Antineoplastic
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Acute myeloid leukaemia: case report A man [age at event onset not stated] developed acute myeloid leukaemia following treatment with cisplatin, cyclophosphamide, cytarabine, doxorubicin, etoposide, gemcitabine, ifosfamide, tucidinostat and oxaliplatin for peripheral T-cell lymphoma [not all routes and dosages not stated]. The man presented to a hospital in October 2011 (at the age of 45 years) due to a neck mass. He was subsequently diagnosed with stage IIIA peripheral T-cell lymphoma, unspecified. He received treatment with CHOPE comprising cyclophosphamide, etoposide, doxorubicin, vincristine and prednisone. After 3 cycles of the therapy, the lymph nodes disappeared. In January 2012, the diagnosis was revised as stage IV. He received 2 cycles of ESHAP treatment comprising of cisplatin, methylprednisolone, etoposide, cytarabine. In April 2012, cervical lymph node enlargement recurred. No lymphoma cell infiltration was observed in myelography and bone marrow pathology. Therefore, in April 2012, he was given one cycle of GIFOX chemotherapy comprising of gemcitabine, oxaliplatin and ifosfamide. Subsequently, the neck mass disappeared. Thereafter, in June 2012, he received three cycles of DHAP chemotherapy comprised of cisplatin, cytarabine and dexamethasone. An excellent response was obtained after chemotherapy, and no tumour infiltration was observed throughout the body. On 8 January 2013, he underwent autologous haematopoietic stem cell transplantation. However, in August 2014, a non-Hodgkin’s lymphoma recurrence was noted. He then received two cycles each of DECP-G chemotherapy in August 2014 (dexamethasone, etoposide, cyclophosphamide, gemcitabine and cisplatin) followed by DPP chemotherapy (dexamethasone, cisplatin and paclitaxel) in November 2014. Eventually, complete response was noted. Thereafter, in January 2016, he was diagnosed with T-cell lymphoma with bone marrow involvement. Therefore, he received four cycles of CHOPE therapy. From October 2016 onwards, he started receiving oral tucidinostat [chidamide] 30mg twice a week. In January 2017, PET-CT recheck showed multiple miliary nodular and patchy shadows in both the lungs with low fludeoxyglucose metabolism. No signs of malignancy were noted. Eventually, a complete response was achieved. In August 2017, his CBC findings, myelography recheck and other laboratory tests were found to be suggestive of possible acute myeloid leukaemia. AML1-ETO fusion gene was found to be positive. Chromosomal test was positive for 46, XY, +1, der(1;7)(q10;p10) [6]/46, idem, t(8;21)(q22;q22) [11]/46, XY. The man’s dose of tucidinostat was reduced to 20mg twice a week. He also received MA regimen comprised of mitoxantrone and cytarabine. Subsequently, a completed response was achieved. He continued to receive one cycle of MA regimen followed by one cycle of medium-dose cytarabine. In December 2017, reevaluation showed AML1-ETO fusion gene negative with chromosomes 46, XY [20]. He continued to receive maintenance chemotherapy with medium-dose cytarabine. In May 2018, flo
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