The survival rate for pediatric cancers has remarkably improved in recent years. Conventional chemotherapy plays a crucial role in treating pediatric cancers, especially in low- and middle-income countries where access to advanced treatments may be limited. The Food and Drug Administration (FDA) approved chemotherapy drugs that can be used in children have expanded, but patients still face numerous side effects from the treatment. In addition, multidrug resistance (MDR) continues to pose a major challenge in improving the survival rates for a significant number of patients. This review focuses on the severe side effects of pediatric chemotherapy, including doxorubicin-induced cardiotoxicity (DIC) and vincristine-induced peripheral neuropathy (VIPN). We also delve into the mechanisms of MDR in chemotherapy to the improve survival and reduce the toxicity of treatment. Additionally, the review focuses on various drug transporters found in common types of pediatric tumors, which could offer different therapeutic options.
As neoplastic cells proliferate, disseminate, and infiltrate, they undergo substantial alterations in their epigenetic configuration. Among the pivotal enzymes implicated in this phenomenon is the AlkB family of demethylases, notably AlkB homolog 1 (ALKBH1), which demonstrates conspicuous upregulation across various malignancies. The heightened expression of ALKBH1 renders it a compelling candidate for the development of multifaceted anticancer modalities. Despite the commendable progress achieved by investigators in elucidating the perturbations associated with ALKBH1 in malignant tissues, a comprehensive mechanism remains elusive. The present study endeavors to address this lacuna by synthesizing recent advancements pertaining to ALKBH1's involvement in oncogenesis over the preceding decade. Therefore, this research not only furnishes novel insights but also establishes a foundation for prospective initiatives aimed at cancer prophylaxis and therapeutics that exploit epigenetic regulatory mechanisms.