The major limitation of conventional chemotherapy drugs is their lack of specificity for cancer cells. As a selective apoptosis-inducing agent, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has emerged as an attractive alternative. However, most of the cancer cells are found to be either intrinsically resistant to the TRAIL protein or may develop resistance after multiple treatments, and TRAIL resistance can induce epithelial-to-mesenchymal transition (EMT) at a later stage, promoting cancer invasion and migration. Interestingly, E-cadherin loss has been linked to TRAIL resistance and initiation of EMT, making E-cadherin re-expression a potential target to overcome these obstacles. Recent research suggests that re-expressing E-cadherin may reduce TRAIL resistance by enhancing TRAIL-induced apoptosis and preventing EMT by modulating EMT signalling factors. This reversal of EMT, can also aid in improving TRAIL-induced apoptosis. Therefore, this review provides remarkable insights into the mechanisms underlying E-cadherin re-expression, clinical implications, and potentiation, as well as the research gaps of E-cadherin re-expression in the current cancer treatment.
A 7-year-old girl with tonsillar infection with antibiotics. Two weeks later, there was a right sided neck lump. Computed tomography scans demonstrated a predominantly hypodense right retropharyngeal area with peripheral enhancement and mass effect. There was intense enhancement within the postero-superior aspect of the lesion which was continuous with the right internal carotid artery. Ultrasound demonstrated tapering of the right internal carotid artery. Magnetic resonance imaging and magnetic resonance arteriography showed a right internal carotid artery pseudoaneurysm. Surgical exploration confirmed the finding. This case highlights an unusual presentation of an internal carotid pseudoaneurysm and how imaging provided the diagnosis.