World Journal of Gastrointestinal Oncology最新文献

This review comprehensively summarized the potential of artificial intelligence (AI) in the management of esophageal cancer. It highlighted the significance of AI-assisted endoscopy in Japan where endoscopy is central to both screening and diagnosis. For the clinical adaptation of AI, several challenges remain for its effective translation. The establishment of high-quality clinical databases, such as the National Clinical Database and Japan Endoscopy Database in Japan, which covers almost all cases of esophageal cancer, is essential for validating multimodal AI models. This requires rigorous external validation using diverse datasets, including those from different endoscope manufacturers and image qualities. Furthermore, endoscopists' skills significantly affect diagnostic accuracy, suggesting that AI should serve as a supportive tool rather than a replacement. Addressing these challenges, along with country-specific legal and ethical considerations, will facilitate the successful integration of multimodal AI into the management of esophageal cancer, particularly in endoscopic diagnosis, and contribute to improved patient outcomes. Although this review focused on Japan as a case study, the challenges and solutions described are broadly applicable to other high-incidence regions.

Background: SMARCB1/INI1-deficient pancreatic undifferentiated rhabdoid carcinoma is a highly aggressive tumor, and spontaneous splenic rupture (SSR) as its presenting manifestation is rarely reported among pancreatic malignancies.

Case summary: We herein report a rare case of a 59-year-old female who presented with acute left upper quadrant abdominal pain without any history of trauma. Abdominal imaging demonstrated a heterogeneous splenic lesion with hemoperitoneum, raising clinical suspicion of SSR. Emergency laparotomy revealed a pancreatic tumor invading the spleen and left kidney, with associated splenic rupture and dense adhesions, necessitating en bloc resection of the distal pancreas, spleen, and left kidney. Histopathology revealed a biphasic malignancy composed of moderately differentiated pancreatic ductal adenocarcinoma and an undifferentiated carcinoma with rhabdoid morphology and loss of SMARCB1 expression. Immunohistochemical analysis confirmed complete loss of SMARCB1/INI1 in the undifferentiated component, along with a high Ki-67 index (approximately 80%) and CD10 positivity. The ductal adenocarcinoma component retained SMARCB1/INI1 expression and was positive for CK7 and CK-pan. Transitional zones between the two tumor components suggested progressive dedifferentiation and underlying genomic instability. The patient received adjuvant chemotherapy with gemcitabine and nab-paclitaxel and maintained a satisfactory quality of life at the 6-month follow-up.

Conclusion: This study reports a rare case of SMARCB1/INI1-deficient undifferentiated rhabdoid carcinoma of the pancreas combined with ductal adenocarcinoma, presenting as SSR - an exceptionally uncommon initial manifestation of pancreatic malignancy.

This letter addresses challenges in the clinical translation of BIBR1532, a promising telomerase inhibitor, for the treatment of esophageal squamous cell carcinoma (ESCC). BIBR1532 exerts its anti-cancer effect by activating DNA damage response (ATR/CHK1 and ATM/CHK2) pathways and downregulating telomere-binding proteins. Although its therapeutic potential is limited by poor aqueous solubility, solid dispersion (SD) technology may overcome this obstacle. Systematic analysis using PubChem-derived simplified molecular input line entry system identifiers and artificial intelligence-driven FormulationDT platform evaluation (oral formulation feasibility index: 0.38) revealed that the SD technology, with superior scalability (32 approved products by 2021) and lower production risks, outperforms lipid-based formulations as an optimal dissolution strategy. Material analysis revealed hydroxypropyl methylcellulose (HPMC) as the optimal carrier with lower hygroscopicity, higher temperature and no intestinal targeting, thus enabling ESCC therapy. HPMC-based SD enhances BIBR1532 solubility and bioavailability for effective ESCC treatment. Future studies should focus on pilot tests for SD fabrication.

Colorectal cancer remains one of the leading causes of morbidity and mortality worldwide. Despite notable advances in early detection and therapeutic strategies, the molecular mechanisms underlying tumor survival, chemotherapy resistance, and metastasis are not yet fully understood. MicroRNAs (miRNAs) have emerged as pivotal regulators of cancer development, as they modulate gene expression and orchestrate key signaling pathways. However, the epigenetic mechanisms that control miRNA expression and their downstream gene targets remain largely unclear. In this review, we highlight the critical role of the colorectal cancer microenvironment in influencing miRNA expression and discuss how this regulation contributes to tumorigenesis. A better understanding of these processes may lead to the identification of novel therapeutic targets and strategies to prevent recurrence.

Background: Sorafenib has been the conventional treatment for advanced hepatocellular carcinoma (HCC) since 2008. While radiological complete responses are extremely rare, improved supportive care and multidisciplinary approaches in clinical practice may explain the recent increase in case reports and retrospective series documenting such responses.

