Laparoscopic duodenum-preserving pancreatic head resection avoids complicated organ resection and reconstruction. In recent years, it has replaced laparoscopic pancreaticoduodenectomy as the first choice for treating benign and low-grade pancreatic head tumors. During the operation, pancreaticojejunostomy (PJ) is performed, and a small amount of pancreatic head is retained to ensure blood supply. In this study, we innovatively apply modified pancreaticogastrostomy (PG) and remove the pancreatic head further to reduce the occurrence of pancreatic fistula and intraoperative trauma. Clinical data of 53 patients who received laparoscopic duodenum-preserving total pancreatic head resection in our hospital from May 2020 to December 2023 were retrospectively analyzed, including sex, age, operation time, and postoperative complications. According to the reconstruction mode of the residual pancreatic duct, the patients were classified into a modified PG group and a PJ group. There were 25 cases in the modified PG group and 28 in the PJ group. The operation was completed in all patients, with no conversion to laparotomy. The anastomotic time of modified PG was significantly shorter than that of PJ (15.4 ± 0.8 min vs 35.1 ± 4.8 min, P < .05), and the postoperative hospital stay in the modified PG group was also significantly shorter than that in the PJ group (10.1 ± 2.2 min vs 15.1 ± 9.1 min, P < .05). There was no significant difference in the overall incidence of postoperative pancreatic fistula (POPF) between the 2 groups, the rates being 10.7% and 8.0% in the PJ and modified PG groups, respectively. One patient underwent reoperation due to abdominal hemorrhage caused by POPF in the PJ group, and another patient in the modified PG group underwent reoperation due to postoperative gastric fistula. The study provides preliminary evidence of the safety and effectiveness of the modified PG method, leading to shorter gastrointestinal reconstruction and postoperative hospitalization time. However, it is essential to note the limitations of the small sample size and short-term follow-up. Future studies should expand the sample size and assess the long-term outcomes of this anastomosis method.

Colorectal serrated polyps are now recognized as an important pathway in colorectal carcinogenesis. An association between serrated polyposis syndrome (SPS) and duodenal serrated lesions sharing a similar immunophenotype in both the colon and duodenum has been reported in the literature. We present a case of a 38-year-old male who presented in June 2023 with abdominal pain and fever. Initial investigations, including multiple computed tomography scans of the abdomen and pelvis, revealed an appendiceal abscess and small bowel intussusception involving two segments of the jejunum without evidence of obstruction, along with multiple polyps throughout the small and large bowel suggestive of an intestinal polyposis syndrome. Further evaluation with colonoscopy, esophagogastroduodenoscopy, and magnetic resonance enterography confirmed the presence of numerous polyps of varying sizes involving the duodenum, jejunum, ileum, and all segments of the colon. The initial differential diagnosis included familial adenomatous polyposis, Peutz-Jeghers syndrome, and PTEN hamartoma tumor syndrome. The patient subsequently developed complicated small bowel obstruction due to intussusception and underwent open small bowel resection. Multiple intestinal polyps were identified, and histopathological examination confirmed the diagnosis of SPS. At a later stage, the patient was planned for subtotal colectomy, preceded by elective endoscopic polypectomy, which achieved clearance of the left colon up to 20 cm from the anal verge. Gross examination of the colectomy specimen revealed more than 20 large polyps measuring up to 4 cm. Histopathological analysis demonstrated colonic serrated polyposis without evidence of invasive malignancy, wall infiltration, or lymph node involvement, with clear surgical margins.

Androgen deprivation therapy (ADT), a cornerstone of advanced prostate cancer treatment, effectively suppresses androgen signaling but frequently induces systemic metabolic dysregulation. Here, we delineate an unrecognized intestinal steroid/bile acid regulatory axis that mechanistically links androgen suppression to extratumoral metabolic aberrations. HSD3B1 is the most common inherited link to prostate cancer mortality and mediates its effects by regulating steroid metabolism. Integrated metabolomic profiling of patients undergoing ADT revealed a rapid genotype-associated reduction in circulating bile acids, most pronounced in carriers of the adrenal-permissive HSD3B1 (1245C) allele. Surprisingly, analyses in human intestinal tissue and mechanistic investigations in in vitro models identified the terminal ileum as a unique site of HSD3B1 and SLC10A2 (ASBT) coexpression, where catalytically active 3βHSD1 is transcriptionally governed by liver receptor homolog-1 (LRH-1). Pharmacologic or genetic LRH-1 inhibition coordinately suppressed HSD3B1 and SLC10A2 expression and function, while inducing adaptive HSD11B2 upregulation and enhanced glucocorticoid inactivation. This LRH-1-dependent regulatory program persisted independently of androgen and glucocorticoid receptor signaling under in vitro conditions modeling androgen deprivation. These findings establish LRH-1 as a central integrator of intestinal steroidogenesis and bile acid transport and implicate the LRH-1/HSD3B1/SLC10A2 network as a mechanistic driver of ADT-associated metabolic disturbances and a potential target for therapeutic intervention.

