The spleen is a very hostile environment for tumor cells due to its anatomic location, blood supply, and rich immunological property – which makes it one of the most unique organ to be involved in metastatic diseases.15 Splenic metastases from non-hematologic malignancies are rare ranging from 0.6 to 7.1% base on autopsy reports of cancer patients, and 1.1 to 3.4% base on review of splenectomy cases.14 Moreover, isolated splenic metastases are more infrequent with only 31 cases reported from 1969 to October 2015.16 A splenic abscess is an unusual formation and is usually caused by hematogenous spread from an infection. Such expected frequency varies in different autopsy studies between 0.14% and 0.7%.1 Albeit rare, abscess can also result from migration of gut flora brought about by direct invasion of tumor cells from a neighboring neoplasm.17 This is a case of a 36-year-old female who came in with a history of abdominal pain, chills and fever for seven months. CT scan of the whole abdomen revealed splenic abscess with suspicion of a splenic rupture. The patient underwent exploratory laparotomy with abscess evacuation, splenectomy and double barrel colostomy and given with intravenous antibiotics. Histopathology results showed metastatic adenocarcinoma in the spleen. Thorough deliberation of her case was done and she was eventually managed as a case of Colon Cancer Stage IV and underwent chemotherapy. Splenic abscess developing from splenic metastasis from a colonic adenocarcinoma is rare and with concomitant high mortality rate. More often than not, splenic metastasis is discovered in advanced stage together with metastatic tumor in other organs while isolated splenic metastasis is even more uncommon. A splenic abscess as an initial demonstration of a colon cancer is not a common daily encounter of physicians hence a high index of suspicion coupled with sensitive and specific imaging is necessary in order to provide prompt medical and surgical intervention.

Human ; Female ; Adult: 25-44 Yrs Old ; Abdomen ; Adenocarcinoma ; Autopsy ; Colostomy ; Gastrointestinal Microbiome ; Pain ; Research Report ; Infections ; History ; Splenic Rupture ; World Health Organization ; Neoplasms ; Disease ; Fever ; Hematologic Neoplasms

Abstract Ectopic hepatocellular carcinoma (EHCC) is an extremely rare neoplasm, especially in the mediastinum, which shares morphologic characteristics with intrahepatic hepatocellular carcinoma (HCC). Its clinical features remain unclear, posing significant diagnostic and therapeutic challenges. The prognosis is also unclear due to its rarity and potential variability. This study reports the first case of EHCC in the mediastinum with subsequent brain metastasis. A 50-year-old man presented with shoulder and chest discomfort persisting for 5 months, accompanied by progressive weight loss and fatigue over the preceding 2 years. Imaging showed a mediastinal mass initially suspected to be lymphoma due to its malignant characteristics. However, histopathological examination identified the lesion as HCC, supported by characteristic immunohistochemical markers, despite normal abdominal imaging. Two months later, the tumor progressed despite intensive radiotherapy, and the patient experienced recurrent seizures. Subsequent brain imaging confirmed multiple intracranial metastases. Unfortunately, the patient died 6 months after diagnosis. The ectopic liver is more susceptible to hepatocarcinogenesis than the main liver; this is attributed to its incomplete functional structure. EHCC can be considered as differential diagnosis of mediastinal masses, even when no intrahepatic HCC is found. The rarity of EHCC in the mediastinum poses difficulties in developing treatment protocols. This case emphasizes the diagnostic challenges and aggressive nature of ectopic HCC and the need for comprehensive management strategies. There are currently no definite guidelines regarding the diagnosis, treatment, and prognosis of EHCC.
ectopic hepatocellular carcinoma ; mediastinum ; metastasis

