A bone marrow transplantation from an HLA-identical, MLC nonreactive paternal donor has been performed in a patient with acute lymphoblastic leukemia resistant to drug treatment.
The long interval between the onset of ALL and GML, as well as the normal karyotype during remission from the ALL, causes us to favor the hypothesis that two separate diseases are present.
We report here observations on the occurrence of intermediate pre-B/B-cell phenotypes, immunoglobulin isotype switching and the asynchrony of immunoglobulin heavy and light chain expression in 30 cases of ALL and 3 cases of chronic myelogenous leukaemia in lymphoblastic crisis (CML-BC).
Two permanent T-cell leukemia lines designated KH-1 and KH-2 were established from the peripheral blood of a 9-year-old boy with acute lymphoblastic leukemia and a 47-year-old man with adult T-cell leukemia (ATL).No T-cell growth factor was used.
The patient responded to chemotherapy with vincristine, prednisone, and L-asparaginase, first line drugs used for remission-induction of acute lymphoblastic leukemia in childhood.
Lymphocytes from patients with acute lymphocytic leukemia (T-ALL) showed an enzyme profile similar to that of normal thymocytes, i.e., an elevated level of adenosine deaminase (ADA) activity as compared with normal T lymphocytes, reduced activities of purine 5'nucleotidase (5'NT) and purine nucleoside phosphorylase (PNP), and a binomial distribution of the LDH isoenzyme pattern.
Lymphocytes from patients with acute lymphocytic leukemia (T-ALL) showed an enzyme profile similar to that of normal thymocytes, i.e., an elevated level of adenosine deaminase (ADA) activity as compared with normal T lymphocytes, reduced activities of purine 5'nucleotidase (5'NT) and purine nucleoside phosphorylase (PNP), and a binomial distribution of the LDH isoenzyme pattern.
Lymphocytes from patients with acute lymphocytic leukemia (T-ALL) showed an enzyme profile similar to that of normal thymocytes, i.e., an elevated level of adenosine deaminase (ADA) activity as compared with normal T lymphocytes, reduced activities of purine 5'nucleotidase (5'NT) and purine nucleoside phosphorylase (PNP), and a binomial distribution of the LDH isoenzyme pattern.
Normal human cells can be transformed to anchorage-independent growth by transfection with DNA from MOLT-4 lymphoblasts, derived from a patient with acute lymphocytic leukemia.
Six hundred and thirty unselected cases of acute leukemia, with complete data regarding age, karyotype (with breakpoints), and the diagnosis according to the FAB classification, were available in the literature and from our unpublished cases for comparing the incidence of chromosomal abnormalities involving the long arm of chromosome #11 among age groups in acute nonlymphocytic leukemia (ANLL) and acute lymphocytic leukemia (ALL).
Immunoglobulin heavy chain gene rearrangement was evaluated in 19 cases of acute lymphoblastic leukemia (ALL) and correlated with the immunological phenotypic expression on primary or phorbol diester (12-O-tetradecanoylphorbol-13-acetate [TPA])-induced cells.
Lymphoblast immunophenotypes were those of HLA-DR+, CALLA+ ALL (six patients); HLA-DR+, CALLA- ALL (four patients); pre-B cell ALL (two patients); T cell ALL (four patients); and undefined ALL (three patients).
The recognition of early pre-T-ALL cases (T1+, RFT2+, T10+, T6-, T11-, E-) contributed to the overall low proportion of 'null' ALL; prior to the use of MoAb, such cases would probably have been classified as undifferentiated acute leukaemia or 'null' ALL.
DNA and RNA determination in 111 cases of childhood acute lymphoblastic leukaemia (ALL) by flow cytometry: correlation of FAB classification with DNA stemline and proliferation.
Eight (of the 40) patients with non-T, non-B ALL were identified as CALLA- but further analysis indicated T-lineage origin in two patients and three patients were reclassified as acute undifferentiated leukaemia (AUL).
The malignant counterpart of the Tp41+/HLA-DR+/TdT+ cell was detected in a patient with acute lymphoblastic leukemia with the Tp41+/T11+/HLA-DR+/TdT+/T1-/T6- phenotype and germ-line immunoglobulin heavy chain genes.
To determine whether acute lymphoblastic leukemia (ALL) is a clonal disease and to define the pattern of differentiation shown by the involved progenitor cells, we studied the glucose-6-phosphate dehydrogenase (G6PD) types in the cells of 19 girls heterozygous for this X chromosome-linked enzyme.
Three patients with acute lymphoblastic leukemia (ALL) and heterozygous for the Mediterranean variant of glucose-6-phosphate dehydrogenase (G6PD) have been investigated with the 2-deoxyglucose-6-phosphate (2dG6P) method to determine the number and type of progenitor cells in which the disease arose.
Four major phenotypic groups were identified: B lineage ALL (BA-1+T-) (64%), T lineage ALL (T+BA-1-MCS-2-) (13%), unclassified ALL (BA-1-MCS-2-CALLA-T-) (9%) and myeloid antigen ALL (MCS-2+CALLA-T-) (7%).
Sister chromatid exchange (SCE) was studied in PHA-stimulated peripheral blood lymphocytes from 36 newly diagnosed and untreated leukemic patients: 16 with acute lymphoblastic leukemia (ALL), 10 with acute nonlymphocytic leukemia (ANLL), and 10 with chronic myelocytic leukemia (CML).