The Boot Camp Model in Urology: Preparing PGY1 Urology Interns for Practice.

PURPOSE OF REVIEW: The purpose of this review is to highlight literature regarding resident boot camps published across surgical specialties with a focus on urology. Herein, we discuss different boot camp iterations, their results, and the integration of simulation into their curriculum. We review program elements such as curriculum, course length, and efficacy as well as areas for continued investigation. RECENT FINDINGS: The field of urology has grown in both the breadth of knowledge and the complexity of procedures. With urology now being an integrated surgical subspecialty, interns often start on the urology service despite limited experience navigating this unique specialty. The boot camp model is one method by which interns and junior residents participate in consolidated training programs to best prepare them for a patient-facing role and the day-to-day demands of residency. Urology programs, both in the USA and abroad, have begun integrating boot camps into their training programs with positive results. Urology boot camps can be a valuable part of training programs for interns to quickly establish medical knowledge, skills, and efficiency. Boot camps should be easily accessible, have sufficient support from institutions, and provide effective training through various methods such as didactics and simulation.

Metastasis-Directed Therapy for Oligometastatic Castration-Sensitive Prostate Cancer: An Alternative to ADT?

PURPOSE OF REVIEW: The standard treatment of patients with metastatic prostate cancer is systemic treatment with androgen-deprivation therapy (ADT). The spectrum-based model of metastatic disease includes the presence of an oligometastatic state, an intermediary between localized and widespread metastatic disease, in which radical local treatment might improve systemic control. Our purpose is to review the literature on metastasis-directed therapy in the treatment of oligometastatic prostate cancer. RECENT FINDINGS: Several prospective clinical trials have reported improvements in ADT-free survival and progression-free survival with metastasis-directed therapy of oligometastatic prostate cancer. Retrospective studies have found improvements in oncologic outcomes for patients with oligometastatic prostate cancer undergoing metastasis-directed therapy, and several recent prospective clinical trials have confirmed these results. Advancements in imaging as well as an understanding of the genomics of oligometastatic prostate cancer may allow for better patient selection for metastasis-directed therapy and the potential for cure in selected patients.

The Impact of COVID-19 on Surgical Training and Education.

The COVID-19 pandemic disrupted conventional medical education for surgical trainees with respect to clinical training, didactics, and research. While the effects of the COVID-19 pandemic on surgical trainees were variable, some common themes are identifiable. As hordes of COVID-19 patients entered hospitals, many surgical trainees stepped away from their curricula and were redeployed to other hospital units to care for COVID-19 patients. Moreover, the need for social distancing limited traditional educational activities. Regarding clinical training, some trainees demonstrated reduced case logs and decreased surgical confidence. For residents, fellows, and medical students alike, most didactic education transitioned to virtual platforms, leading to an increase in remote educational resources and an increased emphasis on surgical simulation. Resident research productivity initially declined, although the onset of virtual conferences provided new opportunities for trainees to present their work. Finally, the pandemic was associated with increased anxiety, depression, and substance use for some trainees. Ultimately, we are still growing our understanding of how the COVID-19 pandemic has redefined surgical training and how to best implement the lessons we have learned.

Downregulation of miR-375 contributes to ERBB2-mediated VEGFA overexpression in esophageal cancer.

Esophageal cancer (EC) is a lethal cancer with an extremely aggressive nature and poor survival rate. However, the molecular mechanisms driving the occurrence and progression of EC are not well understood. MicroRNAs (miRNAs) are small RNA molecules that regulate the expression of protein-coding genes. miRNA-mediated gene regulation plays an important role in EC. By cross-referencing studies from NCBI, we found that microRNA-375 (miR-375) is one of the most frequently downregulated miRNAs in EC. We assessed expression of miR-375 in EC cell lines and primary EC tissues and their matched normal tissues. We found significant downregulation of miR-375 in both cell lines and EC tissues. Forced expression of miR-375 attenuated EC cell proliferation and invasion. Human epidermal growth factor receptor 2 (HER2, ERBB2), a known proto-oncogene, was identified here as one of the potential target genes of miR-375. Ectopic expression of miR-375 significantly suppressed the expression of ERBB2 and subsequently downregulated one of its target genes, vascular endothelial growth factor A (VEGFA), which is related to cancer invasion and metastasis. These findings suggest that miR-375 acts as a tumor suppressor by blocking the ERBB2/VEGFA pathway with the potential to modulate the occurrence and/ or progression of EC.

