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Crosstalk between PD-L1 and Jak2-Stat3/ MAPK-AP1 signaling promotes oral cancer progression, invasion and therapy resistance
CONCLUSIONS: PD-L1 was regulated mainly by the Jak2-Stat3/ MAPK-AP1 pathway, and besides the routine immunological functions, it supports OSCC survival, invasion, and therapy resistance. PD-L1 can be used as an indicator of severity and can be targeted along with Jak2-Stat3/ MAPK-AP1 for a better outcome OSCC.PMID:37678027 | DOI:10.1016/j.intimp.2023.110894
Source: International Immunopharmacology - September 7, 2023 Category: Allergy & Immunology Authors: Arpita Jha Manzar Alam Tanushree Kashyap Nidhi Nath Anjali Kumari Kamdeo K Pramanik Siddavaram Nagini Rajakishore Mishra Source Type: research

Identification and validation of Osteopontin and receptor for hyaluronic acid-mediated motility (RHAMM, CD168) for potential immunotherapeutic significance of in lung squamous cell carcinoma
CONCLUSIONS: By using integrated bioinformatics, we have identified CD168 and OPN as DEGs with poor prognosis in LUSC and have validated their interaction in the ECM receptor pathway. These genes could be potential diagnostic and therapeutic targets for LUSC patients undergoing immunotherapy.PMID:35334357 | DOI:10.1016/j.intimp.2022.108715
Source: International Immunopharmacology - March 25, 2022 Category: Allergy & Immunology Authors: Gao Shan Li Meihe Kang Minchao Zhao Rui Wen Xiaopeng Zhang Guangjian Zheng Jin Source Type: research

Myeloid Derived Suppressor Cells Interactions With Natural Killer Cells and Pro-angiogenic Activities: Roles in Tumor Progression
Conclusions MDSC are major players in the immunosuppressive scenario in cancer, thanks to their phenotype heterogeneity and critical interaction with several innate immune cells, thus representing a crucial target in oncology. Here we reviewed the interactions of MDSCs with NK cells. The contribution of key cytokines, chemokines and mediators active in this process have been discussed. We also described the contribution of MDSC on angiogenesis directly or indirectly through interactions with NK and immunosuppressive activities. A parallel of the cancer associated to the decidual counterpart of these cells is discussed, a...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Downregulation of p70S6K Enhances Cell Sensitivity to Rapamycin in Esophageal Squamous Cell Carcinoma.
Authors: Lu Z, Peng K, Wang N, Liu HM, Hou G Abstract It has been demonstrated that mTOR/p70S6K pathway was abnormally activated in many cancers and rapamycin and its analogs can restrain tumor growth through inhibiting this pathway, but some tumors including esophageal squamous cell carcinoma (ESCC) appear to be insensitive to rapamycin in recent studies. In the present study, we explored the measures to improve the sensitivity of ESCC cells to rapamycin and identified the clinical significance of the expression of phosphorylated p70S6K (p-p70S6K). The results showed that, after downregulating the expression of p7...
Source: Journal of Immunology Research - September 8, 2016 Category: Allergy & Immunology Tags: J Immunol Res Source Type: research