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Arising from the upper nasal tract, esthesioneuroblastoma is believed to originate from sensory neuroepithelial cells, also known as neuroectodermal olfactory cells. [1] Due to the location of the tumor and its proximity to the cranial cavity, esthesioneuroblastoma can be highly invasive and challenging to treat.
Esthesioneuroblastoma, also known as olfactory neuroblastoma, is believed to arise from the olfactory epithelium and its classification remains controversial. However, since it is not a sympathetic nervous system malignancy, esthesioneuroblastoma is a distinct clinical entity and is not to be confused with neuroblastoma.
Treatment using these targets can supplement or replace some of the intensive chemotherapy that is used for neuroblastoma. These molecular targets of this disease include GD2 , ALK , and CD133 . GD2 is a target of immunotherapy , and is the most fully developed of these treatment methods, but is also associated with toxicities. [ 1 ]
Dinutuximab (Ch14.18, tradename Unituxin) and dinutuximab beta (tradename Qarziba) are monoclonal antibodies used as a second-line treatment for children with high-risk neuroblastoma. Each antibody is made of both mouse and human components and targets glycolipid GD2 , expressed on neuroblastoma cells and on normal cells of neuroectodermal ...
Neuroblastoma is a rare form of a malignant cancer which can start in the olfactory nerve, which is responsible for smell sensation. This cancer can become aggressive and progress into the ethmoid sinuses, brain cavity, surrounds the cribriform plate.
Plexiform neurofibromas (associated with neurofibromatosis type 1) have a higher risk of transforming into malignant tumors and require individual treatment plans. [1] Surgical resection is the treatment of choice for symptomatic plexiform neurofibromas, though a new drug, selumetinib was approved in 2020, as a systemic therapeutic for ...
Another important line of current research targets netrin as a treatment for various diseases, including cancer, myocardial infarction, and Alzheimer's disease. In avian and mouse model organisms suffering from neuroblastoma , interfering with the netrin-1 autocrine loop in malignant tumors leads to cell death. [ 28 ]
Overexpression of LIMK2 in SH-EP cells resulted in resistance to vincristine induced apoptosis. These findings have led to the consideration of LIMK2 as a potential drug target in order to improve treatment of childhood neuroblastoma otherwise resistant to microtubule destabilizing drugs. [32]
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