Fig. 3.
Fig. 3. Examples of 6 patients with FLT3-LM at diagnosis who were evaluated for the mutation at different follow-up time points. / M, molecular weight standard; −C, blank control; +C, positive control; BM, bone marrow; PB, peripheral blood; D, sample at diagnosis; Rel, sample at relapse; Rem, sample from remission; M, months. Patient 1 had FLT3-LM at diagnosis in the bone marrow and in the peripheral blood. At follow-up (Rel1) he had a single mutated band in complete remission 3 weeks before morphologic relapse (Rel2). He lost the wild-type allele, which was confirmed by FISH analysis (data not shown). In second remission, only the wild-type allele could be amplified. Patient 2 was studied at 3 remission time points at 3-month intervals. At all remission time points, only the normal allele was detectable. Patient 3 was hemizygous for the mutation at diagnosis and is still in remission with only the wild-type allele detectable. Patient 4 needed 7 months of conventional chemotherapy to achieve clinical remission. Patient 5 was heterozygous for the mutation at diagnosis and is in continuing clinical and molecular remission for 6 months. Patient 6 was heterozygous at diagnosis, did not achieve clinical remission, and shifted to a hemizygous state for the mutation after 3 months.

Examples of 6 patients with FLT3-LM at diagnosis who were evaluated for the mutation at different follow-up time points.

M, molecular weight standard; −C, blank control; +C, positive control; BM, bone marrow; PB, peripheral blood; D, sample at diagnosis; Rel, sample at relapse; Rem, sample from remission; M, months. Patient 1 had FLT3-LM at diagnosis in the bone marrow and in the peripheral blood. At follow-up (Rel1) he had a single mutated band in complete remission 3 weeks before morphologic relapse (Rel2). He lost the wild-type allele, which was confirmed by FISH analysis (data not shown). In second remission, only the wild-type allele could be amplified. Patient 2 was studied at 3 remission time points at 3-month intervals. At all remission time points, only the normal allele was detectable. Patient 3 was hemizygous for the mutation at diagnosis and is still in remission with only the wild-type allele detectable. Patient 4 needed 7 months of conventional chemotherapy to achieve clinical remission. Patient 5 was heterozygous for the mutation at diagnosis and is in continuing clinical and molecular remission for 6 months. Patient 6 was heterozygous at diagnosis, did not achieve clinical remission, and shifted to a hemizygous state for the mutation after 3 months.

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