Small Intestinal Carcinoma

P=N/A, N=107, Active, not recruiting, Weill Medical College of Cornell University | Trial completion date: Aug 2025 --> Jun 2026 | Trial primary completion date: Aug 2025 --> Jun 2026

P2, N=36, Recruiting, Sun Yat-sen University | Trial completion date: Nov 2025 --> Dec 2027 | Trial primary completion date: Nov 2024 --> Dec 2027

P=N/A, N=420, Not yet recruiting, Alliance for Clinical Trials in Oncology

P2, N=54, Not yet recruiting, Yale University

In heavily pretreated patients with advanced solid tumors, E7386 demonstrated a manageable safety profile and a dose-dependent PK profile. PRs were noted in patients with small bowel carcinoma or desmoid tumor.

Next-generation sequencing of the primary small intestinal tumor identified pathogenic mutations in PTEN, TP53, ataxia telangiectasia mutated, ephrin type-A receptor 5 and EGFR p.F997L, suggesting a DNA-repair-deficient genomic background and providing potential targets for future precision therapy. Further research is warranted to determine the molecular mechanisms underlying SMARCA4-DUC, for the development of targeted therapeutic strategies and to improve the understanding of the aggressiveness of SMARCA4-DUC.

Notably, weak DOG1 positivity was observed, a rare finding that may complicate distinction from gastrointestinal stromal tumours. This case highlights the diagnostic challenges of small bowel LMS, the central role of surgical resection in management, and the need for careful pathological evaluation to avoid misclassification and guide prognosis.

Compared with the absence of tracer uptake on 18F-FDG PET/CT, 18Ga-FAPI-04 PET/CT showed high tracer uptake and prominent tumor-to-background contrast. The final pathology confirmed an infiltrating adenocarcinoma, originating from the primary duodenal ampullary carcinoma.

Bile acids and the microbiota are necessary for duodenal adenoma development and are potentially modifiable risk factors in humans at risk of duodenal adenomas. The recruitment of myeloid cells may promote tumor progression via the release of reactive oxygen species.

P4, N=400, Recruiting, Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)

In conclusion, aberrant mucin signatures reflect distinct molecular pathways in (pre)malignant GIT lesions and highlight their potential utility as biomarkers and therapeutic targets. Schematic representation of the main findings regarding altered mucin signalling in several precancerous lesions (adenomatous (i.e., conventional pathway 1) and serrated polyps (i.e. pathway 2)) and small intestinal (SIA) and colorectal (CRC) adenocarcinomas and its clinicopathological significance (outcome, anatomical location (proximal/distal), molecular subtypes (MSI, (non)-mucinous).

It underscores the importance of careful clinicopathological correlation and multidisciplinary evaluation in atypical metastatic scenarios, while illustrating how surgery can provide symptom control and enable systemic therapy. Given its rarity, these observations should be interpreted with caution and regarded as descriptive rather than generalizable.