Introduction: Pancreatic neuroendocrine tumors (PNETs) are rare, comprising less than 3% of all pancreatic neoplasms. These tumors are broadly classified as functioning or nonfunctioning. Insulinoma is the most common functioning PNET. Non-functioning PNETs often present significant diagnostic issues and may be misdiagnosed as pancreatic adenocarcinoma, especially when immunohistochemical evaluation is omitted during histological examination. We describe a case of metastatic insulinoma that was misdiagnosed as a poorly differentiated pancreatic adenocarcinoma. Case: A 65-year-old female first presented to a private hospital in 2023 with obstructive jaundice and was found to have a pancreatic head lesion that was causing biliary obstruction. As a result, a biliary stent was placed. She underwent aortocaval lymph node biopsy, and the result showed poorly differentiated pancreatic adenocarcinoma. Nonetheless, she refused surgical and oncological intervention. Even so, she remained clinically stable and maintained good functional status for 2 years. In 2025, she presented to Hospital Canselor Tuanku Muhriz with recurrent hypoglycemia fulfilling Whipple’s triad. The unexpectedly indolent clinical course prompted reassessment of the initial diagnosis. Biochemical evaluation confirmed endogenous hyperinsulinemic hypoglycemia, with inappropriately elevated insulin (11.03 µIU/mL) and C-peptide levels (1,089 pmol/L). Computer tomography of the abdomen revealed multiple hepatic lesions and progressive lymphadenopathy, suggestive of metastatic disease. Re-evaluation of the initial histopathological specimen showed a well-differentiated neuroendocrine tumor (Grade 1, Ki-67 ~2%). Hence, the diagnosis was revised to metastatic insulinoma. She was referred to the hepatobiliary surgical team for surgical debulking, but the procedure was deemed highrisk and likely to have high mortality due to the extent of the disease. She was managed with diazoxide and longacting somatostatin analogues for glycemic control. Conclusion This case highlights the critical importance of diagnostic vigilance when evaluating pancreatic neoplasms. Persistent or unexplained clinical courses, especially when endocrine symptoms arise, should prompt thorough reassessment. Immunohistochemical confirmation is essential to avoid misdiagnosis and ensure optimal patient management.
Adenocarcinoma ; Insulinoma ; Pancreatic Neoplasms

China is a high-incidence region for gastric cancer globally. The disease is characterized by a high morbidity rate, low early diagnostic rate, and poor long-term outcomes, imposing a significant burden on both patients and society. Therefore, exploring the pathogenesis of gastric cancer, developing novel therapeutic strategies, and identifying new drug targets is of great importance. Telomerase expression is broadly associated with cancer cell targeting, and its up-regulation is one of the key factors driving the initiation and progression of gastric cancer. Additionally, telomerase is intricately involved in the regulation of autophagy and autophagy-associated cell death. While autophagy can induce chemoresistance, excessive autophagy may lead to cell death, which also constitutes one of the mechanisms of chemotherapy. Telomerase not only directly contributes to gastric cancer pathogenesis but also indirectly influences its development and treatment by modulating autophagy and autophagic cell death. Therefore, telomerase holds promise as a novel therapeutic target in gastric cancer.
Humans ; Stomach Neoplasms/genetics* ; Telomerase/genetics* ; Autophagy/physiology*

Acquired hemophilia A (AHA) is a rare autoimmune bleeding disorder. Its occurrence secondary to hepatobiliary malignancies is even rarer, and without timely diagnosis and treatment, the mortality rate is extremely high. There is a need to raise awareness of this disease. This report describes a case of a 70-year-old female patient diagnosed with AHA 2 months after surgery for cholangiocarcinoma, admitted to the Second Affiliated Hospital of Bengbu Medical College in October 2022. The patient presented with subcutaneous hematoma in both lower limbs. Coagulation function tests showed a markedly prolonged activated partial thromboplastin time (APTT) of 74.5 seconds, with no correction in the APTT mixing test. Coagulation factor assays revealed a severely reduced coagulation factor VIII activity (FVIII:C) of 0.3%, and an inhibitor titer of 25.6 BU/mL was detected. After ruling out other potential causes, the patient was diagnosed with cholangiocarcinoma-associated AHA. With chemotherapy to control the primary tumor, alongside hemostatic and immunosuppressive therapy for inhibitor eradication, AHA was brought under control. The patient had no further coagulation abnormalities or bleeding, enabling timely and full-course chemotherapy for cholangiocarcinoma and significantly improving survival and quality of life. Therefore, in patients with malignancies who present with spontaneous bleeding or unusual bleeding following surgery, trauma, or invasive procedures, clinicians should be alert to the possibility of secondary AHA. Timely diagnosis and treatment can significantly improve prognosis.
Humans ; Cholangiocarcinoma/surgery* ; Female ; Hemophilia A/drug therapy* ; Aged ; Bile Duct Neoplasms/surgery* ; Factor VIII

