RESUMEN
Gastrointestinal stromal tumors (GIST) are the most common mesenchymal-derived tumors of the GI tract. They can occur throughout the GI tract, and the survival time of some patients can be improved by first-line targeted therapy with imatinib. However, there are some limitations with imatinib treatment. Immunotherapy for GIST has attracted much attention in recent years, and as one of the most abundant cells in the GIST microenvironment, M2 macrophages play an important role in disease progression. They have unique anti-inflammatory and pro-tumorigenic effects and are one target for immunotherapy. This review summarizes the connection between different factors and the programmed death receptor-1/programmed death ligand-1 pathway and M2 macrophages to reactivate or enhance anti-tumor immunity and improve imatinib efficacy, and to provide new ideas for GIST immunotherapy.
RESUMEN
Background: The molecular mechanisms underlying gastric cancer (GC) progression are unclear. The authors examined key genes associated with the prognosis and tumor-infiltrating immune cells in patients with GC. Materials and Methods: Gene expression omnibus (GEO) was used to filter and obtain GC-related differentially expressed genes (DEGs). The molecular functions, biological processes, and cellular components of the DEGs were subjected to enrichment analysis. Protein-protein interaction networks of proteins encoded by the DEGs were analyzed using STRING. The authors also identified hub genes of GC, as well as their expression levels in GC and their relationship with patient prognosis. The relationship between hub genes and tumor-infiltrating immune cells was analyzed by Tumor IMmune Estimation Resource. Results: Six GEO datasets were included in this study, and 265 DEGs were identified. These DEGs were enriched in different signaling pathways and had different biological functions. Six hub genes were potentially significantly related to the molecular mechanisms of GC (TOP2A, FN1, SPARC, COL3A1, COL1A1, and TIMP1). These genes are potential markers of prognosis. Five hub genes were significantly positively correlated with the number of macrophages, neutrophils, and dendritic cells. Conclusions: The authors provide a theoretical basis for exploring the molecular regulation mechanism underlying GC and identifying therapeutic targets.
Asunto(s)
Biomarcadores de Tumor/genética , Regulación Neoplásica de la Expresión Génica/inmunología , Neoplasias Gástricas/mortalidad , Microambiente Tumoral/inmunología , Biología Computacional , Conjuntos de Datos como Asunto , Células Dendríticas/inmunología , Gastrectomía , Mucosa Gástrica/inmunología , Mucosa Gástrica/patología , Mucosa Gástrica/cirugía , Humanos , Estimación de Kaplan-Meier , Linfocitos Infiltrantes de Tumor/inmunología , Neutrófilos/inmunología , Pronóstico , Mapas de Interacción de Proteínas/genética , Transducción de Señal/genética , Transducción de Señal/inmunología , Neoplasias Gástricas/genética , Neoplasias Gástricas/inmunología , Neoplasias Gástricas/cirugía , Tasa de Supervivencia , Microambiente Tumoral/genética , Macrófagos Asociados a Tumores/inmunologíaRESUMEN
BACKGROUND: Despite increasing evidence demonstrated robot-assisted distal gastrectomy (RADG) is safe and feasible for the treatment of advanced gastric cancer (AGC), robot-assisted total gastrectomy (RATG) remains a challenging procedure due to its technical difficulties and possible postoperative complications (POCs). This study aimed to systematically evaluate POCs following RATG. METHODS: Between January 2017 and January 2019, 319 AGC patients with pathological stage T2-4aN0-3M0 who underwent RADG or RATG were enrolled. POCs were stratified using the Clavien-Dindo classification. One-to-one propensity score matching was performed to reduce confounding differences. RESULTS: After matching, 266 patients met the criteria for further analysis. Ultimately, 64 patients (24.1%) who developed POCs had 126 clinical manifestation events. Overall the POCs rate was significantly greater after RATG in comparison with RADG (29.3% vs. 18.8%; Pâ¯=â¯0.045), and more major POCs (Clavien-Dindo gradeâ¯≥â¯IIIa) were observed in the RATG group (14.3% vs. 5.3%; Pâ¯=â¯0.013). The POCs were then classified into local and systemic POCs. The rates of local POCs (35.3% vs. 19.5%; Pâ¯=â¯0.004) and systemic POCs (24.8% vs. 15.0%; Pâ¯=â¯0.046) were significantly higher in the RATG group than the RADG group. Subgroup analysis showed that the anastomotic leakage rate was higher after RATG (5.3% vs. 0.8%; Pâ¯=â¯0.031), whereas the remaining POCs were similar between the two groups. Patients with higher POCs significantly had longer postoperative length of stay (Râ¯=â¯0.895, Pâ¯=â¯0.003). Multivariate analysis confirmed age, extent of resection, and TNM stage were risk factors for all POCs. CONCLUSIONS: These findings demonstrated that RATG is technically feasible and safe for treatment of AGC with acceptable morbidity and mortality rates. The POCs rate of RATG was higher than RADG, especially for anastomotic leakage. More effective anastomotic techniques are needed in RATG to prevent leakage.