Hematological malignancies remain a significant cause of morbidity and mortality worldwide. A major pathological feature of these cancers is the presence of structural variants, such as deletions, duplications, translocations and inversions, which can lead to the activation of oncogenes or the inactivation of tumor suppressor genes. These genomic alterations are complex and varied, with multiple molecular mechanisms contributing to their formation, evolution, and impact on disease progression. In addition to primary structural changes, hematological cancers often exhibit secondary genomic events that contribute to disease complexity and therapeutic resistance. These include additional mutations that can affect disease outcome and patient survival. A primary goal of our research is to elucidate the detailed mechanisms of structural variant formation and evolution in hematological malignancies. By integrating cutting-edge genomic sequencing and bioinformatics tools, we aim to map these variants more precisely and understand their exact structure and mechanisms of formation and role in cancer biology. This knowledge is crucial for developing targeted therapies that can more effectively treat these malignancies and improve patient outcomes.