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The targeted molecular therapy for neuroblastoma involves treatment aimed at molecular targets that have a unique expression in this form of cancer. Neuroblastoma, the second most common pediatric malignant tumor, often involves treatment through intensive chemotherapy. A number of molecular targets have been identified for the treatment of high-risk forms of this disease. Aiming treatment in this way provides a more selective way to treat the disease, decreasing the risk for toxicities that are associated with the typical treatment regimen. 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. ALK has more recently been discovered, and drugs in development for this target are proving to be successful in neuroblastoma treatment. The role of CD133 in neuroblastoma has also been more recently discovered and is an effective target for treatment of this disease. ==Identifying High-Risk Patients== High-risk cases of neuroblastoma are difficult to treat, even through intensive chemotherapy. For this reason, molecular targets have been identified and are being developed for treatment in patients who have more difficulty responding to treatment. There are a number of genetic factors that can be used to identify high-risk patients. In neuroblastoma cells, there can be amplification of genomic DNA regions, loss of genomic DNA regions, and genetic abnormalities.〔 All of these factors can contribute to an advanced disease state in high-risk patients. Amplification occurs within a protein called the MYCN oncogene. This protein is amplified in approximately 20% of primary neuroblastoma tumors and is associated with advanced disease state and treatment failure.〔 Loss of genomic regions by deletion can occur at chromosomes 1p and 11q. Loss at 1p is correlated with MYCN amplification and advanced disease state.〔 The loss at 11q is not related to MYCN, but is correlated with adverse patient outcomes.〔 Genetic abnormalities frequently occur in a tumor-suppressor gene called caspase 8. Inactivation of this gene will result in tumor cell survival.〔 Table 1 summarizes the genomic factors used to identify high-risk patients.〔〔〔〔 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Targeted molecular therapy for neuroblastoma」の詳細全文を読む スポンサード リンク
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