DSP30 and interleukin-2 as a mitotic stimulant in B-cell disorders including those with a low disease burden.

Chromosome abnormalities detected during cytogenetic investigations for B-cell malignancy offer prognostic information that can have wide ranging clinical impacts on patients. These impacts may include monitoring frequency, treatment type, and disease staging level. The use of the synthetic oligonucleotide DSP30 combined with interleukin 2 (IL2) has been described as an effective mitotic stimulant in B-cell disorders, not only in chronic lymphocytic leukemia (CLL) but also in a range of other B-cell malignancies. Here, we describe the comparison of two B-cell mitogens, lipopolysaccharide (LPS), and DSP30 combined with IL2 as mitogens in a range of common B-cell disorders excluding CLL. The results showed that DSP30/IL2 was an effective mitogen in mature B-cell disorders, revealing abnormal cytogenetic results in a range of B-cell malignancies. The abnormality rate increased when compared to the use of LPS to 64% (DSP30/IL2) from 14% (LPS). In a number of cases the disease burden was proportionally very low, less than 10% of white cells. In 37% of these cases, the DSP30 culture revealed abnormal results. Importantly, we also obtained abnormal conventional cytogenetics results in 3 bone marrow cases in which immunophenotyping showed an absence of an abnormal B-cell clone. In these cases, the cytogenetics results correlated with the provisional diagnosis and altered their staging level. The use of DSP30 and IL2 is recommended for use in many B-cell malignancies as an effective mitogen and their use has been shown to enable successful culture of the malignant clone, even at very low levels of disease.

BCR-ABL1 gene rearrangement as a subclonal change in ETV6-RUNX1-positive B-cell acute lymphoblastic leukemia.

We report here on a case of ETV6-RUNX1-positive B-cell acute lymphoblastic leukemia (B-ALL) that has acquired a BCR-ABL1 gene rearrangement as a subclonal change. The 19-year-old female patient presented with B symptoms, pancytopenia, and circulating blasts. The bone marrow aspirate was hypercellular and was infiltrated by an immature blast population that was confirmed as B-ALL by flow cytometry. Sequential fluorescent in situ hybridization was performed on the patient's leukemic cells, which were shown to contain both ETV6-RUNX1 and BCR-ABL1 gene rearrangements. The majority of nuclei (85%) showed only the ETV6-RUNX1 gene rearrangement; however, an additional 10% also showed a variant BCR-ABL1 gene rearrangement, indicating the ETV6-RUNX1 gene rearrangement was the primary change. A review of the literature has shown that acquisition of a BCR-ABL1 gene rearrangement as a secondary change in B-ALL is a very rare occurrence, and the effect it may have on prognosis is uncertain in the modern therapy age.