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

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

OBJECTIVE: To explore the differences in perioperative clinical and pathological characteristics of patients with different pathological types of prostate cancer undergoing radical prostatectomy, and to analyze the influencing factors that may affect the extraglandular invasion of ductal adenocarcinoma of the prostate. METHODS: Retrospective collection was made of the radical prostatectomy patients who were admitted to Peking University Third Hospital from December 2011 to April 2021. The patients were screened based on inclusion criteria to obtain basic clinical features and postoperative pathological results. According to the pathological results, the patients were divided into ductal adenocarcinoma group (mixed with ductal adenocarcinoma) and acinar adenocarcinoma group, and a 1 ∶1 propensity score matching was performed to compare the differences in clinical characteristics between the two groups. Univariate and multivariate analyses of the factors related to extraglandular invasion were performed in the matched ductal adenocarcinoma groups. RESULTS: A total of 764 patients with prostate cancer were enrolled in this study, of which 62 patients were confirmed to have ductal adenocarcinoma components by postoperative pathology. There was a statistically significant difference in the proportion of the patients with a history of diabetes in baseline characteristics between the two groups before propensity score matching (29.5% vs. 17.7%, P=0.027). A total of 61 patients with simple acinar adenocarcinoma were successfully matched with the patients with ductal adenocarcinoma, and there was no statistically significant difference in baseline characteristics between the two groups after matching (P>0.05). The comparison of perioperative clinical and pathological features showed that International Society of Urology Pathology (ISUP) grade (P=0.003), pT stage (P=0.004), extraglandular invasion rate (P=0.018) and vascular thrombus rate (P=0.019) in ductal adenocarcinoma group were significantly higher than those in simple acinous adenocarcinoma group. Univariate analysis of the influence factors of extraglandular invasion showed that prostate-specific antigen (PSA) level, prostate volume, ISUP grade, seminal vesicle invasion and perineural invasion might be the influencing factors of extraglandular invasion (P < 0.10). Binary Logistic regression analysis showed that perineural invasion was an independent factor of extraglandular invasion (OR=11.78, 95%CI: 1.97-70.56, P=0.007). CONCLUSION Prostatic ductal adenocarcinoma has a worse prognosis than simple acinar adenocarcinoma. Perineural invasion is the influencing factor of extraglandular invasion of ductal adenocarcinoma.
Humans ; Male ; Prostatic Neoplasms/surgery* ; Retrospective Studies ; Prostatectomy ; Neoplasm Invasiveness ; Middle Aged ; Aged ; Carcinoma, Ductal/surgery* ; Propensity Score ; Adenocarcinoma/surgery*

Neoplasms characterized by the expression of markers of neuroendocrine differentiation in neoplastic cells are defined as neuroendocrine neoplasms. A case of neuroendocrine carcinomas (NECs) with a small amount of papillary adenocarcinoma and significantly vacuolar nucleus at the esophagogastric junction was reported in this article. A 77-year-old male had dysphagia for one week. Endoscopy revealed early-stage esophagogastric junction carcinoma, and biopsy was diagnosed as poorly differentiated carcinoma. Endoscopic submucosal dissection was performed. Histologically, the papillary adenocarcinoma progresses from typically branching papillary structures (well-differentiated) to hyperplasia of the lining epithelium of the papilla to form a cribriform structure (moderately differentiated), to solid area lacking papillary structures (poorly differentiated). There was a continuous process, and during this process, the vacuoles in the nuclei of tumor cells showed progressive changes from mild to obvious and finally to significant vacuoles. The tumor was mainly composed of solid areas (about 95%), with single cell, large cell, round or oval to irregular nuclei, and significantly vacuolar nuclei, nuclei with larger vacuoles appeared in a loop, a few thin weakly basophilic or weakly eosinophilic fine particles could be seen in the vacuoles, and the vacuoles had rough edges. The nucleus chromatin at the outer edge of the vacuoles was fine particles, and mitosis was common (20-30/mm²), atypical mitosis could be seen, and nucleoli could be seen easily, the cytoplasm was weakly eosinophilic, and the boundaries of cells were unclear. The cells were arranged in a nested, trabecular, or diffuse sheet shape, with some arranged in a glandular tube shape. Tumor thrombus was found in the vein of submucosa; the interstitial tissue rich in capillaries within the tumor was accompanied by a large number of neutrophil infiltration. Immunohistochemical staining showed that the solid area of the tumor was positive for synaptophysin (Syn) and chromogranin A (CgA), while papillary adenocarcinoma was negative. Mucin 5AC (MUC5AC) was diffusely positive in papillary adenocarcinoma, while the proportion of positive cells in the solid area of the tumor was about 10% to 15%. In a word, this case showed the extreme situation of the vacuolar nuclear characteristics of NECs, extremely rare, in a sense, this case expanded the boundary of the morphological spectrum of NECs. Understanding the extreme vacuolar features of this nucleus is helpful to make a correct pathological diagnosis.
Humans ; Male ; Esophagogastric Junction/pathology* ; Aged ; Carcinoma, Neuroendocrine/pathology* ; Vacuoles/pathology* ; Esophageal Neoplasms/pathology* ; Cell Nucleus/pathology* ; Adenocarcinoma, Papillary/pathology* ; Stomach Neoplasms/pathology*

