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We describe two patients with primary diffuse large B-cell lymphoma of the central nervous system (PCNS-DLBCL). The first patient (case 1) was a woman in her late 70s who presented with a tumor in the left frontal lobe, whereas the second patient (case 2) was a man in his early 70s who presented with a left frontal lobe tumor associated with intratumoral hemorrhage. The histopathology of the tumor specimen disclosed the proliferation of large cells with centroblastic (case 1) or immunoblastic/plasmablastic (case 2) cytomorphology and an accumulation of the tumor cells within the perivascular space. The cells in both cases were positive for CD20, CD79a, BCL6, IRF4/MUM1, MYC, and BCL2 and negative for CD5 and CD10. G-banding revealed t(8;14)(q24;q32) in case 1, and the tetraploid-range karyotype including two or three copies of der(3)t(3;14)(q27;q32) and der(14)t(3;14)(q27;q32) in case 2. Fluorescence in situ hybridization applied to metaphase spreads confirmed colocalization of MYC and IGH (case 1) and BCL6 and IGH (case 2) hybridization signals on the relevant derivative chromosomes. Case 1 carried the MYD88 L265P mutation. This case report provides clear evidence for the occurrence of t(8;14)(q24;q32) and t(3;14)(q27;q32) in PCNS-DLBCL using metaphase-based cytogenetic analysis.

The bone marrow (BM) was infiltrated with large cells with features of Burkitt lymphoma, whereas lymphoma cells in the peripheral blood (PB) exhibited indolent cytomorphology indicative of follicular lymphoma (FL). Multicolor flowcytometry and fluorescence in situ hybridization revealed that BM lymphoma cells were CD10 + , CD24 bright , and CD38 bright and had t(14;18)(q32;q21)/ BCL2-IGH and t(8;14)(q24;q32)/MYC-IGH. In contrast, the majority of PB lymphoma cells were small to medium sized and CD10 − , CD24 −/dim , and CD38 − and had t(14;18)/BCL2-IGH but lacked t(8;14)/MYC-IGH, and we identified a intermediate population composed of medium-sized cells that were CD10 dim , CD24 dim/+ , and CD38 + and had both t(14;18)/BCL2-IGH and t(8;14)/MYC-IGH. Multiplex polymerase chain reaction confirmed that BM and PB lymphoma cells shared common IGK rearrangement and BCL2-IGH fusion sequence. It is indicated that, in this case, indolent FL and MYC/BCL2 double-hit highgrade B-cell lymphoma (HGBL) transformed from FL developed concurrently and acquisition of t(8;14)/ MYC-IGH may not immediately lead to transformation to HGBL, but instead, florid cytomorphologic transformation may occur in BM.

A woman in her seventies presented with leukocytosis. Her white cell count was 33.87 × 10 3 /μL with 80.5% leukemia cells. Her bone marrow was replaced with peroxidase-negative leukemia blasts that were CD10 +/− , CD19 + , CD20 − , CD13 + , CD33 −/dim , CD34 + , CD117 −/dim , CD66c +/− , cytoplasmic (cy-) CD79a + , terminal doxynucleotidyl transferase + , and cy-IGHM − . G-banding revealed t(9;22)(q34;q11.2) as the sole chromosome abnormality, and reverse transcriptase polymerase chain reaction (PCR) and nucleotide sequencing confirmed that the fusion encompassed exon 19 of BCR and exon 2 of ABL1, which generate p230 micro (μ)-BCR-ABL1 mRNA. We treated her with a second-generation tyrosine kinase inhibitor, dasatinib, in combination with low-intensity chemotherapy (vincristine and dexamethasone) followed by consolidation, leading to a hematological complete response (CR) and 10 −4 level reduction of leukemia cell burden as measured by LightCycler ® -based real-time quantitative PCR assay. The patient received maintenance treatment with dasatinib followed by ponatinib and achieved hematological CR for 2 years and 8 months. This report showed that patients with the p230 μ-BCR-ABL1 fusion gene may present with not only chronic myeloid leukemia with mild clinical features but also Philadelphiapositive acute lymphoblastic leukemia (Ph+ ALL) with precursor B-cell immunophenotype; moreover, dasatinib-based induction, consolidation, and maintenance therapies are as effective for Ph+ ALL with μ-BCR-ABL1 as those with minor-and major-BCR-ABL1.

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