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Oncotarget
Genetic Alterations in Thyroid Cancer: Resistance to BRAFi and Anaplastic Transformation
Feb 8, 2024
This podcast discusses genetic alterations in thyroid cancer that lead to resistance to BRF inhibitors and anaplastic transformation, highlighting the emergence of resistance mechanisms and the use of BRF inhibitors in combination with immune checkpoint inhibitors. The effectiveness of combined targeted therapy and immunomodulatory agents in enhancing anti-tumor immune activity and overcoming resistance in thyroid cancer patients is explored, along with ongoing clinical trials and the potential for personalized therapies.
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Quick takeaways
- Genetic alterations in the BRF gene contribute to resistance to therapy and tumor progression in thyroid cancer. Targeted agents inhibiting BRF show promise but long-term efficacy is limited due to resistance mechanisms, highlighting the need for alternative treatment strategies.
- Genetic alterations associated with resistance to BRF inhibitors overlap with the development of anaplastic thyroid cancer, emphasizing the complexity of compensatory mechanisms. Combined targeted therapy with immunotherapy may be a potential strategy to address both resistance and anaplastic transformation.
Deep dives
Genetic Alterations and Resistance to BRF Inhibition
Thyroid cancer is a complex disease that can be challenging to treat due to resistance to therapy and the development of aggressive forms of the disease. Genetic alterations, such as mutations in the BRF gene, have been identified in a significant proportion of thyroid cancers, leading to de-differentiation and tumor progression. Targeted agents that inhibit BRF, such as Vemaraffanib and Dabrophanib, have shown promising results, but long-term efficacy is limited due to the emergence of resistance mechanisms. Genetic alterations associated with resistance to BRF inhibitors, including mutations in the PI3K-AKT-M-Tor pathway, have been identified, providing insights into potential therapeutic targets.
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