OBJECTIVE: To entrap carvacrol (CAR) in bovine serum albumin nanoparticles (BSANPs) to form CAR-loaded BSANPs (CAR@BSANPs) and to explore the anti-cancer effects in breast adenocarcinoma cells (MCF-7 cells) treated with CAR and CAR@BSANPs. METHODS: A desolvation method was used to synthesize BSANPs and CAR@BSANPs. The BSANPs and CAR@BSANPs were characterized by several physicochemical methods, including visual observation, high-resolution field emission scanning electron microscopy, Fourier transform infrared spectroscopy, and high-performance liquid chromatography. MCF-7 cells were used and analyzed after 24 h of exposure to CAR and CAR@BSANPs at half-maximal inhibitory concentration. The anti-proliferative, apoptotic, reactive oxygen species (ROS), and nitric oxide (NO) scavenging activity as well as gene expression analysis were investigated by the cell viability assay, phase-contrast microscopy, 2',7'-dichlorofluorescein-diacetate assay, Griess-Illosvoy colorimetric assay, and quantitative real-time polymerase chain reaction, respectively. RESULTS: CAR and CAR@BSANPs showed anti-proliferative, apoptotic, ROS generation, and NO scavenging effects on MCF-7 cells. Expression profile of B-cell lymphoma 2-like 11 (BCL2L11), vascular endothelial growth factor A (VEGFA), hypoxia inducible factor factor-1α (HIF1A), BCL2L11/apoptosis regulator (BAX), and BCL2L11/Bcl2 homologous antagonist/killer 1 (BAK1) ratios revealed downregulated genes; and BAX, BAK1, and CASP8 were upregulated by CAR and CAR@BSANPs treatment. In vitro anticancer assays of the CAR and CAR@BSANPs showed that CAR@BSANPs demonstrated higher therapeutic efficacy in the MCF-7 cells than CAR. CONCLUSIONS CAR and CAR@BSANPs affect gene expression and may subsequently reduce the growth and proliferation of the MCF-7 cells. Molecular targeting of regulatory genes of the MCF-7 cells with CAR and CAR@BSANPs may be an effective therapeutic strategy against breast cancer.
Humans ; Cymenes ; Nanoparticles/ultrastructure* ; MCF-7 Cells ; Breast Neoplasms/genetics* ; Apoptosis/drug effects* ; Serum Albumin, Bovine/chemistry* ; Monoterpenes/therapeutic use* ; Adenocarcinoma/genetics* ; Cell Proliferation/drug effects* ; Reactive Oxygen Species/metabolism* ; Female ; Cell Survival/drug effects* ; Animals ; Gene Expression Regulation, Neoplastic/drug effects* ; Nitric Oxide/metabolism* ; Cattle

OBJECTIVES: To explore the molecular mechanism by which lncRNA SNHG15 regulates proliferation, invasion and migration of lung adenocarcinoma cells. METHODS: The lncRNA microarray chip dataset GSE196584 and LncBase were used to predict the lncRNAs that interact with miR-30b-3p, and their association with patient prognosis were investigated using online databases, after which lncRNA nucleolar RNA host gene 15 (SNHG15) was selected for further analysis. The subcellular localization of lncRNA SNHG15 and its expression levels in normal human lung epithelial cells and lung adenocarcinoma cell lines were detected using fluorescence in situ hybridization and qRT-PCR. In cultured A549 cells, the changes in cell proliferation, migration, and invasion following transfection with a SNHG15 knockdown plasmid (sh-SNHG15), a miR-30b-3p inhibitor, or their co-transfection were assessed with EdU, wound healing, and Transwell assays. Bioinformatics analyses were used to predict the regulatory relationship between lncRNA SNHG15 and COX6B1, and the results were verified using Western blotting and rescue experiments in A549 cells transfected with sh-SNHG15, a COX6B1-overexpressing plasmid, or both. RESULTS: LncRNA SNHG15 was shown to target miR-30b-3p, and the former was highly expressed in lung adenocarcinoma, and associated with a poor patient prognosis. LncRNA SNHG15 was localized in the cytoplasm and expressed at higher levels in A549 and NCI-H1299 cells than in BEAS-2B cells. In A549 cells, lncRNA SNHG15 knockdown significantly inhibited cell migration, invasion and proliferation, and these changes were reversed by miR-30b-3p inhibitor. A regulatory relationship was found between lncRNA SNHG15 and COX6B1, and their expression levels were positively correlated (r=0.128, P=0.003). MiR-30b-3p knockdown obviously decreased COX6B1 expression in A549 cells, and COX6B1 overexpression rescued the cells from the inhibitory effects of lncRNA-SNHG15 knockdown. CONCLUSIONS LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.
Humans ; MicroRNAs/metabolism* ; RNA, Long Noncoding/genetics* ; Cell Proliferation ; Cell Movement ; Lung Neoplasms/genetics* ; Adenocarcinoma of Lung ; Neoplasm Invasiveness ; A549 Cells ; Adenocarcinoma/genetics* ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor

