Inhibiting BCR-ABL1 fusion in chronic myeloid leukemia (CML) patients with tyrosine-kinase inhibitors is the classic example of molecular targeted therapy. This approach has revolutionized CML therapy and provides long-term survival to patients. Some patients show persistent, deep molecular response following cessation of treatment despite the presence of detectable BCR-ABL1 transcripts. BCR-ABL1 fusion may appear in other hematological diseases as well, it is unclear what is the exact relationship between the fusion and the observable disease phenotype. The translocation may rarely appear as a secondary genetic abnormality, thus the genotype – phenotype association needs further clarification.
The aim of our research is to determine which additional genetic parameters determine prognosis, the efficacy of tyrosine-kinase inhibitor treatment and development of blastic crisis in CML. We will investigate which prognostic parameters can reliably detect a stable, deep molecular response following cessation of therapy. CML patients who demonstrate BCR-ABL1 fusion as a secondary abnormality will be investigated. Besides conventional cytogenetic and molecular methods, next generation sequencing will be utilized as well.
felvehető hallgatók száma: 1
Jelentkezési határidő: 2023-05-19
2024. IV. 17. ODT ülés Az ODT következő ülésére 2024. június 14-én, pénteken 10.00 órakor kerül sor a Semmelweis Egyetem Szenátusi termében (Bp. Üllői út 26. I. emelet).
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