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Blood, Vol. 108, Issue 5, 1684-1689, September 1, 2006
Interstitial uniparental isodisomy at clustered breakpoint intervals is a frequent mechanism of NF1 inactivation in myeloid malignancies
Blood Stephens et al.
108: 1684
Supplemental materials for: Stephens et al
Files in this Data Supplement:
- Table S1. Selected Characteristics and Previous Reports of Patients Included in This Study (PDF, 10.4 KB)
- Table S2. Interphase Fluorescence in Situ Hybridization Analysis of Bone Marrow Samples (PDF, 73.7 KB)
- Figure S1. LOH at chromosome 17 loci in leukemic cells (JPG, 152 KB)
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Selected examples of LOH analysis at loci in the tumors of patient 1, 2,3, and 6 are shown. For patient 1, the maternal allele of D17S1830 was lost, while both parental alleles were retained at D17S928. Similarly, patient 2 showed LOH for a maternal allele at D17S1830 and retention of both alleles at D17S928. The bone marrow of patients 3 and 6 lost heterozygosity at D17S1830, but retained heterozygosity at D17S928. DNA sources were BM, patient bone marrow; F, Father’s leukocytes; M, mother’s leukocytes. The genotype of each individual is given above the lane; patient genotypes are shown as having only one allele, as these data only document LOH not isodisomy.
- Figure S2. Sequence of D17S928 in bone marrow of Patient 1 (JPG, 149 KB)
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To confirm heterozygosity of D17S928 in Patient 1, the locus was amplified and sequenced directly. D17S928 is a dinucleotide repeat and heterozygosity at this locus is confirmed by the frame shift in the sequence at position 60 in this figure.
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