ABSTRACT
B-ALLs have been historically divided into pro-B-ALL (earlypre-B-ALL; TdT+/CD19+/CD10−), common acute lymphoblastic leukemia (ALL; CD10+ or CALLA+), pre-B-ALL (CD10+/−; cytoplasmic IgM+) and mature B-ALL (surface IgM+). e majority of mature B-ALLs, which are characterized by basophilic cytoplasm with prominent vacuoles, expression of surface immunoglobulins, and higher incidence of CNS involvement, are now classied as Burkitt lymphoma (BL) in leukemic phase. Common and pre-B-ALL are oen positive for t(9;22)/BCR-ABL1 (30%–50%). e pro-B-ALLs show t(4;11)(q34;q11)/ALL1-AF4. In a series by Cimino et al., adult patients with pro-B-ALL had the ALL1/AF4 fusion transcript, originating from the t(4;11) translocation in 36.4%, and the t(9;22)/BCR-ABL1 in 9% [17]. B-ALL with t(9;22) oen displays aberrant expression of pan-myeloid antigens (CD33 or less oen CD13). Adult patients with earlypre-B-ALL and t(4;11) or t(9;22) have a poor prognosis, and the absence of both of these translocations correlates with a signicantly better clinical outcome aer intensive chemotherapy treatment [17]. CD10− pre-B-ALL has been identied as a highrisk subgroup of adult ALL, associated with a high frequency of KMT2A aberrations and worse prognosis [18]. Pro-B and/or t(4;11)+ ALL is associated with worse prognosis but responds well to high-dose cytarabine therapy and stem cell transplantation.
