Thirty-seven of them were common-ALL positive for CD10 "common-ALL antigen (CALLA)" (NL-1), CD19(B4) and HLA-DR. One was pre-B ALLnegative for CALLA and another null-ALL which expressed HLA-DR alone.
Thirty-seven of them were common-ALL positive for CD10 "common-ALL antigen (CALLA)" (NL-1), CD19(B4) and HLA-DR. One was pre-B ALLnegative for CALLA and another null-ALL which expressed HLA-DR alone.
The cases were classified as common ALL (TdT+, CALLA+, pan-T-, and pan-B-) (41 cases), null-ALL (TdT+, CALLA-, pan-T-, and pan-B-) (19 cases), T-ALL (TdT+, CALLA-, pan-T+, and pan-B-) (nine cases), B-ALL (TdT-, CALLA-, pan-T-, and pan-B+) (six cases), pre-B-ALL (TdT+/-, CALLA+, pan-T-, and pan-B+) (four cases), or pre-T-ALL (TdT+, CALLA+, pan-T+, and pan-B-) (two cases).
Interestingly, 18% (2/11) of the cytoplasmic immunoglobulin (cIg)-positive cALLA+ (pre-B) ALLs involved TCR gene rearrangements, compared to 60% (21/35) of the cIg-negative cases, suggesting the possibility that the majority of functional B cells are derived from the cALLA+ pool that contains immunoglobulin but not TCR gene rearrangements.
We now report that spontaneous T-cell colonies could also be obtained during complete remission of 13 out of 21 patients with T-ALL and T-NHL, but none of eight patients with common (pre-B) ALL (cALL).
The terminal deoxynucleotidyltransferase-positive phenotype of the patient's leukemic cells further suggests that the pre-B-cell leukemia was derived from a pre-B cell carrying a t(14;18) translocation in the original follicular lymphoma.
The E2A gene is involved by the t(1;19)(q23;p13) in acute pre-B-cell leukemias and the LYL1 gene is structurally altered by a t(7;19)(q34;p13) in T-cell ALL.
Using a specific E2A gene probe spanning the DNA binding and dimerization domain obtained by PCR methodology, we were able to detect the rearrangement of the E2A gene in four cases (three patients and one cell line) of pre-B acute lymphoblastic leukemia with t(1;19) translocation.
The E2A gene is involved by the t(1;19)(q23;p13) in acute pre-B-cell leukemias and the LYL1 gene is structurally altered by a t(7;19)(q34;p13) in T-cell ALL.
Thus rearrangement of the E2A gene is not restricted to cases with pre-B ALL but may also occur in acute leukemias with other immunological phenotypes.
Effective immunochemotherapy of CALLA+C mu+ human pre-B acute lymphoblastic leukemia in mice with severe combined immunodeficiency using B43 (anti-CD19) pokeweed antiviral protein immunotoxin plus cyclophosphamide.
We used this SCID mouse model of human pre-B ALL to evaluate and compare, in a total of 434 SCID mice, the antileukemic efficacy of B43 (anti-CD19)-pokeweed antiviral protein (PAP) immunotoxin and cyclophosphamide (CPA) as individual reagents and as combined immunochemotherapeutic regimens.
We used this SCID mouse model of aggressive human pre-B ALL to evaluate the in vivo antileukemic efficacy of B43 (anti-CD19)-pokeweed antiviral protein (PAP) immunotoxin.
We analyzed the CDR-III sequences of B cell precursor acute lymphoblastic leukemia (pre-B ALL) cells in 23 newly diagnosed and 10 relapsed patients, in order to elucidate the organization of CDR-III in B cell precursors.
The gene for the insulin receptor has been assigned to chromosome 19 near the breakpoint of the translocation t(1;19) which occurs in 25% of pre-B-cell leukemias.
We analyzed the CDR-III sequences of B cell precursor acute lymphoblastic leukemia (pre-B ALL) cells in 23 newly diagnosed and 10 relapsed patients, in order to elucidate the organization of CDR-III in B cell precursors.