mercaptopurine and Leukemia--Myelogenous--Chronic--BCR-ABL-Positive

The patient was a 62-year-old man. His hematological data in April 2000 had shown no abnormalities, but he was referred to our hospital because of a fever and leukocytosis in June 2000. The peripheral blood showed 29.8 x 10(9)/L white blood cells, with 68.0% blasts. A bone marrow aspirate showed hypercellularity with a proliferation of large leukemic blasts. The leukemic cells were positive for CD13 (91%), CD33 (54.8%), CD34 (94.5%), and HLA-DR (97.9%). Some leukemic cells (15.6%) also expressed CD14. Cytogenetic analysis revealed 92,XXYY,t(9;22)(q34;q11)x2 in all 20 metaphase cells. Reverse transcriptase polymerase chain reaction analysis detected the minor BCR/ABL messenger RNA (mRNA) but failed to detect the major BCR/ABL mRNA. The patient achieved complete remission after induction chemotherapy, with no evidence of Philadelphia chromosome (Ph) or minor BCR/ABL mRNA. Ph-positive acute myeloid leukemia (Ph-AML) has rarely been reported. Herein, we report a case of Ph-AML with tetraploidy and review the previously reported Ph-AML cases.

Topics: Acute Disease; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumor; Cytarabine; Daunorubicin; Fusion Proteins, bcr-abl; Humans; Karyotyping; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Middle Aged; Mitoxantrone; Polyploidy; Prednisolone; Remission Induction; RNA, Messenger; RNA, Neoplasm

Ph1-positive chronic myelocytic leukemia (CML) developing in a treated case of acute promyelocytic leukemia (APL) is reported. The patient was a 62-year-old male who was diagnosed as having APL in December 1978. He was treated with daunorubicin, Ara-C and 6MP and a complete remission was obtained 4 months later. But APL recurred in February 1981. He was treated with BHAC, aclarubicin, 6MP and prednisolone. He remained in continuous complete remission for 5 years, when all therapy was discontinued. After then, the leukocytes count continued to rise and a diagnosis of Ph1-positive CML was made in September 1986. His leukocytes count has been well controlled with the use of busulfan. The event in this case suggests a possibility of the Ph1-positive CML being a secondary disease related to prior long term chemotherapy.

Topics: Aclarubicin; Antineoplastic Combined Chemotherapy Protocols; Cytarabine; Daunorubicin; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Promyelocytic, Acute; Male; Mercaptopurine; Methotrexate; Middle Aged; Prednisolone; Remission Induction

Currently, no effective treatment is available for the nonlymphoid blast crisis (BC) of chronic myeloid leukemia (CML) and because of this the prognosis for such patients remains invariably poor. In an attempt to determine the results provided by palliative treatment with oral 6-mercaptopurine (6-MP) in the above hematological condition, 30 such patients were analyzed for hospital stay, days of intravenous (i.v.) antibiotics, transfusion requirements, response rate, and survival. Thirty patients with nonlymphoid BC matched for their initial characteristics and treated with different i.v. regimens were used for comparison purposes. Patients managed with 6-MP spent less days in hospital (median: 9, range: 0-46 vs median: 42, range: 5-140; P<0.0001), needed antibiotics for less days (median: 0. range: 0-46 vs median: 20, range: 0-57; P<0.0001), and received less platelet transfusions (median: 0, range: 0-20 vs median: 6, range: 0-63; P=0.004) than those treated with i.v. chemotherapy. Although no complete or partial remission was achieved by patients receiving 6-MP vs six in the i.v. chemotherapy group, no significant difference was observed when the survival of both groups was compared (median: 4.7 months, range: 0.1-22.7 vs median: 3.8 months, range: 0.2-12, respectively). These results indicate that 6-MP therapy constitutes a good palliative treatment for patients with nonlymphoid BC of CML. However, new treatment strategies for this hematological condition are required.

