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Strategies Based on Genes for Extended Lymphocytic Leukemia

Abstract

Gatalica Zoran

Strategies based on genomic insights are increasingly becoming a cornerstone in the management of Chronic Lymphocytic Leukaemia (CLL), offering a more targeted and personalized approach to treatment. Genomic profiling has revealed a complex landscape of genetic alterations in CLL, guiding the development of innovative therapeutic strategies. One notable breakthrough involves the identification of specific genetic mutations, such as TP53, NOTCH1, and SF3B1, which are associated with distinct clinical behaviours and treatment responses. Tailoring therapeutic interventions based on the presence or absence of these mutations allows for a more nuanced prognosis and treatment plan. Precision medicine approaches, guided by genomic findings, have led to the development of novel targeted therapies that aim to disrupt specific molecular pathways involved in the progression of CLL. Burton’s Tyrosine Kinase (BTK) inhibitors, such as ibrutinib, and B-cell lymphoma 2 (inhibitors, like venetoclax, exemplify this paradigm shift. These agents have shown remarkable efficacy, particularly in cases with specific genomic alterations, offering patients a more tolerable and effective alternative to traditional chemotherapy. Furthermore, the emergence of immunotherapies, particularly those harnessing the power of Chimeric Antigen Receptor (CAR) T-cell therapy, holds promise for CLL patients. CAR T-cell therapy involves genetically modifying a patient's own T cells to express receptors targeting CLL cells, providing a highly personalized and targeted immunotherapeutic approach. The success of these strategies is closely linked to the genomic landscape of each patient's CLL cells, emphasizing the importance of comprehensive genomic profiling for treatment decision-making.

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