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Unfortunately, in our series mutational status and cytogenetic abnormalities were determined in only 15% of patients rendering statistical analysis impossible; ZAP-70 expression was not determined and there was no correlation with CD38 expression.
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Abnormalities were determined as being of maternal origin in all dup(15) cases except for a 22-year-old female with undetermined origin of two extra copies of the 15q11.2-q13.1 region.
Chromosomal abnormalities were determined based on the karyotype.
The number of abnormalities (0-5) was determined in the 214 male and 91 female patients, and the association with each polymorphism evaluated by means of ordinal regression analysis.
The length of ETC abnormality was determined by counting the number of slides the abnormality appeared in and multiplying by 10 μm.
Importantly, direct neuronal loss was determined in the work rather than recording abnormalities in behavior.
Predicted copy number abnormalities greater than 10 Mb in size were determined, as previously described, by plotting the number of mate pairs mapping within a given window (W 9 11 kB) against the position on each chromosome.
Safety and adverse events (AE) were determined through the biochemical abnormalities documented in medical records according to the Department of Health and Human Services - Common Terminology Criteria for Adverse Events (DHHS-CTCAE v.3.0) classification [ 12].
Based on these data, the presence of the abnormality and its shape and location in the imaging window were determined.
Genotypes were determined based on coat color, as the W sh mutation causes abnormalities in pigmentation.
Identification of chromosomal abnormalities is mandatory for classification of acute myeloid leukemia (AML), and the abnormalities have to be determined quickly, to allow patient enrollment in multicenter protocols and/or for selecting therapeutic strategies.
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