Introduction: The 2019 coronavirus, known as SARS-CoV-2 and COVID-19, was named a pandemic by the WHO in March 2020. It binds to the ACE-2 receptor and transmembrane serine protease 2 and is highly virulent. There are many sequelae of this virus, including neurological consequences. We have performed a literature review of the neurological sequelae of COVID-19 with relation to neuroimaging and then present a case series. Case Series: Seven cases were seen by neurology consultants at the Hospital for Special Surgery in New York City between February and May of 2020; 5 met criteria. The majority of these consultations were called for encephalopathy. Some had neuroimaging of brain MRI or head CT, which all showed microvascular disease. One case had prior imaging without microvascular disease. Summary/Conclusion: It is known that vascular disease is a risk factor for severe COVID-19 infection. This case series demonstrates presence of microvascular disease in patients with encephalopathy. We know that microvascular disease can be a risk factor for toxic metabolic encephalopathy. It is unclear if the microvascular disease was present prior to infection, although at least one patient had prior imaging without microvascular disease. More research is needed to determine if COVID-19 infection can cause vascular disease.

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Prostate cancer is the second most common cancer in men worldwide and causes over 250,000 deaths each year1. Overtreatment of indolent disease also results in significant morbidity2. Common genetic alterations in prostate cancer include losses of NKX3.1 (8p21)3,4 and PTEN (10q23)5,6, gains of the androgen receptor gene (AR)7,8 and fusion of ETS-family transcription factor genes with androgen-responsive promoters9–11. Recurrent somatic base-pair substitutions are believed to be less contributory in prostate tumorigenesis12,13 but have not been systematically analyzed in large cohorts. Here we sequenced the exomes of 112 prostate tumor/normal pairs. Novel recurrent mutations were identified in multiple genes, including MED12 and FOXA1. SPOP was the most frequently mutated gene, with mutations involving the SPOP substrate binding cleft in 6–15% of tumors across multiple independent cohorts. SPOP-mutant prostate cancers lacked ETS rearrangements and exhibited a distinct pattern of genomic alterations. Thus, SPOP mutations may define a new molecular subtype of prostate cancer.

Small-cell lung cancer (SCLC) is an aggressive lung tumor subtype with poor survival1–3. We sequenced 29 SCLC exomes, two genomes and 15 transcriptomes and found an extremely high mutation rate of 7.4±1 protein-changing mutations per million basepairs. Therefore, we conducted integrated analyses of the various data sets to identify pathogenetically relevant mutated genes. In all cases we found evidence for inactivation of TP53 and RB1 and identified recurrent mutations in histone-modifying genes, CREBBP, EP300, and MLL. Furthermore, we observed mutations in PTEN, in SLIT2, and EPHA7, as well as focal amplifications of the FGFR1 tyrosine kinase gene. Finally, we detected many of the alterations found in humans in SCLC tumors from p53/Rb1-deficient mice4. Our study implicates histone modification as a major feature of SCLC, reveals potentially therapeutically tractable genome alterations, and provides a generalizable framework for identification of biologically relevant genes in the context of high mutational background.

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