POSTER 6
PH+ ALL RELAPSE IN THE CNS WITH THE T315I MUTATION
Maria Eduarda Couto, Isabel Oliveira and José Mariz
Onco-hematology Service, Instituto Português de Oncologia do Porto, F.G., E.P.E., Porto, Portugal
Introduction: ALL is an aggressive hematologic disease with high risk of relapse, particularly in the
central nervous system (CNS). This location worsens the prognosis of these patients, being difficult to
achieve high cure rates, mainly when the T315I mutation is found (there is low evidence in the
literature about the ability of ponatinib to cross the hematoencephalic barrier efficiently).
Objective and Methods: The clinical file of an ALL patient diagnosed and treated in our center was
reviewed, in order to characterize the disease course.
Results: A 62 year-old female was diagnosed with Ph+ ALL in 2017. This patient was treated with the
standard chemotherapy protocol HCVAD (8 cycles) plus imatinib, achieving a complete molecular
response after the induction. There were no relevant adverse events or infections to report. Along
the 15th month of the maintenance treatment (with vincristine, prednisolone, 6-mercaptopurine,
methotrexate and imatinib) the patient progressively increased the molecular level of the BCR-ABL1
transcript in two different measures. She also complained about disequilibrium, nausea and asthenia.
A disease relapse was identified in the CNS and bone marrow, so she started a second line therapy
with dasatinib, vincristine and dexamethasone for 4 weeks, with lumbar punctures twice a week
(cytarabine/methotrexate) until achieving undetectable disease by CSF flow cytometry. She was not
candidate for bone marrow transplant at the relapse time for comorbidities. After one week, the
T315I mutation was identified in the bone marrow, so dasatinib was replaced by oral ponatinib.
Besides not crossing the hemato-encephalilic barrier so efficiently, after 15 days of therapy with
ponatinib (plus chemotherapy and 8 lumbar punctures) there was a significant reduction in the BCR-ABL1
expression (with the T315I mutation) in the bone marrow. Additionally, there is no evidence of
disease in the CNS by flow cytometry and the patient improved clinically.
Conclusion: In this clinical case of Ph+ ALL relapse in the SNC with the T315 mutation, oral ponatinib
with a classical and palliative chemotherapy regiment and lumbar punctures were sufficient to
eliminate the malignant cells from the CNS. This patient is achieving remission from the ALL and with
good quality of life.
SCIENTIFIC
PROGRAMME
RARE SUBSETS OF
ACUTE LEUKAEMIA
TRACKING LEUKAEMIC
STEM CELLS (LSCs)
ROUTINE DIAGNOSIS
GENE EXPRESSION
AND MUTATIONAL
PROFILING
DEBATE 1 – ALL
PATIENTS WITH
INTERMEDIATE-RISK
AML MUST BE
TRANSPLANTED
INTERACTIVE
CASES 1 – MUTATION-BASED
THERAPY
OFF-LABEL
ROUNDTABLE –
SHOULD WE REALLY
USE NEW TARGETED
INHIBITORS AS SINGLE
AGENTS ?
ADDITION OF A 3RD
AGENT TO FRONTLINE
7+3
ROUNDTABLE –
CURATIVE OPTIONS
FOR OLDER AML
INTERACTIVE CASES 2
DEBATE 2 - BEST
TREATMENT FOR
NPM1-MUTATED AML IN
THE NEXT FUTURE ?
ALLOGENEIC
HAEMATOPOIETIC
STEM CELL
TRANSPLANTATION
(HSCT)
IMMUNOTHERAPY FOR
ACUTE LEUKAEMIA
DEBATE 3 - T-ALL:
WHERE ARE WE GOING
NOW?
SELECTED ABSTRACTS
AND CLINICAL
CASES FOR AN ORAL
PRESENTATION
SELECTED ABSTRACTS
FOR A POSTER
PRESENTATION
DISCLOSURES