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. 2017 Jul 3;5(8):1320–1322. doi: 10.1002/ccr3.1032

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© 2017 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Disease course evolution after the 2nd Ph+ ALL relapse (1.12.2012) treated with FLAG salvage chemotherapy (■ fludarabine 30 mg/m²/day+ cytarabine 2 g/m²/day (days 1–5) and G‐CSF 5 mg/kg/day (FLAG)) followed by maintenance ponatinib (45 mg/day) after the second HSCT (▲). After 12 months of complete molecular remission, ponatinib was reduced to 15 mg/day. Six months later, ALL relapsed (1.9.2014) and T315I mutation were identified by Sanger sequencing. Ponatinib was immediately increased to 45 mg/day, and the patient received a unique dose of 2 mg of Vincristine () and three DLIs () leading to rapid and persistent complete molecular response, bcr‐abl transcript remaining undetectable in bone marrow until today.

Inline graphic — Disease course evolution after the 2nd Ph+ ALL relapse (1.12.2012) treated with FLAG salvage chemotherapy (■ fludarabine 30 mg/m²/day+ cytarabine 2 g/m²/day (days 1–5) and G‐CSF 5 mg/kg/day (FLAG)) followed by maintenance ponatinib (45 mg/day) after the second HSCT (▲). After 12 months of complete molecular remission, ponatinib was reduced to 15 mg/day. Six months later, ALL relapsed (1.9.2014) and T315I mutation were identified by Sanger sequencing. Ponatinib was immediately increased to 45 mg/day, and the patient received a unique dose of 2 mg of Vincristine () and three DLIs () leading to rapid and persistent complete molecular response, bcr‐abl transcript remaining undetectable in bone marrow until today.