OBJECTIVES: To investigate the prognostic significance of PDZ-binding kinase (PBK) in pan-cancer and its potential as a therapeutic target for pancreatic cancer. METHODS: PBK expression levels were investigated in 33 cancer types based on data from TCGA, GEO and CPTAC databases. RT-PCR and Western blotting were employed to examine PBK expression in clinical pancreatic cancer specimens and cell lines. The diagnostic and prognostic value of PBK in pancreatic cancer was evaluated using survival analysis, Cox regression analysis, ROC curve analysis, and clinical correlation studies. Gene enrichment and immune correlation analyses were conducted to explore the potential role of PBK in tumor microenvironment, and its correlation with drug sensitivity was investigated using GDSC and CTRP datasets. In pancreatic cancer BXPC-3 cells, the effects of lentivirus-mediated PBK knockdown on cell proliferation, migration, and invasion were examined using CCK-8, colony formation, and Transwell assays. The interaction between PBK and non-SMC condensin II complex subunit G2 (NCAPG2) was analyzed using co-immunoprecipitation and Western blotting. RESULTS: PBK was overexpressed in multiple cancer types, including pancreatic cancer. A high PBK expression was associated with a poor prognosis of the patients and correlated with immune infiltration and alterations in the tumor microenvironment. Elevated PBK expression was positively correlated with the sensitivity to MEK inhibitors (Trametinib) and EGFR inhibitors (Afatinib) but negatively with the sensitivity to Bcl-2 inhibitors (TW37) and niclosamide. In BXPC-3 cells, PBK knockdown significantly suppressed NCAPG2 expression and inhibited cell proliferation, migration, and invasion. Co-immunoprecipitation confirmed a direct binding between PBK and NCAPG2. CONCLUSIONS PBK is a key regulator of pancreatic cancer and interacts with NCAPG2 to promote tumor progression, suggesting its value as a potential biomarker and therapeutic target for pancreatic cancer.
Humans ; Pancreatic Neoplasms/genetics* ; Prognosis ; Biomarkers, Tumor/genetics* ; Cell Line, Tumor ; Cell Proliferation ; Adenocarcinoma/metabolism* ; Tumor Microenvironment ; Cell Movement ; Mitogen-Activated Protein Kinase Kinases

Objective To investigate whether PLCB1 expression leads to gastric adenocarcinoma metastasis and poor prognosis, and to preliminarily analyze its mechanism. Methods 122 gastric adenocarcinoma patients and their adjacent non-cancerous tissues were selected, and tissue microarray technology was used to detect the expression levels of PLCB1, epithelial cadherin(E-cadherin), vimentin and CD8⁺ T cells by immunohistochemistry, and scored by two pathologists. According to the immunohistochemical score of PLCB1, the patients were divided into PLCB1 high expression group (IHC>90) and PLCB1 low expression group (IHC≤90). The clinical pathological characteristics, epithelial mesenchymal transition(EMT)-related proteins and CD8⁺ T cells expression differences between the two groups were compared. The overall survival of the patients was collected, and COX regression analysis and Kaplan-Meier curve were used to evaluate the relationship between PLCB1 expression level and prognosis. Results PLCB1 was highly expressed in 55 cases of gastric adenocarcinoma tissues, while only 12 cases in adjacent non-cancerous tissues. The tumor invasion depth, lymph node metastasis degree and TNM stage of the PLCB1 high expression group were higher than those of the PLCB1 low expression group. Chi-square test showed that PLCB1 expression level was negatively correlated with E-cadherin (r=-0.339), positively correlated with vimentin (r=0.211), and negatively correlated with CD8⁺ T cells (r=-0.343). Kaplan-Meier curve analysis showed that the overall survival and disease-free survival of gastric adenocarcinoma patients with high PLCB1 expression were significantly reduced. Multivariate COX regression analysis showed that except for lymph node metastasis, tumor invasion depth, TNM stage, E-cadherin and vimentin were also independent prognostic factors for gastric adenocarcinoma patients. Conclusion PLCB1 is highly expressed in gastric adenocarcinoma, and is closely related to tumor aggressiveness and prognosis. PLCB1 may induce EMT and inhibit CD8⁺ T cell infiltration to affect gastric adenocarcinoma metastasis and immune response.
Humans ; Stomach Neoplasms/genetics* ; Epithelial-Mesenchymal Transition ; Male ; Female ; Middle Aged ; Prognosis ; Adenocarcinoma/genetics* ; Cadherins/metabolism* ; Aged ; Adult ; CD8-Positive T-Lymphocytes/immunology* ; Vimentin/metabolism* ; Lymphatic Metastasis ; Neoplasm Metastasis

