Context The COVID-19 pandemic led to shutting of education faculties, including clinical clerkships for medical students. Objective To review a selective for a course in diagnostic pathology geared toward undergraduate medical students, including its design, technical implementation, instructor and student evaluations, and suggestions for options for further adjusting and optimizing the selective. Design Whole slide images (WSI) were anonymized and students were given remote access to university computers, which were prepared with two freely available WSI viewers. Each topic was taught in a four-part module: Self-assigned reading, lecture via Zoom, quiz based on digital slide sets, and a frontal review of the slides via Zoom. Fifty-nine students participated in the selective. Following the course, students completed an anonymous questionnaire. Results Of the 59 participants, 42% (n = 25) responded. None of the respondents had any previous instruction in diagnostic pathology. Overall, the course was rated very favorably: 68% (n = 17) gave at least 3 points on a 4-point scale on questions relating to course interest, improvement in understanding of the covered diseases, and how strongly they would recommend a student take this course if given an option. The most significant disadvantage of the class, as reported by 80% (n = 20) were technical challenges in accessing the slides. Conclusion We believe the course was a success and can be a model for future virtual pathology electives. Great effort should be done to provide technical support to the students. The selective demonstrated value for students and provided much-needed exposure to diagnostic pathology in clinical practice.

BackgroundUbiquitin‐Specific Peptidase 26 (USP26), located on the X chromosome, encodes a deubiquitinating enzyme expressed mainly in testis, where it regulates protein turnover during spermatogenesis and modulates the ubiquitination levels of the Androgen Receptor (AR), and as a consequence, affects AR signaling.MethodsThe patient was thoroughly characterized clinically. He was genetically tested by chromosome analysis and whole exome sequencing (WES).ResultsThe patient was diagnosed with Sertoli cell‐only syndrome pattern (SCOS). The WES analysis revealed only the variation in USP26: causing p.P469S in a highly evolutionary conserved amino acid as the possible cause for SCOS. The literature search identified 34 single variations and 14 clusters of variations in USP26 that were associated with male infertility. Only one of the 22 variations and of one cluster of three mutations tested for ubiquitination activity was found as damaging. Only one out of six variations tested for effect on AR function was found as damaging. Thus, the association of USP26 with male fertility was questioned.ConclusionsThe finding in our patient and the discussion on the reviewed literature support a possible role for USP26 in male fertility.

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Context.— Medical education in pathology relies on the accumulation of experience gained through inspection of numerous samples from each entity. Acquiring sufficient teaching material for rare diseases, such as Hirschsprung disease (HSCR), may be difficult, especially in smaller institutes. The current study makes use of a previously developed decision support system using a decision support algorithm meant to aid pathologists in the diagnosis of HSCR. Objective.— To assess the effect of a short training session on algorithm-assisted HSCR diagnosis. Design.— Five pathologists reviewed a data set of 568 image sets (1704 images in total) selected from 50 cases by the decision support algorithm and were tasked with scoring the images for the presence or absence of ganglion cells. The task was repeated a total of 3 times. Each pathologist had to complete a short educational presentation between the second and third iterations. Results.— The training resulted in a significantly increased rate of correct diagnoses (true positive/negative) and a decreased need for referrals for expert consultation. No statistically significant changes in the rate of false positives/negatives were detected. Conclusions.— A very short (<10 minutes) training session can greatly improve the pathologist's performance in the algorithm-assisted diagnosis of HSCR. The same approach may be feasible in training for the diagnosis of other rare diseases.

<b><i>Introduction:</i></b> Lobular breast cancer represents 10%–15% of breast cancers in women but is virtually nonexistent in men, related to the typical absence of the anatomic breast lobule structure in male breast tissue. We describe donor-transmitted metastatic lobular carcinoma to a male after kidney transplantation. Determining whether a post-transplant cancer is transplant associated, donor transmitted, or donor derived is significant for treatment, prognosis, and possibly management of other organ recipients. <b><i>Case Report:</i></b> A 74-year-old Caucasian male presented to the emergency department with lower abdominal pain and macro-hematuria. Past medical history included two renal transplantations. Computed tomography identified a 4–5-cm space-occupying lesion in the native left kidney. A left native nephrectomy was performed. Histology pathologic examination demonstrated lobular (as opposed to ductal) breast carcinoma. Fluorescent in situ hybridization probes to identify X- and Y-chromosomes showed tumor cells with an XX genotype, whereas the surrounding host cells were of XY genotype. These findings confirmed the female-sex origin (donor) of the tumor within the XY native male (current patient) tissues. <b><i>Discussion/Conclusion:</i></b> Due to discordance between the donor and recipient sex, fluorescent in situ hybridization as a molecular technique correctly identified the origin of an individual’s cancer in the post-transplant setting. The metastatic breast cancer behaved more indolently than usually seen. Expanded criteria donors (ECD) are those who cannot donate under standard criteria for organ transplantation; expanded criteria widen the potential organ donor pool at the expense of increased risk for post-transplant complications (e.g., graft failure, the transmission of malignancy). The case provides a potential area of future research into considering allowing ECDs with a distant history of cancer with very low transmission risk when the biochemical environment of the recipient would, in the unlikely event of transmission, induce the tumor to pursue an indolent clinical course.

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Splenic micronodular T-cell/histiocyte-rich large B-cell lymphoma is derived from diffuse large B-cell lymphoma N.O.S., perhaps with some affinity with nodal T-cell/histiocyte-rich large B-cell lymphoma. Of note, in contrast with the latter, the only lymph nodes involved in association with the splenic micronodular pattern of the disease are the splenic hilar lymph nodes. The possibility that corticosteroids, when prescribed prior to splenectomy, cause histopathological and functional modulations, apoptosis, necrosis, tissue shrinkage, which may obscure the diagnostic morphological features of this variant lymphoma and cause and underdiagnosis of this condition. The indications for glucocorticoid therapy are either related to the lymphoma itself, or else to other comorbidities, like asthma and autoimmune disorders. We propose that patients with the splenic subset of the disease are likely to have been prescribed corticosteroids prior to histopathologic examination of the involved spleen, causing disparate morphologies. However, a reviewer might accidentally dismiss the corticosteroid pretreatment which is thus overlooked. Apoptosis, induced by corticosteroids, is hypothesized as the major mechanism initiating the histopathological and functional changes in the splenic micronodular variant of the lymphoma.

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