The non-small-cell lung cancer drug market

2016 ◽  
Vol 15 (4) ◽  
pp. 229-230 ◽  
Author(s):  
Khurram Nawaz ◽  
Rachel M. Webster
2020 ◽  
Vol 19 (8) ◽  
pp. 507-508
Author(s):  
Joshua B. N. Dawkins ◽  
Rachel M. Webster

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Tae Woo Kim ◽  
Da-Won Hong ◽  
Sung Hee Hong

Abstract Peroxisome proliferator-activated receptor gamma (PPARγ) is a well-known therapeutic target for type 2 diabetes as well as is a potential target for effective anti-cancer drug, since PPARγ ligands such as ciglitazone (Cig) frequently cause cell death in many types of cancer cells and suppress tumor growth. However, many cancer patients acquire chemo-resistance or radio-resistance after chemo or radiotherapy, and it is still unclear. In the difficulty of well-known anti-cancer drugs, we developed a novel PPARγ agonist CB13 (1-benzyl-5-(4-methylphenyl) pyrido [2,3-d]pyrimidine-2,4(1H,3H)-dione) and investigated the anti-cancer effect and cell death mechanism on human non-small cell lung cancer (NSCLC) cells. With anti-cancer effect of Cig, CB13 also causes inhibition of cell growth by decreasing cell viability, increasing the release of LDH, and increasing caspase-3, and caspase-9 activities. CB13 generates reactive oxygen species (ROS) and causes cell death via ER stress in NSCLC and radio-resistant NSCLC cells (A549R and H460R), and a combination of CB13 and radiation induces greater ER stress and cell death when compared to CB13 alone. Taken together, our results suggest that a combination of CB13 and radiation may overcome radio-resistance caused by radiotherapy.


2018 ◽  
Vol 10 (8) ◽  
pp. 879-894 ◽  
Author(s):  
Marina Pifano ◽  
Juan Garona ◽  
Natasha T Sobol ◽  
Marina Albertó ◽  
Daniel F Alonso ◽  
...  

2013 ◽  
Vol 8 (11) ◽  
pp. 1381-1397 ◽  
Author(s):  
Sabrina Vari ◽  
Sara Pilotto ◽  
Marcello Maugeri-Saccà ◽  
Ludovica Ciuffreda ◽  
Ursula Cesta Incani ◽  
...  

2021 ◽  
Author(s):  
Nhung NGUYEN ◽  
Nghia TRAN ◽  
Quang LE ◽  
Oanh NGUYEN ◽  
Hai PHAM

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