatologists. There was a general trend towards electronic versus nonelectronic reporting from 2012 to 2014.
Prostaglandin D2 (PGD2) is a lipid mediator that promotes androgenic alopecia and inhibits wound-induced hair follicle neogenesis. Although the activation of its receptor, GPR44, has been implicated in this action, other mechanisms may exist as well. The role of testosterone and its reduced metabolite, dihydrotestosterone, as drivers of androgenic alopecia is well established. Our previous data showed that human keratinocytes treated with PGD2 upregulated the transcription of aldo-keto reductase 1C3 (AKR1C3), an enzyme that converts androstenedione (AD) a relatively weak androgen, to testosterone. We hypothesized that AKR1C3 upregulation in PGD2-treated keratinocytes increases their capacity to generate testosterone from AD. Our data suggest that testosterone production was elevated by PGD2-treated keratinocytes while another prostaglandin, PGE2, had no effect. Surprisingly, knock down of AKR1C3 by siRNA, or specific inhibition of its enzymatic activity, had no effect on PGD2-induced testosterone production. Thus, following preliminary findings, we speculated that PGD2 stimulation of testosterone synthesis occurs through ROS and changes in REDOX potential. We tested this assumption by using the ROS scavenger, n-acetyl-cysteine (NAC). Remarkably and consistent with our hypothesis, NAC completely blocked PGD2-induced testosterone increase. Attempting to identify genes involved in this response, we further investigated the effects of PGD2 on ROS-associated gene regulation using qPCR. Upregulation of a number of REDOX-associated genes was detected, including enzymes involved in GSH metabolism, ROS clearance, and NADPH synthesis. In ongoing experiments, we are testing the possible role of these genes to identify novel targets for the treatment of androgenic alopecia or other testosterone-driven skin pathologies.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.