A 74-year-old man presented with abdominal pain. Preoperative evaluation for small bowel perforation revealed a 74-mm tumour shadow obstructing the right lower lobe bronchus. Endobronchial biopsy from the truncus intermedius was diagnostic of squamous cell carcinoma (SCC). Pathological findings in the small intestine were consistent with SCC. Based on other radiological findings, the patient was diagnosed with stage IVB (cT4N3M1c) lung SCC (LUSC). Serum amylase levels were elevated at 1693 U/L (pancreatic amylase 184 U/L) prior to treatment. AMY1 (2D4) immunohistochemistry was positive, confirming amylase-producing LUSC, a rarely reported entity. Amylase levels decreased to 203 U/L following combination therapy with carboplatin, nab-paclitaxel and pembrolizumab. The patient had no symptoms or signs of pancreatic or salivary gland disease. To our knowledge, this is the first reported case of LUSC with both histological evidence of amylase production and hyperamylasemia. This case provides new evidence that LUSC can produce amylase and cause hyperamylasemia.

We previously reported that the murine lncRNA Epr is essential for maintaining colon mucosal integrity and permeability. Mice lacking Epr in the colon are more vulnerable to colitis and tumor development. Additionally, we demonstrated that human EPR expression is reduced in ulcerative colitis and in a small cohort of colon adenocarcinoma patients. Here, we present evidence that human and mouse EPR share several key physiological features: preferential binding to the KH1 domain of their interacting protein, KSRP; specific expression in canonical and immature goblet cells of the large intestine; and a functional role in intestinal goblet cell development. The correlation between EPR levels and survival in large cohorts of metastatic colon adenocarcinoma patients, combined with the capacity of human EPR to inhibit cell proliferation and induce apoptosis in two distinct human colon adenocarcinoma cell lines, suggests that EPR may serve as both a valuable prognostic marker for goblet cell-derived adenocarcinomas and a potential therapeutic target.

Calcifying fibrous tumor (CFT) is a rare benign tumor of mesenchymal origin that may develop in several sites in the body, including the gastrointestinal tract. CFTs could present with clinical symptoms or remain asymptomatic. We report a rare case of CFT located at the jejunal mesentery and attached to a mesenteric band causing small bowel obstruction. This case is distinctive due to the presence of a mesenteric CFT combined with a mesenteric band, causing constriction of the small bowel. To our knowledge, this is the first case in the literature to report a congenital band associated with CFT. The mass was surgically removed, and the band was released and ligated.

Primary small-bowel adenocarcinoma (SBA) is a rare malignancy. As early symptoms are nonspecific, diagnosis is frequently delayed, and patients often present with advanced disease. Ovarian metastasis from SBA - classified as a Krukenberg tumor - is exceptionally uncommon and may obscure the underlying gastrointestinal origin, posing a significant diagnostic challenge. We report the case of a 39-year-old woman with a history of ulcerative colitis who presented with abdominal distension and was found to have a rapidly enlarging left ovarian mass. Left adnexectomy revealed adenocarcinoma, and further evaluation identified a circumferential ulcerative lesion in the upper jejunum. Immunohistochemical analysis demonstrated CK7 positivity, CK20 positivity, CDX2 positivity, and PAX8 negativity in both ovarian and jejunal specimens, confirming a diagnosis of primary jejunal adenocarcinoma with ovarian metastasis. The patient subsequently underwent laparoscopic partial jejunal resection. Histopathology confirmed stage IV disease (pT3 NX M1). Postoperatively, capecitabine and oxaliplatin (CAPOX) plus bevacizumab chemotherapy was initiated following colorectal cancer protocols. This case illustrates several diagnostic challenges associated with SBA, particularly when presenting as an ovarian mass. Ovarian metastasis from SBA is exceedingly rare, and the presence of bilateral, non-synchronous disease further complicates diagnosis. Immunohistochemistry played a key role in distinguishing the jejunum as the primary site. Ulcerative colitis may have contributed to carcinogenesis. Despite therapeutic advances, stage IV SBA remains associated with poor prognosis. This rare case of primary upper jejunal adenocarcinoma presenting as a Krukenberg tumor underscores the importance of thorough diagnostic evaluation, including immunohistochemical analysis. Multidisciplinary management and timely surgical intervention remain essential for both diagnosis and symptom control in advanced SBA.

