Background: The ongoing pandemic is having a collateral health effect on delivery of surgical care to millions of patients. Very little is known about pandemic management and effects on other services, including delivery of surgery. Methods: This was a scoping review of all available literature pertaining to COVID-19 and surgery, using electronic databases, society websites, webinars and preprint repositories. Results: Several perioperative guidelines have been issued within a short time. Many suggestions are contradictory and based on anecdotal data at best. As regions with the highest volume of operations per capita are being hit, an unprecedented number of operations are being cancelled or deferred. No major stakeholder seems to have considered how a pandemic deprives patients with a surgical condition of resources, with patients disproportionally affected owing to the nature of treatment (use of anaesthesia, operating rooms, protective equipment, physical invasion and need for perioperative care). No recommendations exist regarding how to reopen surgical delivery. The postpandemic evaluation and future planning should involve surgical services as an essential part to maintain appropriate surgical care for the population during an outbreak. Surgical delivery, owing to its cross-cutting nature and synergistic effects on health systems at large, needs to be built into the WHO agenda for national health planning. Conclusion: Patients are being deprived of surgical access, with uncertain loss of function and risk of adverse prognosis as a collateral effect of the pandemic. Surgical services need a contingency plan for maintaining surgical care in an ongoing or postpandemic phase.

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The contextual signals that regulate the expansion of prostate tumor progenitor cells are poorly defined. We found that a significant fraction of advanced human prostate cancers and castration-resistant metastases express high levels of the β4 integrin, which binds to laminin-5. Targeted IntroductionProstate cancer, the most common noncutaneous malignancy diagnosed in men, progresses from carcinoma in situ, termed prostatic intraepithelial neoplasia (PIN), to invasive and metastatic cancer, suggesting that multiple genetic and epigenetic lesions contribute to its development. Although significant progress has been made toward early detection and treatment, once it has become metastatic, prostate cancer cannot be cured (1, 2). Patterns of allelic loss in human prostate cancer specimens and reverse genetic approaches in the mouse have suggested that loss of function mutations in NKX3.1, PTEN, RB, and P53 and overexpression of MYC promote prostate cancer progression (3). Studies using outlier gene expression analysis have revealed that oncogenic gene fusions juxtaposing 5′ androgen-controlled regulatory elements to Ets transcription factors, such as ERG, are prevalent in human prostate cancer (4). In addition, integrative genomic profiling of a large data set (n = 218) has provided evidence that allelic losses and gains disrupting the Rb and p53 signaling networks and activating the PI-3K and the Ras/Raf signaling pathways are also common in primary prostate cancers, whereas amplifications and mutations of the androgen receptor (AR) are restricted to metastatic lesions (5).Increasing evidence suggests that oncogenic mutations exert their action by transforming adult stem cells or transit-amplifying cells into neoplastic progenitor cells, thereby spurring the develop-

Standard lymph node dissection yields positive nodes more frequently and retrieves a higher total nodal count than the often performed pelvic lymph node dissection limited to the external iliac nodes. Standard pelvic lymph node dissection is feasible through a transperitoneal laparoscopic approach.

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