OBJECTIVES: The application of photodynamic therapy in solid tumors has attracted increasing attention in recent years, and the efficiency of photosensitizers is a crucial determinant of therapeutic efficacy. This study aims to evaluate the cytotoxic effects of a novel photosensitizer, PEG-MTPABZ-PyC, in photodynamic therapy against gastric cancer cells. METHODS: Gastric cancer MKN45 cells were treated with PEG-MTPABZ-PyC. A high-content live-cell imaging system was used to assess the cellular uptake kinetics and subcellular localization of the photosensitizer. The cytotoxic effects of PEG-MTPABZ-PyC-mediated photodynamic therapy were examined using the cell counting kit-8 (CCK-8) assay and flow cytometry, while the intrinsic cytotoxicity of the photosensitizer alone was verified by the CCK-8 assay. Intracellular reactive oxygen species (ROS) generation after photodynamic therapy was detected using 2'-7'-dichlorodihydrofluorescein diacetate (DCFH-DA). RESULTS: PEG-MTPABZ-PyC alone exhibited no cytotoxicity toward MKN45 cells, indicating excellent cytocompatibility. The compound efficiently entered cells within 6 hours and localized predominantly in lysosomes. Upon light irradiation, PEG-MTPABZ-PyC-mediated photodynamic therapy induced significant cytotoxicity compared with the control group (P<0.05) and generated abundant intracellular ROS. CONCLUSIONS The novel photosensitizer PEG-MTPABZ-PyC demonstrates potent photodynamic cytotoxicity against gastric cancer cells, showing promising potential for further development in gastric cancer photodynamic therapy.
Humans ; Stomach Neoplasms/drug therapy* ; Photochemotherapy/methods* ; Photosensitizing Agents/pharmacology* ; Cell Line, Tumor ; Polyethylene Glycols/chemistry* ; Reactive Oxygen Species/metabolism* ; Mesoporphyrins/pharmacology*

Objective:Paragangliomas （PGLs） are chromaffin cell tumors originating from paraganglia and are classified as neuroendocrine neoplasms.They predominantly occur along the distribution area of the paraganglia, commonly occurring between the ages of 20 and 40, with a slight male predominance.They are most frequently found in the axial regions from the skull base to the pelvic cavity. Paragangliomas in the head and neck region typically lack endocrine functionality and primarily manifest through local mass effects. However, clinical signs and symptoms alone cannot reliably distinguish between metastatic and non-metastatic cases. Clinically apparent metastatic paragangliomas are relatively rare. Herein, we present a case of a paraganglioma located in the region of the jugular foramen with liver, bone, and lymph node metastases, and discuss the treatment and prognosis of head and neck paragangliomas.
Humans ; Head and Neck Neoplasms/pathology* ; Jugular Foramina/pathology* ; Liver Neoplasms/secondary* ; Lymphatic Metastasis ; Paraganglioma/pathology*

Nuclear factor erythroid 2-related factor 2 (Nrf2) is an intracellular transcription factor that helps protect against oxidative stress in different types of cells under pathological conditions. Mitochondria are vital organelles that function in diverse metabolic processes in the body, including redox reactions, lipid metabolism, and cell death. Mitophagy, a specific form of autophagy for damaged mitochondria, plays a critical role in the pathophysiology of liver diseases. In this review, we explain in detail the roles of the Nrf2 signaling pathway and mitophagy, and the relationship between them, in various hepatic diseases (nonalcoholic fatty liver disease, viral hepatitis, alcoholic liver disease, drug-induced liver injury, autoimmune hepatitis, hepatic ischemia‒reperfusion injury, and liver cancer). We also offer some potential insights and treatments relevant to clinical applications.
Humans ; NF-E2-Related Factor 2/metabolism* ; Mitophagy/physiology* ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Signal Transduction ; Liver Diseases/etiology* ; Animals ; Oxidative Stress ; Mitochondria/metabolism* ; Non-alcoholic Fatty Liver Disease ; Liver Neoplasms

