These leukaemic cells retain their undifferentiated membrane characteristics C.M.L. patients in blast crisis who are A.L.L.-antigen-positive and have terminal transferase enzyme activity might benefit from therapy usually given in typical Philadelphia-chromosome-negative A.L.L.
These leukaemic cells retain their undifferentiated membrane characteristics C.M.L. patients in blast crisis who are A.L.L.-antigen-positive and have terminal transferase enzyme activity might benefit from therapy usually given in typical Philadelphia-chromosome-negative A.L.L.
Forty-four patients with Ph positive leukemia (36 developing blast crisis after chronic phase and eight presenting in acute leukemia) were classified into subgroups on the basis of reactivity of blasts with an anti-serum made against non-T,non-B acute lymphoid leukemia (ALL+), levels of terminal transferase enzyme (TdT+) and morphology.
A 46-year-old female with chronic myelogenous leukemia (CML) in blast crisis was monitored for terminal deoxynucleotidyltransferase (TdT) activity of marrow and peripheral blood throughout the course of her illness.
Forty-four patients with Ph positive leukemia (36 developing blast crisis after chronic phase and eight presenting in acute leukemia) were classified into subgroups on the basis of reactivity of blasts with an anti-serum made against non-T,non-B acute lymphoid leukemia (ALL+), levels of terminal transferase enzyme (TdT+) and morphology.
Cytogenetic studies in a patient with chronic myelocytic leukemia (CML) demonstrated the emergence of an extremely hypodiploid cell line at the time of blast crisis, a modal chromosome number of 35, with the modal karyotype 35,XY, -3, -4, -5, -7, -9, -11, -12, -13, -15, -16, -17, -19, -20, -22, + t(9;22) (q34;q11, + Mar1, + Mar2, + Mar3.
Cytogenetic studies in a patient with chronic myelocytic leukemia (CML) demonstrated the emergence of an extremely hypodiploid cell line at the time of blast crisis, a modal chromosome number of 35, with the modal karyotype 35,XY, -3, -4, -5, -7, -9, -11, -12, -13, -15, -16, -17, -19, -20, -22, + t(9;22) (q34;q11, + Mar1, + Mar2, + Mar3.
Cytogenetic studies in a patient with chronic myelocytic leukemia (CML) demonstrated the emergence of an extremely hypodiploid cell line at the time of blast crisis, a modal chromosome number of 35, with the modal karyotype 35,XY, -3, -4, -5, -7, -9, -11, -12, -13, -15, -16, -17, -19, -20, -22, + t(9;22) (q34;q11, + Mar1, + Mar2, + Mar3.
Cytogenetic studies in a patient with chronic myelocytic leukemia (CML) demonstrated the emergence of an extremely hypodiploid cell line at the time of blast crisis, a modal chromosome number of 35, with the modal karyotype 35,XY, -3, -4, -5, -7, -9, -11, -12, -13, -15, -16, -17, -19, -20, -22, + t(9;22) (q34;q11, + Mar1, + Mar2, + Mar3.
Cytogenetic studies in a patient with chronic myelocytic leukemia (CML) demonstrated the emergence of an extremely hypodiploid cell line at the time of blast crisis, a modal chromosome number of 35, with the modal karyotype 35,XY, -3, -4, -5, -7, -9, -11, -12, -13, -15, -16, -17, -19, -20, -22, + t(9;22) (q34;q11, + Mar1, + Mar2, + Mar3.
The present study shows that when glycophorin-A is used as a marker for erythroid blasts, involvement of the erythroid lineage during blast crisis of chronic myelogenous leukemia seems to occur more frequently than previously recognized.
The present study shows that when glycophorin-A is used as a marker for erythroid blasts, involvement of the erythroid lineage during blast crisis of chronic myelogenous leukemia seems to occur more frequently than previously recognized.
The present study shows that when glycophorin-A is used as a marker for erythroid blasts, involvement of the erythroid lineage during blast crisis of chronic myelogenous leukemia seems to occur more frequently than previously recognized.
Twenty-five patients with Ph CML who eventually developed a blast crisis were karyotyped at regular intervals in order to correlate the evolution of abnormal clones with clinical changes.
Rosetted (E+) lymphocytes (T lymphocytes) from nine patients in chronic phase and one patient in blast crisis were stimulated with T cell growth factorinterleukin 2 (IL-2) and/or phytohemagglutinin (PHA).
Three cases were classified as myeloid BC based on histochemistry and/or ultrastructure and immunology (OKM1+, MCS2+, IG10+); two as lymphoid BC (CAE-, lysozyme-, TdT+), one of them expressing a T-cell phenotype.
The aberrant abl protein product of a chronic myelogenous leukemia (CML) blast crisis cell line (K562) and of five Philadelphia chromosome-positive CML patients in blast crisis were analyzed by an immune complex kinase assay using two antipeptide sera generated against the hydrophilic domain of v-abl and a region within the third exon of the breakpoint cluster region (bcr) respectively.
Additionally, rearrangement of the breakpoint cluster region (bcr) was demonstrated in the pretransplant blast crisis sample, but not in the posttransplant lymphoproliferation samples, thus confirming that these lymphoproliferative disorders were distinct.