Feline alimentary lymphoma encompasses a diverse group of neoplastic subtypes, each presumably arising from distinct cell populations and exhibiting significant variability in biological behaviour and prognosis. Whilst next-generation sequencing technologies have become a more common aid in the diagnosis, prognostication and treatment of lymphoma in humans, these techniques have been sparsely applied to investigate feline alimentary lymphoma. Specifically, current research in this field is mostly focused on differentiating indolent intestinal lymphomas from inflammatory enteropathies. The aim of the study was to apply transcriptomic analysis to identify differentially expressed genes that may correlate with the aggressiveness of various subtypes of feline alimentary lymphoma. Differential gene analysis was applied to RNA sequencing data from 19 cases of feline alimentary lymphoma split into five phenotypes (small T cell, B cell, CD56+ B cell, Large Granular T cell and Large Granular NK cell lymphomas) according to histomorphology and immunohistochemistry. The analysis identified overexpression of several genes involved in extracellular matrix remodelling, transcription factor expression and cellular division, signalling and metabolism in aggressive lymphoma types (ADAMTS14, ADAMTSl2, FOXI3, ELAVL2, CCR1, GCGR, NMUR1, MARC1, SLC29A4, CENPF, IGF2BP3); and overexpression of several tumour suppressor genes in the indolent lymphoma type (RAB17, SYNPO2, GRM4). The differential expression correlated with biologic behaviours. Future investigation into expression of these genes or gene products using molecular, immunohistochemical or in-situ hybridisation techniques could yield significant advancements in the prognostication of feline alimentary lymphoma as well as pave the way for the development of targeted immunotherapeutic strategies to aid in the treatment of specific feline alimentary lymphoma subtypes.

The majority of intestinal tumors harbor mutations in canonical Wnt pathway genes such as APC, whereas the lack of such alterations in a subset of tumors implies alternative tumorigenic routes. Here we identify recurrent in-frame deletion in COPA, frequently co-occurring with USP9X-truncating mutation, in small intestinal adenoma and adenocarcinoma. Patient-derived and CRISPR-engineered small intestinal organoids carrying COPA in-frame deletions exhibit R-spondin-independent yet Wnt ligand-dependent growth, maintaining LGR5 expression without canonical Wnt drivers. Mechanistically, COPA mutation stabilizes the Frizzled coreceptor LRP6 irrespective of R-spondin, sustaining Wnt pathway activation under growth factor-restricted conditions. USP9X loss further potentiates this phenotype. Unlike canonical Wnt pathway members, COPA encodes the α-subunit of coatomer complex I, which engages in vesicle trafficking with little prior linkage to intestinal tumorigenesis. Our findings establish COPA mutation as a unique and atypical intestinal tumor driver and implicate USP9X loss as a cooperating lesion.

Colorectal cancer (CRC) frequently harbors activating mutations in the WNT and MAPK pathways. While KRAS mutations alone can drive tumor initiation in many tissues, they are insufficient in the intestine. Leveraging allele-specific properties of RAS, we developed a mouse model to investigate MAPK hyperactivation. Here we show that KRAS mutations drive a regenerative state while antagonizing the Lgr5[+] intestinal stem cell state; however, this regenerative state cannot initiate tumorigenesis. Instead, tumor initiation requires a stem-like state dependent on mutational activation of the WNT pathway. We identify two aberrant states-a WNT-driven stem-like state for tumor initiation and MAPK-driven transit-amplifying-like state for tumor growth. These plastic states, essential for tumorigenesis, also impact drug response, potentially explaining lower response rates and shorter duration of response to KRAS-G12C inhibitors in CRC compared to non-small cell lung cancer. These findings highlight the need to target both pathways and their associated cell states for effective CRC treatment.

