About this Research Topic
Osteosarcoma (OS) is the most common primary bone tumor, with a bimodal age distribution. The highest incidence is in children and adolescents, and the second highest is among older adults (>60 years). Surgery and neoadjuvant chemotherapy are the main clinical treatments for OS, yet the 5-year survival rate is just 20% for individuals with metastases or recurrent OS. Most standard treatments were established in the 1980s, which can achieve long-term survival in approximately 60% of patients with localized OS. However, in the face of inoperable surgery, we are still limited in what we can do for OS patients who are insensitive or intolerant to chemotherapy drugs. Resistance to chemotherapeutic drugs is also a problem that hinders breakthroughs in OS treatment. Although survival rates have not improved during the past four decades, the heterogeneity and potential molecular aberrations of OS have been revealed as the biology of OS has come to be better understood. With the recent advancements in molecular profiling technology for OS, new technologies and concepts are undergoing sublimation.
What is the reason for the stagnation of OS treatment? And the potential molecular mechanisms. Surgery is the main clinical treatment and will be difficult to replace with future treatment. Due to the vast genomic instability and heterogenicity of OS, maybe a highly intensive combination of therapies was required. Natural bioactive compounds can combat cancer cells by non-specifically affecting macromolecules, such as DNA, enzymes, and microtubules, which are also found in normal proliferating cells but have a greater impact on cancer cells, as well as by targeting oncogenic signal transduction pathways activated in cancer cells. Ferroptosis plays a critical role in the treatment of OS, in particular chemotherapy resistance OS cells. Immunogenic cell death (ICD) is considered one of the most promising ways to achieve total tumor cell elimination. It activates the T-cell adaptive immune response and results in the formation of long-term immunological memory. Both ferroptosis and ICD can be triggered by many anticancer treatment modalities, including optical therapy (PDT, PTT). Nanoparticles-based drug delivery systems (NDDSs) are designed to induce ferroptosis and ICD by incorporating photosensitizers (PSs) for photodynamic therapy (PDT), and photothermal conversion agents for photothermal therapy (PTT).
This Research Topic welcomes submissions including, but not limited to, the following themes:
• Synergistic therapy
• Ferroptosis and chemotherapy resistance osteosarcoma cells
• Immunotherapy of osteosarcoma
• Targeted Therapies for osteosarcoma
• Molecular mechanisms
What is the reason for the stagnation of OS treatment? And the potential molecular mechanisms. Surgery is the main clinical treatment and will be difficult to replace with future treatment. Due to the vast genomic instability and heterogenicity of OS, maybe a highly intensive combination of therapies was required. Natural bioactive compounds can combat cancer cells by non-specifically affecting macromolecules, such as DNA, enzymes, and microtubules, which are also found in normal proliferating cells but have a greater impact on cancer cells, as well as by targeting oncogenic signal transduction pathways activated in cancer cells. Ferroptosis plays a critical role in the treatment of OS, in particular chemotherapy resistance OS cells. Immunogenic cell death (ICD) is considered one of the most promising ways to achieve total tumor cell elimination. It activates the T-cell adaptive immune response and results in the formation of long-term immunological memory. Both ferroptosis and ICD can be triggered by many anticancer treatment modalities, including optical therapy (PDT, PTT). Nanoparticles-based drug delivery systems (NDDSs) are designed to induce ferroptosis and ICD by incorporating photosensitizers (PSs) for photodynamic therapy (PDT), and photothermal conversion agents for photothermal therapy (PTT).
This Research Topic welcomes submissions including, but not limited to, the following themes:
• Synergistic therapy
• Ferroptosis and chemotherapy resistance osteosarcoma cells
• Immunotherapy of osteosarcoma
• Targeted Therapies for osteosarcoma
• Molecular mechanisms
Keywords: Osteosarcoma, Chemotherapy, Optical therapy, Immunotherapy, Drug synergy, Targeted Therapy, Molecular mechanisms
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