Figure 1.
Treatment and disease characteristics. (A) Absolute lymphocyte counts (ALCs) and MRD of the patients during lenalidomide maintenance therapy. Red lines show the time point of ALL diagnosis, and green lines show the threshold for undetectable MRD (10−4 leukemic cells). Patient 1: CLL MRD levels in peripheral blood (PB) decreased steadily from 8.6 × 104 to 1.6 × 104 after 16 months of lenalidomide treatment. BCR-ABL1–positive common B-ALL was diagnosed but no bone marrow (BM) infiltration of CLL cells could be detected morphologically (panel C). Patient 2 received lenalidomide for 15 months before discontinuing because of increased creatinine levels. Undetectable MRD in PB (<10−4) was achieved after 6 months and maintained at month 12 of lenalidomide therapy. When BCR-ABL1–positive common ALL was diagnosed, there were no signs of CLL cells in the PB or BM by cytomorphology or immunophenotyping. Patient 3 received lenalidomide for 45 months before treatment was stopped after a data safety monitoring board recommendation. Although his MRD level in PB had dropped sustainably below 10−4 after receiving lenalidomide for 6 months, a reciprocal increase of residual CLL cells to 8 × 10−3 was observed 2 months after lenalidomide was discontinued. Three months after the end of maintenance treatment, Philadelphia chromosome–negative common ALL was diagnosed after a BM biopsy prompted by persisting pancytopenia. (B) Summary of selected genetic alterations at CLL and ALL time points, including fluorescence in situ hybridization (FISH) analysis for recurrent aberrations in CLL, IGHV status, cancer-related mutations according to next-generation sequencing (NGS), and BCR/ABL status. We performed BCR-ABL1 reverse transcriptase quantitative polymerase chain reaction (PCR) in earlier PB samples from patients 1 and 2. No BCR-ABL1 fusion transcripts were detected in a blood sample 12 months after initiation of maintenance in patient 2 and 11 months after start of lenalidomide treatment in patient 1. (C) Giemsa stains of BM samples from all 3 patients at the time of ALL diagnosis (magnification ×100). BR, bendamustine, rituximab; FCR, fludarabine, cyclophosphamide, rituximab.

Treatment and disease characteristics. (A) Absolute lymphocyte counts (ALCs) and MRD of the patients during lenalidomide maintenance therapy. Red lines show the time point of ALL diagnosis, and green lines show the threshold for undetectable MRD (10−4 leukemic cells). Patient 1: CLL MRD levels in peripheral blood (PB) decreased steadily from 8.6 × 104 to 1.6 × 104 after 16 months of lenalidomide treatment. BCR-ABL1–positive common B-ALL was diagnosed but no bone marrow (BM) infiltration of CLL cells could be detected morphologically (panel C). Patient 2 received lenalidomide for 15 months before discontinuing because of increased creatinine levels. Undetectable MRD in PB (<10−4) was achieved after 6 months and maintained at month 12 of lenalidomide therapy. When BCR-ABL1–positive common ALL was diagnosed, there were no signs of CLL cells in the PB or BM by cytomorphology or immunophenotyping. Patient 3 received lenalidomide for 45 months before treatment was stopped after a data safety monitoring board recommendation. Although his MRD level in PB had dropped sustainably below 10−4 after receiving lenalidomide for 6 months, a reciprocal increase of residual CLL cells to 8 × 10−3 was observed 2 months after lenalidomide was discontinued. Three months after the end of maintenance treatment, Philadelphia chromosome–negative common ALL was diagnosed after a BM biopsy prompted by persisting pancytopenia. (B) Summary of selected genetic alterations at CLL and ALL time points, including fluorescence in situ hybridization (FISH) analysis for recurrent aberrations in CLL, IGHV status, cancer-related mutations according to next-generation sequencing (NGS), and BCR/ABL status. We performed BCR-ABL1 reverse transcriptase quantitative polymerase chain reaction (PCR) in earlier PB samples from patients 1 and 2. No BCR-ABL1 fusion transcripts were detected in a blood sample 12 months after initiation of maintenance in patient 2 and 11 months after start of lenalidomide treatment in patient 1. (C) Giemsa stains of BM samples from all 3 patients at the time of ALL diagnosis (magnification ×100). BR, bendamustine, rituximab; FCR, fludarabine, cyclophosphamide, rituximab.

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