Fig. 1.
Fig. 1. Analysis of TEL-AML1 translocation in a set of triplet twins. / (A) Scheme of TEL and AML1 genes showing where the primers anneal in both genes (small horizontal arrows). The vertical arrows show the map location of the breakpoint betweenTEL and AML1 shared by the 2 leukemic twins. (B) Sequence neighboring the TEL-AML1 breakpoint found in the twins. The normal TEL sequence is shown at the top, the sequence found in the patients is shown in the center, and theAML1 sequence is shown at the bottom. There is a 4-base homology between TEL and AML1 in the breakpoint, which is shown in italics. (C) PCR analysis of the TEL-AML1translocation on the blood DNA of the triplet twins. The predicted PCR product of 521 bp was amplified with primers A and E in twins T1 and T2 but not in twin T3 or any of the control DNA samples. M, marker; T1 and T2, affected twins; T3, healthy twin; C, negative control DNA samples.

Analysis of TEL-AML1 translocation in a set of triplet twins.

(A) Scheme of TEL and AML1 genes showing where the primers anneal in both genes (small horizontal arrows). The vertical arrows show the map location of the breakpoint betweenTEL and AML1 shared by the 2 leukemic twins. (B) Sequence neighboring the TEL-AML1 breakpoint found in the twins. The normal TEL sequence is shown at the top, the sequence found in the patients is shown in the center, and theAML1 sequence is shown at the bottom. There is a 4-base homology between TEL and AML1 in the breakpoint, which is shown in italics. (C) PCR analysis of the TEL-AML1translocation on the blood DNA of the triplet twins. The predicted PCR product of 521 bp was amplified with primers A and E in twins T1 and T2 but not in twin T3 or any of the control DNA samples. M, marker; T1 and T2, affected twins; T3, healthy twin; C, negative control DNA samples.

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