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MEDTECH A compendium of research data on the likelihood and treatment of ocular side effects brought on by the use of MEK and BRAF inhibitors is provided by clinical professionals.
In the evolving landscape of cancer treatment, targeted therapies like MEK inhibitors (MEKi) and BRAF inhibitors (BRAFi) have shown promise but come with ocular adverse events (OAEs) that require vigilant monitoring by ophthalmologists. These OAEs can manifest soon after treatment initiation and vary in severity, affecting both the patient’s vision and quality of life. Proper management and interdisciplinary communication between oncologists and ophthalmologists are crucial for balancing effective cancer treatment with ocular health.
HCN Medical Memo
Understanding the ocular side effects of targeted cancer therapies like MEKi and BRAFi is essential. Early detection and management of OAEs can significantly impact the patient’s quality of life and the efficacy of cancer treatment. Therefore, a collaborative approach with oncologists is imperative for tailoring individualized treatment plans that consider both cancer therapy and ocular health.
Key Points
- MEKi and BRAFi target the MAPK/ERK pathway, crucial for cellular growth and survival.
- OAEs such as MEKi-associated retinopathy (MEKAR) and intraocular inflammation occur early in treatment.
- Management options for OAEs include observation, corticosteroids, and anticancer treatment tapering or discontinuation.
- Outcomes are generally favorable with proper management, often regressing without permanent visual impairment.
- Perspectives: Physicians stress the importance of early monitoring and interdisciplinary communication for individualized cancer therapy.
The incidence of OAEs in asymptomatic patients undergoing treatment with MEKi has been reported to be up to 90%.
Additional Points
- MEKAR can manifest within hours to weeks, while intraocular inflammation from BRAFi can take weeks to months.
- Researchers are investigating the molecular mechanisms behind these OAEs, including the role of the MAPK pathway and aquaporin density.
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