BACKGROUND: Ferroptosis-related genes play a crucial role in regulating intracellular iron homeostasis and lipid peroxidation, and they are involved in the regulation of tumor growth and drug resistance. The expression of ferroptosis-related genes in tumor tissues can be used to predict patients' future survival times, aiding doctors and patients in anticipating disease progression. Based on the sequencing data of lung adenocarcinoma (LUAD) patients from The Cancer Genome Atlas (TCGA) database, this study identified genes involved in the regulation of ferroptosis, constructed a prognostic model, and evaluated the predictive performance of the model. METHODS: A total of 1467 ferroptosis-related genes were obtained from the GeneCards database. Gene expression profiles and clinical data from 541 LUAD patients were collected from the TCGA database. The expression data of all ferroptosis-related genes were extracted, and differentially expressed genes were identified using R software. Survival analysis was performed on these genes to screen for those with prognostic value. Subsequently, a prognostic risk scoring model for ferroptosis-related genes was constructed using LASSO regression model. Each LUAD patient sample was scored, and the patients were divided into high-risk and low-risk groups based on the median score. Receiver operating characteristic (ROC) curves were plotted, and the area under the curve (AUC) was calculated. Kaplan-Meier survival curves were generated to assess model performance, followed by validation in an external dataset. Finally, univariate and multivariate Cox regression analyses were conducted to evaluate the independent prognostic value and clinical relevance of the model. RESULTS: Through survival analysis, 121 ferroptosis-related genes associated with prognosis were initially identified. Based on this, a LUAD prognostic risk scoring model was constructed using 12 ferroptosis-related genes (ALG3, C1QTNF6, CCT6A, GLS2, KRT6A, LDHA, NUPR1, OGFRP1, PCSK9, TRIM6, IGF2BP1 and MIR31HG). The results indicated that patients in the high-risk group had significantly shorter survival time than those in the low-risk group (P<0.001), and the model demonstrated good predictive performance in both the training set (1-yr AUC=0.721) and the external validation set (1-yr AUC=0.768). Risk scores were significantly associated with the prognosis of LUAD patients in both univariate and multivariate Cox regression analyses (P<0.001), suggesting that this score is an important prognostic factor for LUAD patients. CONCLUSIONS This study successfully established a LUAD risk scoring model composed of 12 ferroptosis-related genes. In the future, this model is expected to be used in conjunction with the tumor-node-metastasis (TNM) staging system for prognostic predictions in LUAD patients.
Humans ; Ferroptosis/genetics* ; Prognosis ; Adenocarcinoma of Lung/pathology* ; Lung Neoplasms/pathology* ; Male ; Female ; Gene Expression Regulation, Neoplastic ; Middle Aged ; ROC Curve

Fusion variations of neurotrophic receptor tyrosine kinase (NTRK) are oncogenic drivers in various solid tumors such as breast cancer, salivary gland carcinoma, infant fibrosarcoma, etc. Gene rearrangements involving NTRK1/2/3 lead to constitutive activation of the tropomyosin receptor kinase (TRK) domain, and the expressed fusion proteins drive tumor growth and survival. NTRK fusions are estimated to occur at a frequency of approximately 0.1% to 1% in non-small cell lung cancer (NSCLC). Epidermal growth factor receptor (EGFR) mutations are prevalent in NSCLC, but the frequency of EGFR G719A mutation is relatively low (about 2%), and EGFR mutations are typically mutually exclusive with NTRK fusion variants. The study presented the first documented case of lung adenocarcinoma harboring both EGFR G719A mutation and LMNA-NTRK1 fusion. A review of the literature was conducted to elucidate the role of NTRK fusion mutations in NSCLC and their relationship with EGFR mutations, aiming to enhance the understanding of NTRK fusion mutations in NSCLC.
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Humans ; Adenocarcinoma/genetics* ; Adenocarcinoma of Lung ; ErbB Receptors/genetics* ; Lamin Type A/genetics* ; Lung Neoplasms/genetics* ; Mutation ; Oncogene Proteins, Fusion/genetics* ; Receptor, trkA/metabolism*