OBJECTIVES: To investigate the active ingredients in Hedyotis diffusa-Scutellaria barbata D. Don and the main biological processes and signaling pathways mediating their inhibitory effect on primary hepatocellular carcinoma (HCC). METHODS: The core intersecting genes of HCC and the two drugs were screened from TCMSP, Uniport, Genecards, and String databases using Cytoscape software, and GO and KEGG enrichment analyses of the intersecting genes were conducted. Molecular docking between the active ingredients of the drugs and the core genes was carried out using Pubcham, RCSB and Autoduckto to identify the active ingredients with the highest binding energy, whose inhibitory effect on HepG2 cells was verifies using CCK-8 assay, flow cytometry and Western blotting. RESULTS: TP53 and ESR1 were identified as the core genes of HCC and the two drugs. GO and KEGG analyses showed that the two genes were mainly involved in regulation of apoptotic signaling pathway, cell population proliferation, methane raft, and protein kinase activity, and participated in the signaling pathways of apoptosis, proteoglycans in cancer, PI3K Akt signaling pathway, and hepatitis B. Molecular docking studies showed that the active ingredients of the drugs could be docked with TP53 and ESR1 genes under natural conditions, and ursolic acid had the highest binding energy to ESR1 (-4.98 kcal/mol). The results of CCK-8 assay, flow cytometry and Western blotting all demonstrated significant inhibitory effect of ursolic acid on HepG2 cells. CONCLUSIONS The inhibitory effect of Hedyotis diffusa-scutellariae barbatae on HCC is mediated by multiple active ingredients in the two drugs.
Humans ; Molecular Docking Simulation ; Liver Neoplasms/drug therapy* ; Hep G2 Cells ; Network Pharmacology ; Carcinoma, Hepatocellular/drug therapy* ; Hedyotis/chemistry* ; Signal Transduction/drug effects* ; Cell Proliferation/drug effects* ; Tumor Suppressor Protein p53/metabolism* ; Apoptosis/drug effects* ; Estrogen Receptor alpha/metabolism* ; Drugs, Chinese Herbal/pharmacology*

OBJECTIVES: To investigate the association of NUF2 expression with tumor prognosis and its regulatory role in tumor microenvironment. METHODS: We analyzed NUF2 expression, its prognostic value, and is immune-related functions across different cancer types using datasets from the Human Protein Atlas (HPA), TCGA, GTEx, CCLE, and TIMER. RT-qPCR, Western blotting, and immunohistochemistry were used to detect NUF2 expression in liver cancer cell lines and tissue and blood samples from patients with liver cancer. GO, KEGG, and GSEA analyses were conducted to explore the molecular mechanisms of NUF2 and its related genes, and a competitive endogenous RNA (ceRNA) network for NUF2 in liver cancer was constructed. RESULTS: NUF2 expression was upregulated in the tumor tissues of 27 cancers and was associated with clinical stages in several cancers. High NUF2 expressions were correlated with poor overall survival, disease-specific survival, progression-free survival, and disease-free survival of cancer patients. NUF2 expression levels were positively correlated with tumor mutational burden, microsatellite instability, infiltrating immune cells, immune cell marker genes and immune checkpoint genes in different cancers. RT-qPCR, Western blotting, and immunohistochemistry confirmed that NUF2 expression was upregulated in liver cancer cell lines and tumor tissues and blood samples of liver cancer patients, and was decreased significantly after operation. GO, KEGG and GSEA analyses indicated that NUF2 was involved in chromosome segregation and cell cycle and was associated with glycine, serine and threonine metabolism. CONCLUSIONS NUF2 expression is upregulated in 27 cancers and is associated with clinical stage and poor prognosis in some malignancies. NUF2 expression is closely correlated with immune cell infiltration in different cancers, suggesting its potential value for predicting immunotherapy response in these cancers.
Humans ; Prognosis ; Immunotherapy ; Tumor Microenvironment ; Liver Neoplasms/metabolism* ; Cell Line, Tumor ; Neoplasms/genetics* ; Gene Expression Regulation, Neoplastic ; Biomarkers, Tumor/genetics*