Tumour necrosis factor (TNF)-α plays an important role in inflammatory, infectious, and tumor processes, and it is closely related to the early stages of gastric cancer. It is a pro-inflammatory cytokine, produced not only by macrophages and monocytes but also by the lymphocytes, mast cells, neutrophils, keratinocytes, smooth muscle cells, and some tumor cell lines. Large amounts of TNF are released upon contact of macrophages, CD4 + T lymphocytes, and natural killer (NK) cells with lipopolysaccharides, bacterial products, and interleukin 1. TNF-alpha inducing protein (Tipa) is a unique carcinogenic factor of Helicobacter pylori, secreted into culture broth. The biological activities of TNF alpha and deletion mutant were studied. TNF alpha protein specifically binds to cell-surface nucleolin and then enters the gastric cancer cells, where TNF-a and chemokine gene expressions are induced by NF-jB activation. Nucleolin localizes on the surface of gastric cancer cells, and interaction between TNF alpha and cell-surface nucleolin causes a cancer-oriented microenvironment that increases the risk of gastric cancer. This paper discusses a mechanism of gastric cancer development and the clinical significance of tumor necrosis-alpha and carcinoembryonic antigen in gastric cancer.

Type 2 diabetes mellitus (DM) is a chronic metabolic disorder posing multifaceted challenges to global public health. Among its numerous complications, infected diabetic foot ulcers (IDFUs) represent a particularly debilitating consequence. Beyond cardiovascular implications, there is an emerging understanding of the interconnectedness among IDFUs, neuropathy, atherosclerosis, and dyslipidemia. IDFUs, peripheral neuropathy, and atherosclerosis share common risk factors and mechanistic pathways. The primary objective of this study was to characterize the lipid profiles in DM patients with IDFUs, comparing them with DM patients without foot ulcers, and with a control group of healthy subjects. The secondary objectives included evaluating apolipoprotein E (ApoE) levels across these study groups and comparing lipid profiles within IDFU subgroups. A total of 160 patients were assessed for this study. After applying exclusion criteria, 140 participants were included, divided into three groups: Group IDFU (80 patients with IDFUs), Group DM (32 patients with DM but no foot ulcers), and Group Controls (28 healthy controls). Compared to Group DM, Group IDFU demonstrated lower levels of high-density lipoprotein cholesterol (HDL-C) (30.9 ± 12.6 mg/dL vs. 40.8 ± 16.6 mg/dL, p = 0.002), but improved levels of ApoE (160.9 ± 68.4 mg/dL vs. 197.2 ± 69.6 mg/dL, p = 0.01), triglycerides (TG) (126.9 ± 56.2 mg/dL vs. 165.8 ± 79.0 mg/dL, p = 0.004), low-density lipoprotein cholesterol (LDL-C) (84.2 ± 32.3 mg/dL vs. 92.3 ± 39.3 mg/dL, p = 0.1), and total cholesterol (133.6 ± 43 mg/dL vs. 164.6 ± 44.4 mg/dL, p = 0.002). The IDFU patients exhibit improved lipid profiles, excepting HDL-C, which is unusual because IDFU follows complications related to dyslipidemia for DM patients. Anemia, impaired renal function, and elevated TG levels were identified as biomarkers for mortality among patients with IDFUs. The data suggest that a lower level of HDL-C and an improved lipid profile may indicate a systemic end-stage disease manifestation in DM patients with IDFUs.

Strategies have been researched and implemented to reduce the number of people with diabetic foot ulcers (DFUs). One problem is the accurate assessment of DFU severity, which is the main factor in resource allocation and treatment choice. The primary objective of this study was to assess pentraxin-3 as a biomarker of an infected DFU (IDFU), the limb amputation level prognosis, and patient survival. The secondary objectives were to evaluate and compare other markers, including white blood cells (WBCs), C-reactive protein (CRP), the erythrocyte sedimentation rate (ESR), and procalcitonin (PCT), for identifying IDFUs. Over a period of two years, 145 patients were followed; 131 of these were analyzed for this study. Pentraxin-3 was found to be a good predictor of death (p = 0.047). A comparison between IDFUs and DFUs revealed the following differences: PCT had the highest AUROC of 0.91, sensitivity of 93.7, and specificity of 83.3%. CRP had a cutoff value of 226 mg/L, an AUROC of 0.89, a sensitivity of 95.5%, and a specificity of 83.3%. Fibrinogen had an AUROC of 0.87 at a cutoff value of 5.29 g/L, with a good sensitivity and specificity of 85% and 87%, respectively. ESR had a cutoff value of 46 mm/h, an AUROC of 85%, a sensitivity of 83.7%, and a specificity of 83.3%. Pentraxin-3 showed promising results in predicting IDFUs and DFUs, and it served as a marker for the risk of death in IDFU patients during the 6 month follow-up. Other markers, including CRP, PCT, ESR, and fibrinogen, were more effective in differentiating between IDFUs and DFUs.

Background/Objectives: Gastric cancer remains a leading cause of cancer mortality worldwide. Reliable biomarkers are crucial for early detection, prognostication, and therapy monitoring. While classical tumor markers such as carcinoembryonic antigen (CEA), cancer antigen (CA)19-9, CA72-4, and alpha-fetoprotein (AFP) are used in clinical practice, their accuracy can be limited. Tumor necrosis factor alpha (TNF-α) is an inflammatory cytokine implicated in tumor progression, yet its relationship with established gastric cancer tumor markers has not been fully clarified. This study aimed to determine whether elevated TNF-α correlates with key tumor markers and disease stage in gastric cancer. Methods: In this prospective observational study, we enrolled 80 gastric cancer patients and 20 non-neoplastic controls. Baseline clinical data, laboratory parameters, and tumor markers (CEA, CA19-9, CA72-4, AFP) were recorded. TNF-α concentrations were measured using enzyme-linked immunosorbent assays. Correlation analyses and multivariate regression were performed to assess the relationship of TNF-α with tumor markers, inflammatory indices, and disease stage. Results: TNF-α was significantly elevated in gastric cancer patients (median 4.5 pg/mL) compared to controls (2.9 pg/mL). TNF-α showed a robust correlation with CA19-9 (rho = 0.502) and CA72-4 (rho = 0.385), and a moderate correlation with CEA (rho = 0.279). TNF-α concentrations were highest in Stage IV disease and in the intestinal-type histology. In regression analysis, only CA19-9 and CA72-4 remained independent predictors of TNF-α after controlling for clinical confounders. Conclusions: TNF-α is strongly associated with CA19-9 and CA72-4 and rises with advancing stage, highlighting its potential as an adjunct marker for assessing gastric cancer burden. These findings provide a rationale for further research on TNF-α as both a prognostic biomarker and a possible therapeutic target in gastric cancer.