Topics: Administration, Oral; Adolescent; Adult; Aged; Antimetabolites, Antineoplastic; Blast Crisis; Female; Humans; Injections, Intravenous; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Middle Aged; Treatment Outcome

A variety of oncogenes are activated by specific chromosomal translocations, which are associated with distinct subtypes of leukemia. The identification of these rearrangements provides critical diagnostic and prognostic information, which may contribute to the selection of specific anti-leukemic therapy. The translocation t(9;22), the equivalent of the BCR/ABL rearrangement, is associated with a poor prognosis. We therefore used RT-PCR to detect this molecular event in a prospective study including 890 children. 673 of them suffered from acute lymphoblastic leukemia (ALL) at primary diagnosis and a transcription of the chimeric gene was detected in 21 of 648 with a successful analysis (3.2%). All children were treated by one of the two German multicenter childhood ALL therapy studies ALL-BFM-90 or COALL-05-92, respectively. Comparison of clinical features between BCR/ABL-positive and -negative children showed no significant differences regarding WBC, percentage of blasts, splenomegaly, hepatomegaly and age. Immunophenotypic studies at diagnosis in 21 BCR/ABL-positive children identified common ALL in 16 patients (76.2%), pre-B-ALL in four (19.0%), and an early T-lineage ALL in one (4.8%). Coexpression of myeloid antigens (CD13 and/or CD33) was observed in six of 16 common ALL patients as well as in the one child with early T-lineage ALL phenotype. The type of breakpoint (m-BCR/ABL: n = 14; M-BCR/ABL: n = 7) showed no correlation with clinical parameters. A comparison of cytogenetic and molecular data was performed in 16 positive patients and was concordant in all of them. We analyzed the response to the prednisone pretreatment and found a higher incidence of poor responders among the BCR/ABL-positive children. Regarding the event-free survival (EFS) of BCR/ABL-positive (0.53) and -negative patients (0.79) after a follow-up of 2 years, significant differences (P < 0.05) between both groups could be demonstrated.

Topics: Adolescent; Antineoplastic Combined Chemotherapy Protocols; Asparaginase; Base Sequence; Child; Child, Preschool; Chromosomes, Human, Pair 22; Chromosomes, Human, Pair 9; Cyclophosphamide; Cytarabine; Daunorubicin; Disease-Free Survival; Female; Fusion Proteins, bcr-abl; Germany; Humans; Incidence; Infant; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Methotrexate; Molecular Sequence Data; Polymerase Chain Reaction; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Prednisone; Prognosis; Prospective Studies; Transcription, Genetic; Translocation, Genetic; Vincristine

Eighty-three patients in the chronic phase of Ph1-positive chronic myelogenous leukemia (CML) have been treated with busulfan or other alkylating agents in a conventional way hitherto acknowledged. During its chronic phase, 31 cases of these 83 had received an additional intermittent therapy every 4 to 6 months, consisting of vincristine 2 mg or vindesine 3 mg per week, prednisolone 20 to 30 mg per day, and partly 6-mercaptopurine 50 to 100 mg, combined with allopurinol 200 to 300 mg per day for 2 to 3 weeks. The 50% survival of these patients using the Kaplan-Meier's method was 73, 7 months and 5-year survival was 70.2%, while those of the remaining patients were 41.2 months and 13.4%, respectively. The second nation-wide survey of long-term survivors of CML in Japan was attempted. CML totalling 195 surviving over 7 years from the initial diagnosis and 113 of CML surviving over one year from the blastic crisis had been collected by the end of March 1988. The longest survivors of the former group was for 21.3 years, while the latter 4.6 years. In addition, recent increase of the annual incidence of the above both groups was clarified. These results strongly support the progress of chemotherapy of CML in recent years.

Topics: Adolescent; Adult; Aged; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Female; Humans; Japan; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid, Chronic-Phase; Male; Mercaptopurine; Middle Aged; Multicenter Studies as Topic; Prednisolone; Survival Rate; Vincristine

Patients with Philadelphia chromosome-positive (Ph+) and/or BCR-ABL+ acute lymphoblastic leukemia (ALL) have extremely poor prognoses. Most of these patients have additional, heterogenous karyotype abnormalities, the majority of which have uncertain clinical significance. In this study we analyzed the clinical characteristics, karyotype abnormalities, and outcome of 77 patients with Ph+ and/or BCR-ABL+ ALL registered in Poland in 1997-2004. In 31/55 patients with known karyotype, the sole t(9;22)(q34;q11) abnormality had been diagnosed; in one patient, variant translocation t(4;9;22)(q21q31.1;q34;q11), and additional abnormalities in 23 (42%) patients, had been diagnosed. The characteristics of the patients with Ph chromosome and additional abnormalities were not significantly different when compared with the entire analyzed group. Out of 77 patients, 54 (70%) achieved first complete remission (CR1) after one or more induction cycles. The overall survival (OS) probability of 2 years was 63, 43, and 17% for patients treated with allogeneic stem cell transplantation (alloSCT), autologous SCT, and chemotherapy, respectively (log rank p=0.002). Median OS from the time of alloSCT was significantly longer for patients transplanted in CR1 compared with alloSCT in CR >1 (p=0.032). There were no significant differences in CR rate, disease-free survival (DFS), and OS for patients with t(9;22) and additional abnormalities compared with the whole group. Only WBC >20 G/l at diagnosis adversely influenced OS probability (log rank p=0.0017). In conclusion, our data confirm poor outcome of Ph+ and/or BCR-ABL+ ALL. Only patients who received alloSCT in CR1 had longer DFS and OS. We have shown that additional karyotype abnormalities did not influence the clinical characteristics of the patients; however, their influence on treatment results needs to be further assessed.

