Medical oncology
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Review Meta Analysis
Cetuximab in patients with esophageal cancer: a systematic review and meta-analysis of randomized controlled trials.
Esophageal cancer is one cause of the most common cancer death and diagnosed in approximately half a million people annually worldwide, as well as has resulted in worse status, which is responsible for an estimated 482,300 new cases and 406,800 deaths in 2008, and is the fifth highest in the mortality rate among tumor sites. Esophageal cancer mainly occurred in southern and eastern Africa, eastern Asia and some areas of China. ⋯ Moreover, collated differences in overall survival rate and progression-free survival remained the most common grade 3/4/5 toxicities, and quality of life after intervention revealed no evidence of a difference between the two groups. With the present evidence, there is no role for cetuximab combined with standard approaches for esophageal cancer.
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Estrogen classically drives lung cancer development via estrogen receptor β (ERβ). However, fulvestrant, an anti-estrogen-based endocrine therapeutic treatment, shows limited effects for non-small cell lung cancer (NSCLC) in phase II clinical trials. G protein-coupled estrogen receptor (GPER), a third estrogen receptor that binds to estrogen, has been found to be activated by fulvestrant, stimulating the progression of breast, endometrial, and ovarian cancers. ⋯ Importantly, the pro-tumorigenic effects of GPER induced by E2 were significantly reduced by co-administering the GPER inhibitor G15 and the ERβ inhibitor fulvestrant, as compared to administering fulvestrant alone both in vitro and in vivo. Moreover, the phosphorylation of MAPK and Akt was involved in E2/G1-induced GPER activation. In conclusion, our results indicated that a pro-tumor function of GPER exists that mediated E2-/G1-dependent NSCLC progression and showed better efficiency regarding the co-targeting of GPER and ERβ, providing a rationale for further investigation of anti-estrogen clinical therapy.