Robotic duodenum-preserving pancreatic head resection (R-DPPHR) is a technically feasible procedure for benign or borderline tumors of the pancreatic head. Among these, pancreatic cystic neoplasms (PCNs), particularly intraductal papillary mucinous neoplasms (IPMNs), are ideal candidates for this minimally invasive, organ-preserving approach. While numerous studies have demonstrated the short- and long-term advantages of DPPHR over conventional pancreaticoduodenectomy (PD), detailed video descriptions of the robotic-assisted procedure are scarce. This case report presents a step-by-step technical video of R-DPPHRt for a main duct-IPMN (MD-IPMN) in the pancreatic head. A 65-year-old male patient with upper abdominal discomfort was diagnosed with MD-IPMN, presenting as a 4.3 cm cystic-solid mass in the pancreatic head. R-DPPHRt was performed using the da Vinci Xi system, with an operation time of 350 minutes and an estimated blood loss of 150 mL. The patient had an uneventful postoperative course and was discharged on postoperative day 9. Pathology confirmed MD-IPMN with low-grade dysplasia. R-DPPHRt is an effective, function-preserving treatment for selected patients with pancreatic cystic neoplasms, particularly when performed by experienced surgeons in high-volume centers. While this single-case report limits generalizability, the article offers unique value by providing a clear procedural template.

Copyright: © 2026 Speyer et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Gastrointestinal stromal tumors (GISTs) are molecularly defined by oncogenic alterations that predict clinical behavior and response to therapy. Activating mutations in KIT or PDGFRA characterize most GISTs and confer sensitivity to imatinib, whereas succinate dehydrogenase (SDH)–deficient GISTs lack these mutations and are typically imatinib resistant. These molecular subtypes are generally considered mutually exclusive. We report a rare case of a small bowel GIST harboring both a somatic KIT exon 9 A502_Y503 duplication and a germline inactivating SDHC mutation (p.R50C). The patient received neoadjuvant high-dose imatinib with a marked radiographic and metabolic response, followed by complete surgical resection. Pathology demonstrated spindle cell GIST with significant treatment effect and retained SDHB expression. This case suggests that oncogenic KIT signaling may remain the dominant driver of GIST behavior despite the presence of a germline SDHC mutation and highlights the importance of integrated molecular interpretation in GIST management.

Several HSP90 inhibitors are in use or late-stage trials: pimitespib is approved in Japan for intestinal tumors, hypericin sodium under US regulatory review, and WP-1303 in Phase III development. However, their efficacy depends on tumor HSP90 expression levels, necessitating probes for subtype-specific detection in vivo. Translation is limited by inadequate validation in specific subtypes and off-target accumulation in kidneys and liver. We developed and optimized an HSP90-targeted radiotracer addressing these limitations. Chemical modifications enhanced tumor uptake in colorectal and gastric cancer models (10.02 ± 2.05% and 5.02 ± 0.08% ID/g), while reducing liver and kidney retention (∼2% and ∼5% ID/g), yielding tumor/muscle ratios of 23.28 ± 9.70 and 16.73 ± 2.80. Clinical evaluation confirmed translational potential, enabling tumor delineation and high-contrast imaging (SUVmax ∼ 5). This probe supports comprehensive cancer management and may guide clinical application of emerging HSP90 inhibitors.

Interactions between alcohol and nutrition play an important role in the development and progression of alcohol-associated liver disease (ALD). Although dietary cholesterol was shown to exacerbate fatty liver and liver injury in alcohol-fed mice, findings regarding the combined effect of dietary cholesterol and heavy alcohol drinking on cholesterol homeostasis remain controversial. Ezetimibe has been widely used as a cholesterol-lowering drug in hypercholesterolemic subjects. It is not fully understood whether ezetimibe blunts the adverse effect of cholesterol on lipid and biliary bile acid metabolism in alcohol-exposed mice. In the current study, wild-type mice were subjected to NIAAA alcohol feeding model. Dietary cholesterol (0.2%, w/v) and ezetimibe (0.001%, w/v) were added to the liquid diets. Cholesterol and triglyceride contents in the liver and circulation were determined. Biliary bile acid composition, as well as hepatic and circulating inflammatory markers were analyzed. We found that ezetimibe protected mice from the synergistic effects of dietary cholesterol and alcohol on hepatic triglyceride accumulation, which was accompanied by enhanced expression of genes involved in hepatic beta oxidation. Dietary cholesterol caused great increases in liver cholesterol content and dramatic reductions in the expression of hepatic cholesterol biosynthetic genes in both control- and alcohol-fed mice. These changes were normalized by ezetimibe treatment. Ezetimibe attenuated dietary cholesterol-induced elevations in total biliary bile acids. Moreover, mice fed a diet containing both cholesterol and alcohol exhibited increased expression of monocyte chemoattractant protein 1 (Mcp1) and tumor necrosis factor alpha (Tnfα) in the distal small intestine. Collectively, our findings indicate that ezetimibe effectively mitigates the adverse effects of dietary cholesterol and alcohol consumption on hepatic lipid accumulation and liver injury.