Topics: Adolescent; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Cytarabine; Disease-Free Survival; Female; Fusion Proteins, bcr-abl; Hematopoietic Stem Cell Transplantation; Humans; Karyotyping; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Methotrexate; Middle Aged; Philadelphia Chromosome; Poland; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Remission Induction; Retrospective Studies; Treatment Outcome

A 60-year-old woman presented with night-sweats and increasing weakness. Physical examination revealed no abnormalities. For 27 years she had been treated for Philadelphia-positive chronic myeloid leukemia (CML). Because of progressive disease treatment with the tyrosine kinase inhibitor imatinib (STI571, Glivec (R)) had been started 9 months before. She had achieved complete hematological remission within 8 weeks, but not a cytogenetic response.. Elevated WBC count (26.7/nl) with a differential displaying typical features of acceleration in bone marrow aspirate confirmed CML in accelerated phase. Sequencing of the ATP binding site of the BCR-ABL gene, which - at protein level - is the target for imatinib, revealed the clonal selection of cells harboring a point mutation leading to the exchange of amino acid 253 from tyrosine to histidine. This was considered to be the cause of resistance to imatinib.. Dose increase of imatinib up to 600 mg daily and administration of cytarabine did not overcome resistance. Imatinib therapy was discontinued; hematologic remission was induced by oral therapy with hydroxyurea and mercaptopurine. In the course of the following 6 months a gradual decrease of the resistant clone from 100 % down to lower than the detection limit of the method was demonstrated.. Clonal mutations are often the cause of resistance to imatinib therapy. They can be detected by sequencing of the ATP binding site of BCR-ABL in specialized laboratories. This case shows that discontinuation of imatinib therapy can significantly reduce the mutated (resistant) clone and thereby restore sensitivity to imatinib.

Topics: Amino Acid Substitution; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Clone Cells; Drug Resistance, Neoplasm; Female; Fusion Proteins, bcr-abl; Histidine; Humans; Hydroxyurea; Imatinib Mesylate; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mercaptopurine; Middle Aged; Oncogene Proteins, Fusion; Piperazines; Point Mutation; Pyrimidines; Selection, Genetic; Tyrosine

Retrospective analysis of 102 children with CML from 9 paediatric centres in Poland has been performed. A total number of 102 children: 58 boys and 44 girls aged 1-17 years (median 9.4 years old) with CML, treated in the period 1975-1999 were included in the study. Forty eight of 102 (47.1 %) children were treated with cytostatic drugs without IFN alpha: busulfan, hydroxyurea, 6-mercaptopurine or etoposide (VP-16). Fifty four of 102 (52.9%) patients were treated with interferon alpha (IFN alpha) after cytoreductive pretreatment. Thirty out of 102 (29.4%) patients underwent stem cell transplantation (SCT): 24 - matched related donor allo-BMT, 2 - matched unrelated donor allo-BMT, 1 - partially matched related donor T-cell depleted allo-PBPCT, 1 - syngeneic allo-BMT and 2 - autologous PBPCT. Overall survival analysis revealed that 46 of the 102 (45.1%) children remained alive: 5/35 (14.3%) children treated with cytostatics alone, 22/37 (59.5%) children treated with IFN alpha and 19/30 (63.3%) children treated with SCT. Among SCT survivors there are 10/17 (58.8%) children treated with IFN alpha prior to SCT and 9/13 (69.2%) children treated with cytostatics alone prior to SCT. The probability of 5-year survival is 0.51 in the group treated with SCT (median follow-up 58 months); 0.43 in the group treated with IFN alpha (median follow-up 53 months) and 0.23 in the group treated with cytostatics (median follow-up 31 months). Our data show, that BMT is the treatment of choice in CML in children. IFN alpha could be successfully applied as an alternative treatment for those, who do not have a suitable donor for allogeneic SCT. Better outcome in post BMT children, who were not treated with IFN alpha prior to SCT requires confirmation by studies on larger groups of patients. However, it seems to be justified to stop IFN alpha therapy at least 3 months before SCT. The main reason for unsuccessful treatment outcome in patients with CML in Poland remains the still insufficient access to MUD-BMT.

