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Nano drug delivery systems in upper gastrointestinal cancer therapy
Salapa Julia,Bushman Allison,Lowe Kevin,Irudayaraj Joseph 나노기술연구협의회 2020 Nano Convergence Vol.7 No.38
Upper gastrointestinal (GI) carcinomas are characterized as one of the deadliest cancer types with the highest recurrence rates. Their treatment is challenging due to late diagnosis, early metastasis formation, resistance to systemic therapy and complicated surgeries performed in poorly accessible locations. Current cancer medication face deficiencies such as high toxicity and systemic side-effects due to the non-specific distribution of the drug agent. Nanomedicine has the potential to offer sophisticated therapeutic possibilities through adjusted delivery systems. This review aims to provide an overview of novel approaches and perspectives on nanoparticle (NP) drug delivery systems for gastrointestinal carcinomas. Present regimen for the treatment of upper GI carcinomas are described prior to detailing various NP drug delivery formulations and their current and potential role in GI cancer theranostics with a specific emphasis on targeted nanodelivery systems. To date, only a handful of NP systems have met the standard of care requirements for GI carcinoma patients. However, an increasing number of studies provide evidence supporting NP-based diagnostic and therapeutic tools. Future development and strategic use of NP-based drug formulations will be a hallmark in the treatment of various cancers. This article seeks to highlight the exciting potential of novel NPs for targeted cancer therapy in GI carcinomas and thus provide motivation for further research in this field.
Han, D.,Walsh, Matthew C.,Cejas, Pedro J.,Dang, Nicholas N.,Kim, Youngmi F.,Kim, J.,Charrier-Hisamuddin, L.,Chau, L.,Zhang, Q.,Bittinger, K.,Bushman, Frederic D.,Turka, Laurence A.,Shen, H.,Reizis, B. Cell Press 2013 Immunity Vol.38 No.6
The intracellular signaling molecule TRAF6 is critical for Toll-like receptor (TLR)-mediated activation of dendritic cells (DCs). We now report that DC-specific deletion of TRAF6 (TRAF6ΔDC) resulted, unexpectedly, in loss of mucosal tolerance, characterized by spontaneous development of T helper 2 (Th2) cells in the lamina propria and eosinophilic enteritis and fibrosis in the small intestine. Loss of tolerance required the presence of gut commensal microbiota but was independent of DC-expressed MyD88. Further, TRAF6ΔDC mice exhibited decreased regulatory T (Treg) cell numbers in the small intestine and diminished induction of iTreg cells in response to model antigen. Evidence suggested that this defect was associated with diminished DC expression of interleukin-2 (IL-2). Finally, we demonstrate that aberrant Th2 cell-associated responses in TRAF6ΔDC mice could be mitigated via restoration of Treg cell activity. Collectively, our findings reveal a role for TRAF6 in directing DC maintenance of intestinal immune tolerance through balanced induction of Treg versus Th2 cell immunity.