The integrated analysis of over 1,300 children with T-ALL has revealed 15 distinct subtypes, each characterized by unique genomic drivers and outcomes, reconstructing our understanding of the disease.
The study delineates a new category of 'early T cell precursor-like' leukaemia, highlighting its variable immunophenotype and diverse genomic alterations, challenging previous classifications.
Our findings indicate that specific genetic subtypes and alterations significantly contribute to treatment failure in T-ALL, showing the complexity and heterogeneity of this high-risk leukaemia.
By unveiling the role of noncoding alterations in oncogene deregulation, the research provides critical insights that could influence future therapeutic strategies for T-ALL.
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