Topics: Adolescent; Antineoplastic Combined Chemotherapy Protocols; Bone Marrow Transplantation; Busulfan; Child; Child, Preschool; Combined Modality Therapy; Disease-Free Survival; Etoposide; Female; Humans; Hydroxyurea; Infant; Interferon-alpha; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Poland; Remission Induction; Retrospective Studies; Stem Cell Transplantation; Transplantation, Homologous; Treatment Outcome

The adenine nucleoside analogue, fludarabine phosphate, in combination with cytosine-arabinoside (Ara-C) and granulocyte-colony stimulating factor (G-CSF) (the so called FLAG regimen) has recently been shown to be effective in the treatment of poor-prognosis acute non-lymphoid leukaemia. We used this combination plus novantrone (FLANG regimen) in a case of Ph1+ chronic myeloid leukaemia (CML) unresponsive to interferon alpha that had progressed to an acute phase, after 3 months of treatment with 6-mercaptopurine and hydroxyurea. The patient was treated with two courses of fludarabine 30 mg/m2 (days 1-5) + Ara-C 2 g/m2 (days 1-5) + novantrone 5 mg/m2 (days 1-3) and G-CSF from day 0 to neutrophil recovery. After the first cycle of chemotherapy, bone marrow blasts decreased from 100% to less than 5% (clinical complete remission), with a progressive clearance of Ph1+ metaphases (from 100% to 12%). At the end of the second course, a progressive increase of blasts was observed again and karyotypic detection of Ph+ cells was also documented (from 12% to 42.9%). During this partial remission, the patient underwent an allogeneic bone marrow transplantation from an HLA matched identical brother. At the time of this report, he is still alive and well and in complete karyotypic remission. This partial therapeutic success was compared with the result obtained in another previously reported CML case: differences in the therapeutic efficacy of protocols employing fludarabine nucleosides and the type of blastic cells involved are discussed.

Topics: Antineoplastic Combined Chemotherapy Protocols; Blast Crisis; Bone Marrow; Bone Marrow Transplantation; Chromosome Aberrations; Combined Modality Therapy; Cytarabine; Disease Progression; Granulocyte Colony-Stimulating Factor; Humans; Hydroxyurea; Immunologic Factors; Interferon-alpha; Karyotyping; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Middle Aged; Mitoxantrone; Remission Induction; Vidarabine

A 67-year-old patient with chronic myeloid leukemia for 4 years rapidly developed multiple squamous-cell carcinomas on the scalp. We discuss the role of chemotherapy, chronic immunosuppression, chronic sun exposure and of possible genetic factors.

Topics: Aged; Antimetabolites, Antineoplastic; Antineoplastic Agents; Carcinoma, Squamous Cell; Humans; Hydroxyurea; Immunocompromised Host; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Male; Mercaptopurine; Neoplasms, Multiple Primary; Scalp; Skin Neoplasms; Sunlight

Topics: Alkylating Agents; Animals; Bone Marrow Transplantation; Combined Modality Therapy; Humans; Hydroxyurea; Interferons; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mercaptopurine; Philadelphia Chromosome

Topics: Acute Disease; Antineoplastic Combined Chemotherapy Protocols; Bone Marrow Transplantation; Combined Modality Therapy; Cytarabine; Daunorubicin; Granulocyte Colony-Stimulating Factor; Hematologic Tests; Humans; L-Lactate Dehydrogenase; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mercaptopurine; Prednisolone; Remission Induction

Topics: Child; Coloring Agents; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mercaptopurine; Methotrexate; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Purines; Thioguanine

Seventy-four patients in the chronic phase of Ph1-positive chronic myelogenous leukemia (CML) have been treated with busulfan or other alkylating agents in a conventional way. During its chronic phase, 24 of these 74 cases had received additional intermittent therapy every 4 to 6 months, consisting of vincristine 2 mg or vindesine 3 mg per week, prednisolone 20-30 mg per day and partly 6 mercaptopurine 50 to 100 mg, combined with allopurinol 200 to 300 mg per day for 2 to 3 weeks. The 50% survival of these patients using the Kaplan-Meier's method was 73.7 months and 5-year survival was 69.6%, against 40.5 months and 14.4%, respectively, in the remaining patients. Nine patients in the blastic or accelerated phase of Ph1-positive CML have been treated with new regimens including MCNU. All cases had been refractory for usual types of induction chemotherapy. The new regimen consisted of MCNU 50-100 mg, combined with vindesine or 6-MP plus allopurinol or prednisolone. Five out of 9 cases attained complete remission and 1 partial remission. The major adverse effect of this regimen was slight liver damage. MCNU could be regarded as an useful agent in the blastic phase as well as in the chronic phase of CML.

