Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Purpose: We aimed to comprehensively analyze the immune cell and stromal components of tumor microenvironment at the single-cell level and identify tumor heterogeneity among the major top-derived oncogene mutations in non-small cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNA-seq) data. Materials and Methods: The scRNA-seq dataset utilized in this study comprised 64369 primary tumor tissue cells from 21 NSCLC patients, focusing on mutations in EGFR, ALK, BRAF, KRAS, TP53, and the wild-type. Results: Tumor immune microenvironment (TIM) analysis revealed differential immune responses across NSCLC mutation subtypes. TIM analysis revealed different immune responses across the mutation subtypes. Two mutation clusters emerged: KRAS, TP53, and EGFR+TP53 mutations (MC1); and EGFR, BRAF, and ALK mutations (MC2). MC1 showed higher tertiary lymphoid structures signature scores and enriched populations of C2-T-IL7R, C3-T/NK-CXCL4, C9-T/NK-NKG, and C1-B-MS4A1 clusters than cluster 2. Conversely, MC2 cells exhibited higher expression levels of TNF, IL1B, and chemokines linked to alternative immune pathways. Remarkably, co-occurring EGFR and TP53 mutations were grouped as MC1. EGFR+TP53 mutations showed upregulation of peptide synthesis and higher synthetic processes, as well as differences in myeloid and T/NK cells compared to EGFR mutations. In T/NK cells, EGFR+TP53 mutations showed a higher expression of features related to cell activity and differentiation, whereas EGFR mutations showed the opposite. Conclusion Our research indicates a close association between mutation types and tumor microenvironment in NSCLC, offering insights into personalized approaches for cancer diagnosis and treatment.