As much as SARS-CoV-2 has altered the way humans live since the beginning of 2020,<br/>this virus's deadly nature has required clinical testing to meet 2020's demands of higher<br/>throughput, higher accuracy and higher efficiency. Information technology has allowed<br/>institutions, like Arizona State University (ASU), to make strategic and operational changes to<br/>combat the SARS-CoV-2 pandemic. At ASU, information technology was one of the six facets<br/>identified in the ongoing review of the ASU Biodesign Clinical Testing Laboratory (ABCTL)<br/>among business, communications, management/training, law, and clinical analysis. The first<br/>chapter of this manuscript covers the background of clinical laboratory automation and details<br/>the automated laboratory workflow to perform ABCTL’s COVID-19 diagnostic testing. The<br/>second chapter discusses the usability and efficiency of key information technology systems of<br/>the ABCTL. The third chapter explains the role of quality control and data management within<br/>ABCTL’s use of information technology. The fourth chapter highlights the importance of data<br/>modeling and 10 best practices when responding to future public health emergencies.
The synergistic effects between Vorinostat and Tamoxifen observed through a phase II study on breast cancer patients resistant to hormone therapy may involve more than the modulation of ER-alpha to reverse Tamoxifen resistance in ERBC cells. RT-qPCR of genes expressed in Tamoxifen resistant cells, trefoil factor 1(TFF1) and v-myc avian myelocytomatosis viral oncogene homolog (MYC), were evaluated along with ESR1 and Diablo as a control. MYC was observed to have increased expression in the treated cells, whereas the other genes had a decrease in their expression levels after the cells were treated for 3 days with Vorinostat IC30 of 1 µM. As for targeting the AR, MCF7 Tamoxifen sensitive and resistant cells were not affected by the AR antagonists to determine an IC50. The cell viability for all MCF7 sub-clones only decreased for high concentrations of 5.56 µM - 50 µM in Bicalutamide and 16.67 µM – 50 µM of MDV1300. Furthermore, hormone depletion of MCF7 G11 Tamoxifen resistant sub-clones did not show a great response to DHT stimulation or the AR antagonists. In the RT-qPCR, the MCF7 G11 cells showed an increase in mRNA expression for ER, AR, and PR after 4 hours of treatment with estradiol. As for the DHT treatment, ER, AR, PR, and PSA had a minimal increase in the fold change, but the fold change in AR was less than in the estradiol treatment. The Mayo Clinic will investigate the possible usage of AR as a biomarker through immunohistochemistry.