Topics: Adolescent; Adult; Aged; Allopurinol; Antineoplastic Combined Chemotherapy Protocols; Blast Crisis; Drug Evaluation; Female; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid, Accelerated Phase; Leukemia, Myeloid, Chronic-Phase; Male; Mercaptopurine; Middle Aged; Nitrosourea Compounds; Prednisolone; Remission Induction; Vincristine; Vindesine

Sixteen children with refractory hematological malignancies were treated with a combination of BH.AC, aclacinomycin-A, 6-MP and predonisolone (BH-AC.AMP protocol). They were ALL(6), ANLL(8), CML(1) and NHL(1). The CR ratio was 17% in ALL, 50% in ANLL, and blast crisis of CML was treated successfully but NHL failed in the induction remission. Major complications were vomiting, nausea, gastrointestinal bleeding, hematuria and hemorrhagic cystitis. More than 10 days or 120 mg/m2 administration of aclacinomycin-A was thought to induce more severe side effects.

Topics: Aclarubicin; Adolescent; Antineoplastic Combined Chemotherapy Protocols; Child; Child, Preschool; Cytarabine; Drug Administration Schedule; Female; Humans; Infant; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid, Acute; Lymphoma; Male; Mercaptopurine; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Prednisolone; Remission Induction

Topics: Amsacrine; Blast Crisis; Drug Evaluation; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukocyte Count; Mercaptopurine; Remission Induction

Topics: Alkaline Phosphatase; Antineoplastic Agents; Bone Marrow Examination; Busulfan; Cell Division; Chromosome Aberrations; Colchicine; Humans; Hydrogen-Ion Concentration; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Leukocyte Count; Leukocytes; Mercaptopurine; Philadelphia Chromosome; Vinblastine

Topics: Antineoplastic Agents; Blood Platelets; Busulfan; Chlorambucil; Factor Analysis, Statistical; Hemoglobinometry; Humans; Leukemia; Leukemia, Lymphoid; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Leukocyte Count; Mercaptopurine; Phosphorus Isotopes; Toxicology; Triethylenemelamine

Topics: Blood Chemical Analysis; Blood Platelets; Busulfan; Child; Chromosome Aberrations; Erythrocyte Count; Hematocrit; Humans; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Leukocyte Count; Male; Mercaptopurine; Neoplasms; Pathology; Priapism; Splenomegaly

Topics: Adolescent; Busulfan; Cyclophosphamide; Geriatrics; Leukemia; Leukemia, Lymphoid; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Mercaptopurine; Nitrogen Mustard Compounds; Phenothiazines; Toxicology; Uracil Mustard

Topics: Abnormal Karyotype; Blood Cell Count; Bone Marrow Examination; Busulfan; Chromosome Aberrations; Chromosome Disorders; Geriatrics; Gout; Hemoglobinometry; Humans; Kidney Calculi; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Mercaptopurine; Nephrectomy; Prednisone

Topics: Busulfan; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mercaptopurine; Neoplasms; Radiotherapy

Topics: Alkaline Phosphatase; Antineoplastic Agents; Busulfan; Chromosome Aberrations; Colchicine; Humans; Hydrogen-Ion Concentration; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Leukocytes; Mercaptopurine; Nucleosides; Vinblastine

Topics: Animals; Blood Protein Electrophoresis; Busulfan; Complement System Proteins; Erythrocytes; Guinea Pigs; Hydrazines; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Leukocyte Count; Mercaptopurine; Prednisolone; Sheep

Topics: Blood Transfusion; Busulfan; Cortisone; Erythrocyte Count; Hemoglobinometry; Humans; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Leukocyte Count; Mercaptopurine; Nitrogen Mustard Compounds; Prednisolone; Prednisone; Uracil Mustard

Topics: Busulfan; Disease Management; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Mercaptopurine

Topics: Amino Acids; Humans; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukocytes; Mercaptopurine

Topics: Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mercaptopurine

Topics: Busulfan; Hematinics; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Mercaptopurine; Vitamin B 12

Topics: Humans; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Mercaptopurine