Gastrointestinal stromal tumors (GISTs) are rare, typically sporadic connective tissue tumors, most commonly located in the stomach or small intestine. We report an unusual case of a 59-year-old female who underwent emergency surgery for hemorrhagic shock caused by a small intestinal GIST, resulting in massive hemoperitoneum. GISTs often remain asymptomatic for a long time, only becoming apparent when they enlarge or cause complications. Very rarely, these tumors present as hemoperitoneum. This case highlights that in patients with hemorrhagic shock, massive hemoperitoneum, and an abdominal mass on imaging, a bleeding GIST should be considered, despite its rarity.

Neuroendocrine neoplasms (NENs) are a heterogeneous group of tumors arising from neuroendocrine cells with malignant potential. NENs of the colorectum are uncommon, and colonic neuroendocrine neoplasms (CNENs) are particularly rare. Here, we report the diagnostic and therapeutic course of a man in his 25-year-old with small-cell neuroendocrine carcinoma (SCNEC) of the descending colon. The patient presented with sudden, severe abdominal pain accompanied by nausea and vomiting. Computed tomography (CT) revealed circumferential wall thickening of the descending colon, blurring of the surrounding fat planes, and multiple small regional lymph nodes; contrast-enhanced CT demonstrated marked, homogeneous, and persistent enhancement. The initial imaging findings were easily confounded with inflammatory disease, and the patient declined further evaluation and was discharged. Nine months later, he was readmitted because of progressive intestinal obstruction. Imaging showed substantial progression of the lesion with extension to the sigmoid colon, accompanied by signs of extra-serosal invasion and peritoneal dissemination. Colonoscopy and histopathology confirmed SCNEC. The patient received ascites control, etoposide plus cisplatin chemotherapy, and supportive care, but the response was poor. This combination of young age and tumor location in the descending colon appears to be uncommon in the existing literature. The case is further distinguished by the presence of circumferential colonic wall thickening on imaging, a feature absent in prior reports. This case highlights that colonic SCNEC in young patients may present with atypical imaging features. Colonic NENs should be included in the differential diagnosis, and early endoscopic biopsy should be performed; definitive diagnosis relies on histopathology and immunohistochemistry to facilitate early recognition and standardized management.

How the small intestine ages at the cellular and molecular level has been unclear. Here we profile single nuclei from young and aged primate small intestine and find that aging brings barrier dysfunction, chronic inflammation and a shift in stem cell differentiation away from absorptive cells toward secretory cells. Through integrative multimodal analysis, we identify the transcriptional corepressor NCoR1 as a key player whose decline is conserved in the aging human gut. In human intestinal epithelial cells and organoids, knocking down NCOR1 recapitulates aging phenotypes including senescence, disrupted junctions and lineage imbalance, whereas overexpressing NCoR1 alleviates them. Metformin-a geroprotective drug-restores NCoR1 levels and delays intestinal aging in nonhuman primates. Our work points to NCoR1 as a central regulator of small intestinal aging and suggests a pharmacologically actionable strategy to counter age-related intestinal decline.

Small bowel tumors are rare malignancies, comprising less than 5% of all gastrointestinal (GI) cancers. The most common subtypes are adenocarcinomas, GI stromal tumors, neuroendocrine tumors, and lymphomas. Workup for these masses includes a combination of endoscopic and high-resolution imaging. Small bowel cancers are generally staged using their depth of invasion, regional lymph node involvement, and distant metastasis. While advances in medical oncology have yielded promising results, surgical resection remains central to treatment of small bowel tumors. With a shift toward minimally invasive approaches in surgery, robotic surgery has gained increasing popularity in resection of small bowel tumors.

Small bowel neuroendocrine neoplasms (SB-NENs) are a distinct subgroup of gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs), characterized by marked biological heterogeneity and a high prevalence of metastatic disease at diagnosis. Their frequently nonspecific clinical presentation, together with small and often multifocal primary lesions, poses significant diagnostic and therapeutic challenges. This review provides a comprehensive overview of SB-NENs, focusing on recent epidemiological trends, key elements of the 2022 World Health Organization (WHO) classification and of the American Joint Committee on Cancer (AJCC) Staging System, and the central role of imaging in clinical management. Emphasis is placed on the complementary value of anatomical and molecular imaging modalities for tumor detection, staging, treatment planning, and response assessment. The key radiologist's contribution to surgical planning is discussed, along with imaging strategies for follow-up and evaluation of treatment response.