Contributions
Abstract: PB1953
Type: Publication Only
Background
Chronic Myeloid Leukemia is a myeloproliferative disorder that results due to reciprocal translocation t(9;22)(q34.1;q11.2) leading to the formation of an oncogene. Although Imatinib proved to be revolutionary treatment wise but 20% showed resistance. Point mutations in the ABL Kinase Domain were one of the causes of the resistance of which T315I was found to be the most resilient against all Tyrosine Kinase Inhibitors (TKIs).
Aims
This study observes the frequency of T315I mutation in TKI non-responders in our population.
Methods
Patients labeled as non-responders according to European Leukemianet guidelines to the first line therapy i.e. Imatinib or Nilotinib at our centre were included. The blood sample was collected in an EDTA vacutainer. DNA was extracted and then analyzed for the presence of both wild type and mutant via PCR. Negative controls were healthy individuals and demographically similar to the patients.
Results
Out of 150 patients, 44 were found to be non-responders. Patients were divided into three groups on the basis of TKI administered. Imatinib (n=3), Nilotinib (n=22) and those shifted from one TKI to another (n=19). Of these, 37/44(84.1%) patients had the presence of T315I.
Conclusion
Mutational analysis in the event of resistance and prior to the shift to next generation is mandatory. The presence of mutations will tailor the further treatment plan of the patient. As in our case the presence of T315I mutation will help in counseling the patients for the stem cell transplantation and prevent their further exposure to TKIs which would be an unwanted financial and psychological burden for them.
Session topic: 8. Chronic myeloid leukemia - Clinical
Keyword(s): Chromosomal translocation, Chronic myeloid leukemia, Drug resistance, Tyrosine kinase inhibitor
Abstract: PB1953
Type: Publication Only
Background
Chronic Myeloid Leukemia is a myeloproliferative disorder that results due to reciprocal translocation t(9;22)(q34.1;q11.2) leading to the formation of an oncogene. Although Imatinib proved to be revolutionary treatment wise but 20% showed resistance. Point mutations in the ABL Kinase Domain were one of the causes of the resistance of which T315I was found to be the most resilient against all Tyrosine Kinase Inhibitors (TKIs).
Aims
This study observes the frequency of T315I mutation in TKI non-responders in our population.
Methods
Patients labeled as non-responders according to European Leukemianet guidelines to the first line therapy i.e. Imatinib or Nilotinib at our centre were included. The blood sample was collected in an EDTA vacutainer. DNA was extracted and then analyzed for the presence of both wild type and mutant via PCR. Negative controls were healthy individuals and demographically similar to the patients.
Results
Out of 150 patients, 44 were found to be non-responders. Patients were divided into three groups on the basis of TKI administered. Imatinib (n=3), Nilotinib (n=22) and those shifted from one TKI to another (n=19). Of these, 37/44(84.1%) patients had the presence of T315I.
Conclusion
Mutational analysis in the event of resistance and prior to the shift to next generation is mandatory. The presence of mutations will tailor the further treatment plan of the patient. As in our case the presence of T315I mutation will help in counseling the patients for the stem cell transplantation and prevent their further exposure to TKIs which would be an unwanted financial and psychological burden for them.
Session topic: 8. Chronic myeloid leukemia - Clinical
Keyword(s): Chromosomal translocation, Chronic myeloid leukemia, Drug resistance, Tyrosine kinase inhibitor