Differentially Regulated miRNAs and Their Related Molecular Pathways in Lichen Sclerosus.

Lichen sclerosus (LS) is a chronic inflammatory skin disorder with unknown pathogenesis. The aberrant expression of microRNAs (miRNAs) is considered to exert a crucial role in LS. We used the next-generation sequencing technology (RNASeq) for miRNA profiling and Ingenuity Pathway Analysis (IPA) for molecular network analysis. We performed qRT-PCR, miRNA transfection and Matrigel assays for functional studies. We identified a total of 170 differentially expressed miRNAs between female LS and matched adjacent normal tissue using RNASeq, with 119 upregulated and 51 downregulated. Bioinformatics analysis revealed molecular networks that may shed light on the pathogenesis of LS. We verified the expression of a set of miRNAs that are related to autoimmunity, such as upregulated miR-326, miR-142-5p, miR-155 and downregulated miR-664a-3p and miR-181a-3p in LS tissue compared to the matched adjacent normal tissue. The differentially expressed miRNAs were also verified in blood samples from LS patients compared to healthy female volunteers. Functional studies demonstrated that a forced expression of miR-142-5p in human dermal fibroblast PCS-201-010 cells resulted in decreased cell proliferation and migration. These findings suggest that differentially expressed miRNAs may play an important role in LS pathogenesis; therefore, they could serve as biomarkers for LS management.

microRNA-196b promotes esophageal squamous cell carcinogenesis and chemoradioresistance by inhibiting EPHA7, thereby restoring EPHA2 activity.

Esophageal cancer (EC) is extremely aggressive and has a very poor survival rate. Esophageal squamous cell carcinoma (ESCC) accounts for 80% of all ECs worldwide, with the majority of the remaining 20% being esophageal adenocarcinoma (EAC). Due to its occult and insidious presentation, ESCC is typically diagnosed and treated in its advanced stages, thereby limiting the success of present therapeutic modalities. microRNAs (miRNAs) can function as tumor suppressors or oncogenes, playing critical roles in cancer initiation and progression by regulating target genes in oncogenic pathways. In the current study, we demonstrated that microRNA-196b (miR-196b) is one of the most upregulated miRNAs in both ESCC and EAC. miR-196b was overexpressed in ESCC and EAC cell lines, cellular exosomal RNAs, and ESCC tissue samples. Functional studies revealed that miR-196b acted as an oncomiR by directly targeting a tumor suppressor, ephrin type-A receptor 7 (EPHA7). EPHA7 abrogates the activity of ephrin type-A receptor 2 (EPHA2), a key molecule involved in the epithelial-to-mesenchymal transition (EMT) and MAPK/ERK pathways, mediating resistance to UV and chemoradiotherapy in both ESCC and EAC. Taken together, these findings suggest that miR-196b is a strong candidate molecular target for EC treatment.

Estrogen Receptor, Progesterone Receptor, and HER2 Receptor Markers in Endometrial Cancer.

Background: Endometrial cancer (EC) is a major gynecologic adenocarcinoma that arises from the endometrium. While the incidence of EC is on the rise worldwide, survivorship and clinical advancement have considerably lagged compared to other cancers. Given the sensitive nature of the endometrium and its high expression of hormone receptors, hormonal therapy has become a favorable alternative treatment compared to highly toxic chemotherapeutics and radiation therapy. Methods: Clinical samples from patients diagnosed with EC were obtained. ER and PR staining were performed according to the S-P kit, and HER2 staining was carried out according to the UltrasensitiveTM S-P immunohistochemistry kit protocol. Chi-square analysis was conducted using the SPSS. P-values of less than 0.05 were taken as an a priori value for statistical significance. Results: Immunohistochemical (IHC) analysis showed the overall positive expression rates of ER, PR, and HER2 to be 59.8%, 75.0%, and 71.1%, respectively. Significant co-expression was found among all three receptors, suggesting a cooperative, synergistic effect. More importantly, we found that ER expression was correlated with FIGO staging and cervical invasion, whereas PR expression was associated with histologic type. No clinicopathologic features were correlated with HER2 expression, but HER2 positivity was inversely associated with the degree of HER2 overexpression. Conclusions: These results suggest that EC is a heterogeneous disease that may not conform to traditional, prototypically defined subtypes. The status of ER, PR, and HER2 receptors may have the potential to serve as prognostic indicators for EC, but further analysis is needed to ascertain their prognostic significance.