Objective:To summarize the precise association between pulmonary tuberculosis(PTB)and P2x7 A1513 C gene polymorphism.Methods:PubMed and Google Scholar web-databases were searched for the studies reporting the associat...Objective:To summarize the precise association between pulmonary tuberculosis(PTB)and P2x7 A1513 C gene polymorphism.Methods:PubMed and Google Scholar web-databases were searched for the studies reporting the association of P2x7 A1513 C polymorphism and PTB risk.A meta-analysis was performed for the selected case-control studies and pooled odds ratios(ORs)and 95%confidence intervals(95%CIs)were calculated for all the genetic models.Results:Eleven studies comprising 2678 controls and 2113 PTB cases were included in this meta-analysis.We observed overall no significant risk in all the five genetic models.When stratified population by the ethnicity,Caucasian population failed to show any risk of PTB in all the genetics models.In Asian ethnicity,variant allele(C vs.A:P=0.001;QR=1.375,95%CI=1.159-1.632)and heterozygous genotype(AC vs.AA:P=0.001;OR=1.570,95%CI=1.269-1.944)demonstrated significant increased risk of PTB.Likewise,recessive genetic model(CC+AC vs.AA:P=0.001;OR=1.540,95%CI=1.255-1.890)also demonstrated increased risk of PTB in Asians.Conclusions:Our meta-analysis did not suggest the association of P2x7 A1513 C polymorphism with PTB risk in overall or separately in Caucasian population.However,it plays a significant risk factor for predisposing PTB in Asians.Future larger sample and expression studies are needed to validate this association.展开更多
Hematological malignancies,including leukemia,lymphoma,and multiple myeloma,develop within and remain dependent on a complex and dynamic tumor microenvironment(TME).Malignant cells interact continuously with the cellu...Hematological malignancies,including leukemia,lymphoma,and multiple myeloma,develop within and remain dependent on a complex and dynamic tumor microenvironment(TME).Malignant cells interact continuously with the cellular and molecular components of the TME,which play a critical role in shaping disease progression,therapeutic response,and immune evasion.The TME comprises mesenchymal stromal cells,immune cells,fibroblasts,endothelial cells,and a range of signaling molecules such as chemokines,cytokines,and extracellular vesicles,embedded within a heterogeneous extracellular matrix(ECM).This integrated network,along with recently established mechanisms,establishes a supportive niche that promotes malignant cell survival,clonal evolution,immune modulation,and therapy resistance.This review examines the cellular and molecular architecture of the hematologic TME and its influence on chemoresistance and immune suppression.It further discusses therapeutic interventions that aim to disrupt or reprogram the TME,thereby restoring therapeutic sensitivity and enhancing immune-mediated clearance.展开更多
文摘Objective:To summarize the precise association between pulmonary tuberculosis(PTB)and P2x7 A1513 C gene polymorphism.Methods:PubMed and Google Scholar web-databases were searched for the studies reporting the association of P2x7 A1513 C polymorphism and PTB risk.A meta-analysis was performed for the selected case-control studies and pooled odds ratios(ORs)and 95%confidence intervals(95%CIs)were calculated for all the genetic models.Results:Eleven studies comprising 2678 controls and 2113 PTB cases were included in this meta-analysis.We observed overall no significant risk in all the five genetic models.When stratified population by the ethnicity,Caucasian population failed to show any risk of PTB in all the genetics models.In Asian ethnicity,variant allele(C vs.A:P=0.001;QR=1.375,95%CI=1.159-1.632)and heterozygous genotype(AC vs.AA:P=0.001;OR=1.570,95%CI=1.269-1.944)demonstrated significant increased risk of PTB.Likewise,recessive genetic model(CC+AC vs.AA:P=0.001;OR=1.540,95%CI=1.255-1.890)also demonstrated increased risk of PTB in Asians.Conclusions:Our meta-analysis did not suggest the association of P2x7 A1513 C polymorphism with PTB risk in overall or separately in Caucasian population.However,it plays a significant risk factor for predisposing PTB in Asians.Future larger sample and expression studies are needed to validate this association.
文摘Hematological malignancies,including leukemia,lymphoma,and multiple myeloma,develop within and remain dependent on a complex and dynamic tumor microenvironment(TME).Malignant cells interact continuously with the cellular and molecular components of the TME,which play a critical role in shaping disease progression,therapeutic response,and immune evasion.The TME comprises mesenchymal stromal cells,immune cells,fibroblasts,endothelial cells,and a range of signaling molecules such as chemokines,cytokines,and extracellular vesicles,embedded within a heterogeneous extracellular matrix(ECM).This integrated network,along with recently established mechanisms,establishes a supportive niche that promotes malignant cell survival,clonal evolution,immune modulation,and therapy resistance.This review examines the cellular and molecular architecture of the hematologic TME and its influence on chemoresistance and immune suppression.It further discusses therapeutic interventions that aim to disrupt or reprogram the TME,thereby restoring therapeutic sensitivity and enhancing immune-mediated clearance.
