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Updated: Aug 27, 2025
Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma
Published on: October 14, 2016
An overview of resistance to chemotherapy in osteosarcoma and future perspectives
Dorian Yarih Garcia-Ortega1, Sara Aileen Cabrera-Nieto2, Haydee Sarai Caro-Sánchez3
1Cirugía Oncológica, Instituto Nacional de Cancerología (INCAN), Ciudad de México 14080, México.
Abstract:
Osteosarcoma (OS) is the most common type of bone sarcoma. Despite the availability of multimodal treatment with surgery and chemotherapy, the clinical results remain unsatisfactory. The main reason for the poor outcomes in patients with OS is the development of resistance to methotrexate, cisplatin, doxorubicin, and ifosfamide. Molecular and cellular mechanisms associated with resistance to chemotherapy include DNA repair and cell-cycle alterations, enhanced drug efflux, increased detoxification, resistance to apoptosis, autophagy, tumor extracellular matrix, and angiogenesis. This versatility of cells to generate chemoresistance has motivated the use of anti-angiogenic therapy based on tyrosine kinase inhibitors. This approach has shown that other therapies, along with standard chemotherapy, can improve responses to therapy in patients with OS. Moreover, microRNAs may act as predictors of drug resistance in OS. This review provides insight into the molecular and cellular mechanisms involved in the development of resistance during the treatment of OS and discusses promising novel therapies (e.g., afatinib and palbociclib) for overcoming resistance to chemotherapy in OS.
Insights
Osteosarcoma (OS) treatment faces challenges due to chemoresistance. Novel therapies targeting mechanisms like angiogenesis and utilizing microRNAs show promise for improving patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Osteosarcoma (OS) is the most common bone cancer.
- Current multimodal treatments (surgery, chemotherapy) yield unsatisfactory results.
- Chemoresistance to drugs like methotrexate, cisplatin, doxorubicin, and ifosfamide is a major cause of poor outcomes.
Purpose of the Study:
- To review molecular and cellular mechanisms of chemoresistance in OS.
- To discuss novel therapeutic strategies for overcoming chemoresistance in OS.
Main Methods:
- Literature review of mechanisms driving OS chemoresistance.
- Analysis of emerging therapeutic approaches, including anti-angiogenic therapy and targeted agents.
- Exploration of the role of microRNAs in predicting drug resistance.
Main Results:
- Chemoresistance mechanisms include DNA repair, drug efflux, apoptosis evasion, autophagy, and angiogenesis.
- Anti-angiogenic therapies (e.g., tyrosine kinase inhibitors) combined with chemotherapy improve OS treatment response.
- MicroRNAs show potential as biomarkers for predicting drug resistance.
Conclusions:
- Understanding chemoresistance mechanisms is crucial for developing effective OS treatments.
- Novel therapies like afatinib and palbociclib offer new avenues for overcoming chemoresistance.
- Targeting angiogenesis and utilizing microRNA insights are promising strategies for improving OS patient outcomes.
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