Abstract Background The development of novel therapeutic approaches to cancers requires significant time and labour, especially for uncommon cancers (e.g. of mesenchymal origin). I
The marked heterogeneity of cancer poses a substantial challenge to precision drug therapy, resulting in considerable variability in patient responses to identical treatments. Accu
Cancer subtyping is essential for precision oncology, enabling early diagnosis, targeted therapy, and improved prognosis. DNA methylation is a powerful molecular marker for subtype
Multi-scale computational prediction of a candidate mutp53-FOXP3 interaction mechanism, supported by associational survival data and in silico modelling but lacking experimental validation of physical sequestration or functional causality.