Al toxicity. Based on sequential analysis of BCR-ABL transcripts, the 91 patients were divided into

Al toxicity. Based on sequential analysis of BCR-ABL transcripts, the 91 patients were divided into three subgroups. Subgroup A consisted of patients who had no variation on sequential analysis. Patients who had a single positive variation result obtained in a single sample were allocated to subgroup B. Subgroup C consisted of patients who had variations of BCR-ABL transcripts in at least two consecutive samples. As depicted in Table 2, 57 (62.6 ) patients were assigned to group A, 30 (32.9 ) to group B and 4 (4.39 ) to group C. Of the 34 patients (group B and C) who had at least a single variation in BCR-ABL RT-qPCR, 19 (55.8 ) had a < 1 of BCRABL/BCR ratio, 13 (38.2 ) patients had a 1 to 10 increase and 2 patients had a >10 increase of RT-qPCR. Only 4 patients (group C) had variations of BCR-ABL transcripts in consecutives samples. One of these four patients developed the M244V mutation. Despite having CCyR, the patient’s imatinib was discontinued and dasatinib was started at a dose of 100 mg once daily and regained MMR in the last evaluation (March 2010). Another patient have to take more medications on a daily basis for sickle cell anemia and admitted to having missing some doses. During follow-up, the other two patients who had a >10 increase of RT-qPCR lostCCyR without evidence of mutation on the ABL kinase domain. Of these two cases, one had not achieved CCyR at 18 months while taking imatinib at 400 mg/day. The same patient achieved both CCyR and MMR after 26 months with an increase of imatinib to 800 mg/day; however, 4 months later the transcript levels had increased to 11.54 compared to baseline. As a result, treatment was switched to nilotinib 400 mg twice daily and further to bosutinib 500 mg/day, but without response. The CEP-37440 supplement possibility of non-compliance appeared inevitable and was discussed repeatedly, and finally admitted by the patient. The patient was on dasatinib 100 mg/day and had achieved CCyR after 4 months of therapy. The second patient achieved both CCyR and MMR after 6 and 18 months of therapy, respectively. The same patient maintained MMR for only 4 months, and molecular analysis of peripheral blood revealed a continuous increase of the BCR-ABL transcript from 0.08 to 1.8 and then to 3.6 . However, the latter patient had gastric intolerance of nausea PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26866270 and vomiting despite the use of antiemetic, which may have impaired drug absorption. As a consequence, imatinib was safely switched to nilotinib 400 mg twice daily, and the patient regained CCyR and MMR at 6 months. As shown in table 2, CMR was achieved in 39 patients (29 in group A, 10 in group B, none in group C) and of them, only 9 patients (8 in group A and 1 in group B) have ongoing CMR. There was no significant difference between patients in group B in relation to CMR (P = 0.11). Of the other 30 patients who achieved CMR, 18 had BCR-ABL/BCR ratio increase from 0.005 to 0.01 , 7 had BCR-ABL/BCR ratio raised between 0.005 0.1 , and 5 had increased ratio greater than 0.5 . Of note, these variations were observed in some of the collected samples during follow-up period. Previous exposure to IFN was documented in 29 patients, among whom 17 were in group A, 11 in group B (7 with BCR-ABL transcripts variation < 1 , and 4 with variations between 1-10 ), and 1 in group C.Table 2 Molecular, treatment with imatinib and cytogenetic assessment of clinical samples of CML patients studiedNo. of Patients Variations in BCR-ABL/BCR 0.5-<1 1-10 >10 Imatinib dose during.