Intramural gastric masses arise in the wall of the stomach (generally within the submucosa or muscularis propria), often with intact overlying mucosa. These tumors are typically mesenchymal in origin and have overlapping radiologic appearances. A combination of features such as location, attenuation, enhancement, and growth pattern may suggest one diagnosis over another. Gastrointestinal stromal tumors (GISTs) account for the majority of intramural tumors and can vary widely in appearance, from small intraluminal lesions to exophytic masses that protrude into the peritoneal cavity, commonly with areas of hemorrhage or necrosis. A well-circumscribed mass measuring -70 to -120 HU is a lipoma. Leiomyomas usually manifest as low-attenuation masses at the gastric cardia. Homogeneous attenuation is a noteworthy characteristic of schwannomas, particularly for larger lesions that might otherwise be mistaken for GISTs. A hypervascular mass in the antrum is a common manifestation of glomus tumors. Hemangiomas are also hypervascular but often manifest in childhood. Inflammatory fibroid polyps usually arise as a polypoid mass in the antrum. Inflammatory myofibroblastic tumors are infiltrative neoplasms with a propensity for local recurrence. Plexiform fibromyxomas are rare, usually antral tumors. Carcinoid tumors are epithelial in origin, but often submucosal in location, and therefore should be distinguished from other intramural lesions. Multiple carcinoid tumors are associated with hypergastrinemia, either in the setting of chronic atrophic gastritis or Zollinger-Ellison syndrome. Sporadic solitary carcinoid tumors not associated with hypergastrinemia have a higher rate of metastasis. Histopathologic analysis, including immunohistochemistry, is usually required for diagnosis of intramural masses.

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Similar to previously reported studies, PDAC with a wild type mutational profile has a better prognosis with a longer OS. This improved prognosis is independent of the protocol utilized in therapy for these patients. Our findings suggest that future clinical trials in pancreatic cancer should take into consideration the presence of mutations in their pre-planned analysis when assessing the efficacy of a novel therapeutic approach. This may be a crucial factor in trial concepts and outcomes.

Liver transplantation (LT) provides the only effective therapy for end-stage liver disease. Unfortunately, only two-thirds of the approximately 13,000 patients on the waitlist receive a life-saving LT. 1 Efforts to alleviate the organ shortage include increasing living donation, optimizing allocation models, 2 and improving utilization of grafts from extended-criteria donors (ECD), such as those from older donors and donation after circulatory death (DCD), or those with macrosteatosis, abnormal liver function tests (LFTs), or significant alcohol or drug use history. 3 These livers are often declined because poor post-transplant function and graft survival rates as low as 20% pose too great a risk for the recipient. 4,5 Interestingly, a landmark European clinical trial of normothermic machine perfusion (NMP) demonstrated a 50% lower rate of organ discard with NMP than with cold storage (CS), in spite of longer warm ischemic and total preservation times. Availability of functional metrics during NMP likely increased surgeon confidence in these grafts, a judgment subsequently supported by the finding that more aggressive acceptance of organs in the NMP arm