The coronavirus disease 2019 (COVID-19) has recently been found to cause cutaneous vasculitis in patients. Granulomatosis with polyangiitis (GPA) is a type of small and medium vessel vasculitis that is often associated with pulmonary issues and has been shown to raise diagnostic complications in COVID-19 infection. In this report, we discuss the first case of new-onset GPA in the setting of active COVID-19 infection. Symptoms often overlap between the two diseases, and while there is no current cure for COVID-19, rapid immunosuppressive initiation can be lifesaving for patients with GPA. Thus, this case is essential in expanding our current knowledge of COVID-19 and its many skin manifestations.

Cutaneous diseases such as psoriasis are often the first disease manifestations in HIV+ patients, with greater severity corresponding to a weaker immune system. Despite its prevalence, literature and placebo-controlled studies on the recognition of HIV as a cause of psoriasis are lacking, causing challenges to arise in its treatment. In this article, we illustrate a case of an HIV+ patient whose psoriasis drastically improved after the initiation of highly active antiretroviral therapy (HAART) consisting of bictegravir, emtricitabine, and tenofovir alafenamide. While it is unclear which combination of antiretrovirals is optimal for controlling psoriasis in HIV+ patients, prompt initiation of HAART can significantly improve immune status and psoriasis in HIV+ patients.

Acute generalized exanthematous pustulosis (AGEP) is a rare drug-induced autoimmune disease that presents with hundreds of sterile pustules and systemic symptoms. Genetic predisposition, race, and medications prescribed are all factors in AGEP's frequency, which occurs most commonly in Caucasians and with the use of macrolides and aminopenicillins. Cases of AGEP with sulfonamides or in African American patients are rare. To our knowledge, this is the first documented example of trimethoprim-sulfamethoxazole-induced AGEP in an African American male. In this article, we will further discuss our case and review the literature.

Introduction: Epithelial ovarian cancer is one of the most common gynecological malignancies and the fifth most frequent cause of cancer death in women, affecting over 22,000 women annually. Nearly 15,500 affected women die from this disease annually, and chemoresistance from the commonly prescribed platinum-based drug, carboplatin, is a major contributor to this mortality. Previous studies have identified genes with CpG islands that are methylated and transcriptionally silenced in resistant epithelial ovarian cancer patients. One of these genes is GSK3β, an important regulator of apoptosis and cell growth in the Wnt pathway. Thus, understanding the role of GSK3β suppression in chemoresistance of epithelial ovarian cancer can help contribute to more effective treatments for this disease. By performing different assays our study examined the functional role that GSK3β plays in carboplatin chemoresistance. Procedure: Human ovarian surface epithelium (HOSE) 6-3 cell line was utilized, which is characterized as sensitive to carboplatin therapy. The cells were studied in six groups: 1) untreated; 2) treated with Lithium Chloride (LiCl); 3) treated with carboplatin; 4) treated with carboplatin and LiCl; 5) treated with doxorubicin as control; 6) treated with doxorubicin and LiCl as another control. LiCl is known to suppress GSK3β gene expression. We took images of cells using a fluorescence microscope. We also performed the Neutral Red Dye assay that determines cell viability, Vybrant® MTT Cell Assay which measures amount of non-viable cells, Caspase 3 Assay which measures cell apoptosis, and we did cell counting using a hemocytometer and a light microscope. Data analysis was done by T-tests using Microsoft Excel®, with p < .05 for significance. Summary of Data: More growth was observed in the carboplatin and LiCl group compared to the carboplatin group alone on microscopy. Neutral Red Dye assay: Compared to the cells exposed to carboplatin alone, those exposed to carboplatin and LiCl were more viable (p <0.01). Vybrant® MTT Cell Assay: the cells treated with carboplatin and LiCl showed lesser amounts of nonviable cells as compared to the carboplatin alone group (p<0.01). Caspase 3 Assay: the cells treated with carboplatin and LiCl were less apoptotic, compared to cells treated with carboplatin alone (p <0.01). Cell Counting: cells treated with carboplatin and LiCl had significantly more growth compared to the cells treated with carboplatin alone (p <0.01). Conclusion: Our results show that cells with suppressed GSK3β had increased proliferation and reduced apoptosis, strongly suggesting that silenced GSK3β expression contributes to carboplatin resistance and GSK3β expression is vital to carboplatin chemosensitivity. Future in vivo studies could further investigate the role of GSK3β methylation to facilitate the design of potential genome-guided treatments for patients with chemoresistant epithelial ovarian cancer. Citation Format: Naeha Pathak, Noelle L. Cutter. GSK3β modulates chemoresistance in epithelial ovarian cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2934.

Epithelial ovarian cancer is one of the most common gynecological malignancies and the fifth most frequent cause of cancer death in women, affecting over 22,000 women annually. Nearly 15,500 affected women die from this disease annually, and chemoresistance from the commonly prescribed platinum-based drug, carboplatin, is a major contributor to this mortality rate. Previous studies have identified genes with CpG islands that are methylated and transcriptionally silenced in resistant epithelial ovarian cancer patients. One of these genes is GSK3β, an important regulator of apoptosis and cell growth in the Wnt pathway. Thus, understanding the role of GSK3β suppression in chemoresistance of epithelial ovarian cancer can help contribute to more effective treatments for this disease. By performing assays of cell growth, viability, and apoptosis, our study examined the functional role that GSK3β plays in carboplatin mediated apoptosis. Our results suggest that cells with suppressed GSK3β had increased proliferation and reduced apoptosis. We conclude that silenced GSK3β expression might therefore contribute to carboplatin resistance seen in tumors and our in vitro analysis suggests that GSK3β expression is vital to carboplatin chemosensitivity. Future research is required to further investigate the role of GSK3β methylation to facilitate the design of potential genome-guided treatments for patients with chemoresistant epithelial ovarian cancer.