Review Board at The University of Texas MD Anderson Cancer Center in Houston, Texas, USA. Immunohistochemistry for Bcl-2 and cut-off determination Bcl-2 protein expression was evaluated in all patients using a monoclonal anti-Bcl-2 antibody (Clone-124, Dako, Carpinteria, CA, USA) and standard

the primary leukemia whereas 'type 2' relapse originates from a common pre-leukemic ancestor. Relapse-specific changes included activation of the nucleotidase NT5C2 resulting in resistance to chemotherapy and mutations of epigenetic modulators, exemplified by SUZ12, WHSC1 and SMARCA4. While

's lymphocytes to test for IL12RB1 expression on the cell surface. To this end, primary lymphocytes from the patient and healthy individuals were stimulated for 4 days with phytohemagglutinin/IL2. Whereas lympho- + cells specifically induced in IL12-treated compared to untreated cells is shown. (C) Cultivated

was collected on the last treatment day, and at 1, 2, 5 and 30 days later. From 2 patients, blood samples were also collected after 12 days to better understand the delayed regain of platelet function. Patients with a malignancy, active infection or a known platelet disorder were not included. Blood

-ANT II™; Bio-Rad Laboratories, Hercules, CA, USA). The molecular analysis of the b-globin cluster was achieved including deletion detection using the quantitative multiplex polymerase chain reaction of short fragment (QMPSF) procedure. 9 Precise localization of unknown breakpoints was determined using a

and laboratory determinations. Cases were followed for recurrence in a prospective cohort study. The median lipoprotein (a) concentration did not differ between groups [cases: median 18.0 nmol/L (7.5 mg/dL) and observed range 0.9-259 nmol/L (0.38-108.0 mg/dL), controls: 20.4 nmol/L (8.5 mg/dL) and 0.2-282 nmol

the outcome of CLL patients based on clinical parameters. 1,2 In the last two decades, multiple biological markers have been shown to have prognostic relevance in CLL, most notably chromosomal aberrations, IGHV mutations and expression of surface markers such as ZAP-70 and CD38. Design and Methods Patients

and focal IKZF1-deleted cases Loss of IKZF1 function, a well-known tumor-inducing event in ALL, is conceivably one of the reasons for the recurrent heterozygous loss of chromosome 7, as this would include losing the IKZF1 locus on 7p12.2. We hypothesized that, if loss of IKZF1 were to be one of the driving

significant. All analyses and data management were performed using Stata version 12.0 (StataCorp, College Station, TX, USA), and EZR. 23 Results Patients' characteristics In general, conditioning intensity is selected based on patients' characteristics, such as age and co-morbidity, and donor

), CD14 (M0P9 FITC), CD3 (SK7 PerCp), CD4 (Leu 3 FITC), CD5 (Leu 1 FITC), CD8 (Leu 2 PE) purchased from Becton Dickinson, San José, CA, USA (BDIS); CD19 (SJ25-C1 PE/Cy 5) and MPO (H-43-5 FITC) from Caltag Laboratories, Burlingame, CA, USA; CD 123 (9F5 PE), CD10 (HI10a, Cy-Chrome) from Pharmingen, San