The Potential of Death Receptor 4– and 5–Directed Therapies in the Treatment of Lung Cancer

2007 ◽  
Vol 8 (7) ◽  
pp. 413-419 ◽  
Author(s):  
D. Ross Camidge
Keyword(s):  
Lung Cancer ◽  
Death Receptor ◽  
Death Receptor 4

scholarly journals Downregulation of death receptor 4 is tightly associated with positive response of EGFR mutant lung cancer to EGFR-targeted therapy and improved prognosis

Theranostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 3964-3980
Author(s):  
Shuo Zhang ◽  
Zhen Chen ◽  
Puyu Shi ◽  
Songqing Fan ◽  
Yong He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Positive Response ◽  
Death Receptor ◽  
Egfr Mutant ◽  
Death Receptor 4

There is no Significant Association Between Death Receptor 4 (DR4) Gene Polymorphisms and Lung Cancer in Turkish Population

2013 ◽  
Vol 19 (4) ◽  
pp. 779-784 ◽  
Author(s):  
Deniz Taştemir-Korkmaz ◽  
Osman Demirhan ◽  
Sedat Kuleci ◽  
Serap Hastürk
Keyword(s):  
Lung Cancer ◽  
Gene Polymorphisms ◽  
Death Receptor ◽  
Turkish Population ◽  
Death Receptor 4

scholarly journals Expanded human NK cells from lung cancer patients sensitize patients’ PDL1−negative tumors to PD1-blockade therapy

2021 ◽  
Vol 9 (1) ◽  
pp. e001933
Author(s):  
Sophie M Poznanski ◽  
Tyrah M Ritchie ◽  
Isabella Y Fan ◽  
Abdullah El-Sayes ◽  
Ana L Portillo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Nk Cells ◽  
Tumor Regression ◽  
Checkpoint Inhibitors ◽  
Combined Treatment ◽  
Death Receptor ◽  
High Rate ◽  
Advanced Lung Cancer ◽  
Pd1 Blockade

Lung cancer remains the leading cause of cancer death worldwide despite the significant progress made by immune checkpoint inhibitors, including programmed death receptor-1 (PD1)/PD ligand 1 (PDL1)-blockade therapy. PD1/PDL1−blockade has achieved unprecedented tumor regression in some patients with advanced lung cancer. However, the majority of patients fail to respond to PD1/PDL1 inhibitors. The high rate of therapy non-response results from insufficient PDL1 expression on most patients’ tumors and the presence of further immunosuppressive mechanisms in the tumor microenvironment. Here, we sensitize non-responding tumors from patients with lung cancer to PD1-blockade therapy using highly cytotoxic expanded natural killer (NK) cells. We uncover that NK cells expanded from patients with lung cancer dismantle the immunosuppressive tumor microenvironment by maintaining strong antitumor activity against both PDL1+ and PDL1− patient tumors. In the process, through a contact-independent mechanism involving interferon γ, expanded NK cells rescued tumor killing by exhausted endogenous TILs and upregulated the tumor proportion score of PDL1 across patient tumors. In contrast, unexpanded NK cells, which are susceptible to tumor-induced immunosuppression, had no effect on tumor PDL1. As a result, combined treatment of expanded NK cells and PD1-blockade resulted in robust synergistic tumor destruction of initially non-responding patient tumors. Thus, expanded NK cells may overcome the critical roadblocks to extending the prodigious benefits of PD1-blockade therapy to more patients with lung cancer and other tumor types.

Expression of death receptor 4 induces caspase-independent cell death in MMS-treated yeast

2008 ◽  
Vol 376 (2) ◽  
pp. 305-309 ◽  
Author(s):  
Mi-Sun Kang ◽  
Sung-Keun Lee ◽  
Chang-Shin Park ◽  
Ju-Hee Kang ◽  
Sung-Ho Bae ◽  
...  
Keyword(s):  
Cell Death ◽  
Death Receptor ◽  
Death Receptor 4

Death receptor 4 variants enhanced prostate cancer risk in North Indian population

Tumor Biology ◽  
2015 ◽  
Vol 36 (7) ◽  
pp. 5655-5661 ◽  
Author(s):  
Rama D. Mittal ◽  
Raju K. Mandal ◽  
Abhinav Singh ◽  
Priyanka Srivastava
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Indian Population ◽  
Death Receptor ◽  
Prostate Cancer Risk ◽  
North Indian Population ◽  
Death Receptor 4

scholarly journals Ciprofloxacin Enhances TRAIL-Induced Apoptosis in Lung Cancer Cells by Upregulating the Expression and Protein Stability of Death Receptors through CHOP Expression

2018 ◽  
Vol 19 (10) ◽  
pp. 3187 ◽  
Author(s):  
Eun Lim ◽  
Yu Yoon ◽  
Jeonghoon Heo ◽  
Tae Lee ◽  
Young-Ho Kim
Keyword(s):  
Lung Cancer ◽  
Protein Stability ◽  
Cancer Cells ◽  
Death Receptor ◽  
Proteolytic Processing ◽  
Receptor Expression ◽  
Host Cells ◽  
Lung Cancer Cells ◽  
Regulation Of Transcription ◽  
Induced Apoptosis

Ciprofloxacin (CIP) is a potent antimicrobial agent with multiple effects on host cells and tissues. Previous studies have highlighted their proapoptotic effect on human cancer cells. The current study showed that subtoxic doses of CIP effectively sensitized multiple cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Although TRAIL alone mediated the partial proteolytic processing of procaspase-3 in lung cancer cells, co-treatment with CIP and TRAIL efficiently restored the complete activation of caspases. We found that treatment of lung cancer with CIP significantly upregulated the expression and protein stability of death receptor (DR) 5. These effects were mediated through the regulation of transcription factor CCAT enhancer-binding protein homologous protein (CHOP) since the silencing of these signaling molecules abrogated the effect of CIP. Taken together, these results indicated that the upregulation of death receptor expression and protein stability by CIP contributed to the restoration of TRAIL-sensitivity in lung cancer cells.

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