scholarly journals EKSPRESI PD-L1 PADA MENINGIOMA

2020 ◽  
Vol 6 (1) ◽  
pp. 1-10
Author(s):  
Raudatul Janah

ABSTRAKMeningioma merupakan tumor yang paling umum terjadi pada sistem saraf pusat (SSP), berasal dari sel meningothelial lapisan arakhnoid. Programmed Death Ligand 1 (PD-L1) merupakan protein immune checkpoint yang akan menyebabkan imun antitumor tersupresi. Pada meningioma high grade, sel T regulator dan ekspresi PD-L1 meningkat yang disebabkan karena immunosuppressive tumor microenvironment sehingga tumor menjadi agresif. Tingkat ekspresi PD-L1 tidak ditetapkan dalam meningioma. Tergantung pada tingkat ekspresi, anti-PD-L1, mungkin merupakan pengobatan yang efektif untuk meningioma.Kata Kunci : meningioma, PD-L1, Anti PD-L1

ACS Nano ◽  
2021 ◽  
Vol 15 (1) ◽  
pp. 515-525
Author(s):  
Qiang Liu ◽  
Jiangwei Tian ◽  
Ye Tian ◽  
Qinchao Sun ◽  
Dan Sun ◽  
...  

Biomedicines ◽  
2018 ◽  
Vol 6 (4) ◽  
pp. 114 ◽  
Author(s):  
Ping-Chih Hsu ◽  
Cheng-Ta Yang ◽  
David Jablons ◽  
Liang You

The programmed death-ligand 1(PD-L1)/PD-1 pathway is an immunological checkpoint in cancer cells. The binding of PD-L1 and PD-1 promotes T-cell tolerance and helps tumor cells escape from host immunity. Immunotherapy targeting the PD-L1/PD-1 axis has been developed as an anti-cancer therapy and used in treating advanced human non-small cell lung cancer (NSCLC) and malignant pleural mesothelioma (MPM). Yes-associated protein (YAP) is a key mediator of the Hippo/YAP signaling pathway, and plays important roles in promoting cancer development, drug resistance and metastasis in human NSCLC and MPM. YAP has been suggested as a new therapeutic target in NSCLC and MPM. The role of YAP in regulating tumor immunity such as PD-L1 expression has just begun to be explored, and the correlation between YAP-induced tumorigenesis and host anti-tumor immune responses is not well known. Here, we review recent studies investigating the correlation between YAP and PD-L1 and demonstrating the mechanism by which YAP regulates PD-L1 expression in human NSCLC and MPM. Future work should focus on the interactions between Hippo/YAP signaling pathways and the immune checkpoint PD-L1/PD-1 pathway. The development of new synergistic drugs for immune checkpoint PD-L1/PD-1 blockade in NSCLC and MPM is warranted.


Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 57
Author(s):  
Man-Chin Chen ◽  
Christian Ronquillo Pangilinan ◽  
Che-Hsin Lee

Immunotherapy is becoming a popular treatment modality in combat against cancer, one of the world’s leading health problems. While tumor cells influence host immunity via expressing immune inhibitory signaling proteins, some bacteria possess immunomodulatory activities that counter the symptoms of tumors. The accumulation of Salmonella in tumor sites influences tumor protein expression, resulting in T cell infiltration. However, the molecular mechanism by which Salmonella activates T cells remains elusive. Many tumors have been reported to have high expressions of programmed death-ligand 1 (PD-L1), which is an important immune checkpoint molecule involved in tumor immune escape. In this study, Salmonella reduced the expression of PD-L1 in tumor cells. The expression levels of phospho-protein kinase B (P-AKT), phospho-mammalian targets of rapamycin (P-mTOR), and the phospho-p70 ribosomal s6 kinase (P-p70s6K) pathway were revealed to be involved in the Salmonella-mediated downregulation of PD-L1. In a tumor-T cell coculture system, Salmonella increased T cell number and reduced T cell apoptosis. Systemic administration of Salmonella reduced the expressions of PD-L-1 in tumor-bearing mice. In addition, tumor growth was significantly inhibited along with an enhanced T cell infiltration following Salmonella treatment. These findings suggest that Salmonella acts upon the immune checkpoint, primarily PD-L1, to incapacitate protumor effects and thereby inhibit tumor growth.


2019 ◽  
Vol 79 (16) ◽  
pp. 4149-4159 ◽  
Author(s):  
Renee Clift ◽  
Jennifer Souratha ◽  
Sheryl A. Garrovillo ◽  
Susan Zimmerman ◽  
Barbara Blouw

2020 ◽  
Vol 15 (9) ◽  
pp. 1449-1459 ◽  
Author(s):  
Lingzhi Hong ◽  
Marcelo V. Negrao ◽  
Seyedeh S. Dibaj ◽  
Runzhe Chen ◽  
Alexandre Reuben ◽  
...  

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