Fig. 2.
Fig. 2. Analysis of tissue from the patient and of blood from his parents for LOH at. / NF1. (A) DNA samples were amplified using oligonucleotides corresponding to the intragenic marker EVI-20. DNA obtained from the mother with NF1 (NF1±, lane 1) and the unaffected father (NF1+/+, lane 2). Patient peripheral blood (lane 3) and unfractionated bone marrow (lane 4) were obtained at the time of initial presentation and diagnosis of JMML. Lymph node (lane 5), spleen (lane 6), unfractionated marrow (lane 7), maturing marrow monocytes (lane 8), and marrow-derived neutrophils (lane 9) and the lymph node subpopulations—CD4+sCD3+ (lane 10) and CD4+sCD3− (lane 11)—were obtained at the time of the diagnosis of lymphoma. Different alleles are designated in size order, beginning with the letter a. (B) Identical chromosome 17 loci showed LOH in both primary leukemic and lymphoma cells. Bars represent a schematic of the patient's paternally derived chromosome 17 in bone marrow, lymph node, sCD3+ (phenotypically normal CD4+ T cells), and CD4+sCD3−(abnormal lymphoma) cells, designated as CD4+. The heterozygosity status of informative loci is indicated by the shaded bar for loci that lost heterozygosity or the open bar for loci that retained heterozygosity. Interlocus genetic distances in centiMorgans (cM) are indicated to the left of each interval as estimated from a chromosome 17 sex-averaged map (http://www.marshmed.org/genetics/). Data illustrating the retention of heterozygosity at the D17S805 locus and the loss of heterozygosity at the D17S1294 locus are shown to the right. DNA samples are as follows: lane 1, patient's unaffected father; lane 2, patient's mother affected with NF1; lane 3, patient's unfractionated bone marrow; lane 4, patient's lymph node; lane 5, CD3+ cells from the lymph node; lane 6, CD4+cells from the lymph node; positive and negative controls are not shown. For each locus, 2 alleles, designated simply as a and b, are segregating in this family. Differences in band intensity are caused by differences in the amount of DNA loaded per lane.

Analysis of tissue from the patient and of blood from his parents for LOH at

NF1. (A) DNA samples were amplified using oligonucleotides corresponding to the intragenic marker EVI-20. DNA obtained from the mother with NF1 (NF1±, lane 1) and the unaffected father (NF1+/+, lane 2). Patient peripheral blood (lane 3) and unfractionated bone marrow (lane 4) were obtained at the time of initial presentation and diagnosis of JMML. Lymph node (lane 5), spleen (lane 6), unfractionated marrow (lane 7), maturing marrow monocytes (lane 8), and marrow-derived neutrophils (lane 9) and the lymph node subpopulations—CD4+sCD3+ (lane 10) and CD4+sCD3− (lane 11)—were obtained at the time of the diagnosis of lymphoma. Different alleles are designated in size order, beginning with the letter a. (B) Identical chromosome 17 loci showed LOH in both primary leukemic and lymphoma cells. Bars represent a schematic of the patient's paternally derived chromosome 17 in bone marrow, lymph node, sCD3+ (phenotypically normal CD4+ T cells), and CD4+sCD3−(abnormal lymphoma) cells, designated as CD4+. The heterozygosity status of informative loci is indicated by the shaded bar for loci that lost heterozygosity or the open bar for loci that retained heterozygosity. Interlocus genetic distances in centiMorgans (cM) are indicated to the left of each interval as estimated from a chromosome 17 sex-averaged map (http://www.marshmed.org/genetics/). Data illustrating the retention of heterozygosity at the D17S805 locus and the loss of heterozygosity at the D17S1294 locus are shown to the right. DNA samples are as follows: lane 1, patient's unaffected father; lane 2, patient's mother affected with NF1; lane 3, patient's unfractionated bone marrow; lane 4, patient's lymph node; lane 5, CD3+ cells from the lymph node; lane 6, CD4+cells from the lymph node; positive and negative controls are not shown. For each locus, 2 alleles, designated simply as a and b, are segregating in this family. Differences in band intensity are caused by differences in the amount of DNA loaded per lane.

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