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.
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.
The total uptake of 3H-C 20:4 by platelets from CML patients did not differ from controls, but the release of radioactivity in response to thrombin was significantly lower (p < 0.01) in CML patients (32.3% +/- 4.9% of total radioactivity was released from control platelets; 19.0% +/- 7.4% from CML platelets).
To investigate this further, we established Epstein-Barr virus (EBV)-transformed B-lymphoblastoid cell lines derived from patients with CML and studied chromosomes and G6PD to determine whether progenitor B lymphocytes for any of the cell lines had originated from the CML clone.
It has been shown with glucose 6-phosphate dehydrogenase (G-6-PD) mosaicism that Ph1-positive chronic myelogenous leukemia (CML) is a clonal disease that involves multipotent hematopoietic stem cells.
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).
The requirement of erythropoiesis for erythropoietin were studied in a patient with Ph chronic myelocytic leukemia who had undergone an erythroblastic transformation.
T lymphocytic colony formation by peripheral lymphocytes separated by discontinuous albumin gradient centrifugation was evaluated in 8 patients with Philadelphia (Ph1)-positive chronic myeloid leukemia (CML).
This finding is a direct demonstration of a reciprocal exchange between the two chromosomes and suggests a role for the c-abl gene in the generation of CML.
Granulocytes from patients with chronic myelogenous leukemia (CML) contain both TC I and TC III, and these R proteins can be released in vitro by lithium stimulation.
Granulocytes from patients with chronic myelogenous leukemia (CML) contain both TC I and TC III, and these R proteins can be released in vitro by lithium stimulation.
Granulocytes from patients with chronic myelogenous leukemia (CML) contain both TC I and TC III, and these R proteins can be released in vitro by lithium stimulation.
Clonal origin of the Philadelphia translocation in chronic myeloid leukemia demonstrated in somatic cell hybrids using an adenylate kinase-1 polymorphism.
Granulocytes from patients with chronic myelogenous leukemia (CML) contain both TC I and TC III, and these R proteins can be released in vitro by lithium stimulation.
It was recently suggested that the translocation of the c-abl gene (the human cellular homologue of the transforming sequence of Abelson murine leukaemia virus) from chromosome 9 to 22 in Philadelphia translocation, might have a role in the generation of chronic myeloid leukaemia (CML).
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.
A remarkable concordance between the chromosomal location of human cellular oncogenes and the breakpoints involved in acquired chromosomal translocations is becoming apparent in various cancers: the oncogenes c-mos, c-myc and c-abl are located at the breakpoints that occur in acute myeloblastic leukaemia, Burkitt's lymphoma and chronic myelocytic leukaemia respectively.
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.