Cancer Genetics and Epigenetics 2024, Vol.12, No.6, 317-328 http://medscipublisher.com/index.php/cge 322 sequence, enabling cancer cells to adapt to therapeutic pressures. For instance, epigenetic silencing of tumor suppressor genes can lead to reduced sensitivity to chemotherapeutic agents (Raskov et al., 2019; Das et al., 2020). Figure 2 Comparison of Mutation Status in Plasma and Tissue Samples of Four Colorectal Cancer Patients Before and After Treatment (Adapted from Cao et al., 2020) Image Description: The red squares represent mutations detected in plasma, white squares with a solid black border indicate mutations detected in tissue, and red squares with a solid black border indicate mutations detected in both plasma and tissue. White squares with a light gray border indicate no mutations detected. The results show significant changes in the mutation status of key genes during treatment; some mutations appeared or disappeared post-treatment, suggesting that these mutations may be associated with treatment response or resistance. These findings highlight the importance of dynamically monitoring gene mutations during treatment, aiding in the development of personalized treatment strategies (Adapted from Cao et al., 2020) 5.2 Strategies to overcome resistance To counteract resistance, several strategies have been developed and are being explored in clinical settings. One approach is the use of combination therapies that target multiple pathways simultaneously, reducing the likelihood of resistance development. For example, combining MEK and PI3K inhibitors has shown promise in overcoming resistance in CRC cells with specific mutations (Clarke et al., 2019). Another strategy is to utilize liquid biopsies to monitor the emergence of resistance mutations in real-time, allowing for timely adjustments to treatment plans (Montagut et al., 2018).
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