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7D) could be due to the loss of function mutations in the HLA-A allele in some clones within the tumour, making them unresponsive to neoepitope-driven T-cell activation, thereby contributing to relapse of the disease in LS patient II.2

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Moreover, epigenetic modifications, including redox-sensitive DNA methylation and histone acetylation, may play a pivotal role in sustaining maladaptive tendon remodeling (Sakai and Kumagai, 2025