Case summary: This case series describes 3 patients with advanced HCC who achieved durable complete responses using first-line sorafenib therapy, even in the presence of portal vein thrombosis or extrahepatic spread, and highlights the potential for sustained remission in selected patients. Dermatologic toxicity and non-viral etiology may correlate with favorable outcomes; however, reliable predictive biomarkers for sorafenib response are lacking.

Conclusion: Future research into the etiology and molecular differences in HCC is necessary to develop more personalized therapy options.

Over the past ten years, numerous papers have been published on the use of indocyanine green (ICG) fluorescence in liver surgery for hepatocellular carcinoma (HCC). There are many different applications. The first involves targeting superficial tumors in patients with macronodular cirrhosis and an irregular liver surface. In a minimally invasive setting, the lack of tactile feedback on the hepatic surface makes detecting subcapsular HCC with ultrasound alone challenging. ICG fusion images can mimic the tactile feedback of the hand and act as an ultrasound booster. ICG fluorescence can be used to evaluate tumor residues after minimally invasive thermal ablation. ICG fluorescence imaging can also be used to identify the grade of HCC early on and evaluate the microinvasive component.

Colorectal cancer (CRC) is ranked as the third most common tumor globally, representing approximately 10% of all cancer cases, and is the second primary cause of cancer-associated mortality. Existing therapeutic approaches demonstrate limited efficacy against CRC, partially due to the immunosuppressive tumor microenvironment (TME). In recent years, substantial evidence indicates that dysbiosis of the gut microbiota and its metabolic products is closely associated with the initiation, progression, and prognostic outcomes of CRC. In this minireview, we systematically elaborate on how these microbes and their metabolites directly impair intestinal epithelial integrity, activate cancer-associated fibroblasts, remodel tumor vasculature, and critically, sculpt an immunosuppressive landscape by modulating T cells, dendritic cells, and tumor-associated macrophages. We highlight the translational potential of targeting the gut microbiota, including fecal microbiota transplantation, probiotics, and engineered microbial systems, to reprogram the TME and overcome resistance to immunotherapy and chemotherapy. A deeper understanding of the microbiota-TME axis is essential for developing novel diagnostic and therapeutic paradigms for CRC.

Gastric cancer (GC) is the fifth most prevalent malignancy worldwide and remains a leading cause of cancer-related mortality. Major risk factors for GC include Helicobacter pylori infection, increasing age, high dietary salt intake, and diets deficient in vegetables and fruits. Due to the often subtle and nonspecific early symptoms, coupled with the lack of routine screening programs, a significant proportion of GC cases are diagnosed at advanced stages. The etiology of GC is multifactorial, and diagnosis is confirmed histologically through endoscopic biopsy, followed by staging via computed tomography, positron emission tomography, staging laparoscopy, and endoscopic ultrasound. Treatment strategies typically involve a multidisciplinary approach including chemotherapy, surgical resection, radiotherapy, and emerging immunotherapeutic options. Despite advances in diagnostic and therapeutic modalities, the prognosis of advanced GC remains poor, with high rates of recurrence and metastasis. In recent years, increasing attention has been given to the role of tight junction (TJ) proteins in the pathogenesis and progression of GC. TJ proteins, critical components of epithelial barrier function, have been implicated in various stages of gastric carcinogenesis, from intestinal metaplasia to invasion and metastasis. Infection and inflammation, particularly due to Helicobacter pylori, disrupt TJ integrity, compromising the gastric mucosal barrier and facilitating neoplastic transformation. This review synthesizes current evidence from PubMed, EMBASE, Google Scholar, ScienceDirect, SpringerLink, and other reputable databases to provide a comprehensive overview of the involvement of TJ proteins in GC. By elucidating the molecular interplay between TJ dysregulation and gastric tumorigenesis, this work aims to highlight the potential of TJ proteins as novel diagnostic biomarkers and therapeutic targets in GC management.

Experimental therapies targeting immune and stromal cells, such as mast cells, cancer-associated fibroblasts, dendritic cells, and tumor endothelial cells, in the treatment of gastrointestinal solid tumors pose new and complex surgical and medico-legal challenges. These innovative treatments require that informed consent not be limited to simple acceptance of the medical procedure, but instead reflect a true relational and cognitive process grounded in understanding, free choice, and the ability to revoke consent at any time. In particular, it is essential that the patient understands the experimental nature of the therapy, its development stage, potential benefits and risks, as well as the implications for their health and personal dignity. In the case of stromal cell-based treatments, which may exert complex immunomodulatory effects or activate angiogenic pathways that are not yet fully understood, patients must be made fully aware that they are participating in a non-standardized therapy whose outcomes, whether beneficial or harmful, cannot yet be predicted with certainty. This requires particularly careful medical communication, using simple yet scientifically accurate explanations delivered in appropriate language, along with a final verification of the patient's actual understanding.

[This corrects the article on p. 103198 in vol. 17, PMID: 40547171.].