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Results for “blast phase”

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At least 19 recordsLinked to original sources
PubMed1986

Preliminary observations on the therapy of the myeloid blast phase of chronic granulocytic leukemia with plicamycin and hydroxyurea.

We observed a dramatic improvement in the peripheral blood counts of a patient in the myeloid blast phase of chronic granulocytic leukemia after plicamycin (mithramycin) therapy of concurrent hypercalcemia. We then treated eight additional patients in the blast phase of chronic granulocytic leukemia with a combination of alternate-day plicamycin and daily hydroxyurea. All six patients with myeloid morphology at the time of blast crisis responded with a return to a chronic phase without an intervening pancytopenic period. Of three patients with lymphoid morphology at the time of treatment, only one responded (this patient had recently relapsed and converted from myeloid to lymphoid morphology). Another patient with nonmyeloid, nonlymphoid blast morphology also did not respond. Continual therapy with the two-drug combination appeared to be necessary, since early relapses were seen in responding patients whose therapy was interrupted. These data are preliminary and will need further confirmation, but they suggest that the combination of alternate-day plicamycin and daily hydroxyurea may be effective in the myeloid blast phase of chronic granulocytic leukemia.

Adult↗
PubMed1989

Therapy of the myeloid blast phase of chronic granulocytic leukemia with plicamycin and hydroxyurea.

Treatment of the myeloid blast phase of chronic granulocytic leukemia is still a major problem in clinical hematology. Alternate-day plicamycin and hydroxyurea treatment was reported to induce remissions in the majority of patients with myeloid blast phase by Koller and Miller in 1986 Subsequently we treated eight patients according to this regimen. Complete remissions could not be achieved and no prolongation of median survival was observed. In two patients treatment had to be discontinued due to severe toxicity.

Adult↗
PubMed1987

Association of a chromosomal 3;21 translocation with the blast phase of chronic myelogenous leukemia.

An identical reciprocal translocation between the long arms of chromosomes 3 and 21 with breakpoints in bands 3q26 and 21q22, t(3;21)(q26;q22), was found in three male patients with the blast phase of chronic myelogenous leukemia (CML). The abnormality was clonal in all three patients and was always accompanied by either a standard or variant 9;22 translocation resulting in a Philadelphia chromosome (Ph1). In two cases, the t(3;21) was the only abnormality other than a t(9;22) in the primary clone. Serial studies of one patient demonstrated that the t(3;21) occurred as a result of clonal evolution near the time of development of the blast phase. We have not observed the t(3;21) in greater than 500 patients with CML in the chronic phase. Thus, the t(3;21) is a new recurring cytogenetic abnormality associated with the blast phase of CML.

Adult↗
PubMedDate not supplied

Failure of mithramycin to control the myeloid blast phase of chronic granulocytic leukemia: a report on nine patients and review of the literature.

After reports of the successful use of mithramycin and hydroxyurea in the myeloid blast phase of chronic granulocytic leukemia, we treated nine patients according to the protocol devised by Koller and Miller (1986). There were no complete responses, but one patient had a partial response with a transient return to the chronic phase. Of the remaining eight patients, two experienced lessening of bone pains, and one a reduction in spleen size, but without hematological improvement. The regimen was associated with significant toxicity, and no overall survival advantage. We present a review of published data regarding the use of mithramycin in chronic granulocytic leukemia which supports the results in our series. The combination of mithramycin and hydroxyurea is largely ineffective in the blast phase of chronic granulocytic leukemia, but may be of value in the accelerated phase.

Adult↗
PubMed1975

Identification and characterization: cell membrane antigens associated with the blast phase of human adult leukemia.

Cell membrane antigens which produce delayed skin reactions and are associated with the blast phase of human acute leukemia have been identified and characterized. When patients are in remission, these proteins are not present on their white blood cells. The blast antigens associated with acute lymphatic leukemia (ALL) are also present on early human fetal thymus cells. Blast antigens from acute myelocytic leukemia (AML) appear to have a different structure and are not associated with fetal antigens. The isolation away from blocking factors of purified, solubilized proteins from the leukemic blast cell membranes now permits the possibility of testing to see whether or not such specific antigens will be useful in diagnosis and in immuno-chemotherapy of leukemia.

Antigens, Neoplasm↗
PubMedDate not supplied

Oral idarubicin in the treatment of acute myelogenous leukaemia and the blast phase of chronic myeloid leukaemia.

Fourteen patients with poor-risk acute myelogenous leukaemia (AML) and five patients with accelerated phase/blast crisis chronic myeloid leukaemia (CML) were treated with 3 days of oral idarubicin (25 mg/m2/day). No complete remissions or return to chronic phase CML were observed. A fall in the peripheral blast count was seen in all patients with the first cycle of treatment, and with subsequent cycles in CML patients, but all responses were transient, with eventual reemergence of peripheral blasts. In some patients, there was a clear cut improvement in symptoms such as bone and splenic pain. Five of the AML patients and all of the CML patients were treated as out-patients. In this group of patients oral idarubicin was found to be a useful drug for palliative treatment.

Administration, Oral↗
PubMed1985

Cytogenetically distinct leukemic cell lines displaying in vitro specific proliferative and differentiation capacities may account for early disease relapse in the blast phase of CML.

The cytogenetic features and the proliferative and differentiation capabilities of blast cell fractions purified on a density gradient were studied in one patient with chronic myeloid leukemia (CML) in blast crisis, both at the emergence and at relapse of the disease. The results show that relapse was due to the appearance of a new leukemic cell line that was characterized by peculiar chromosomal, growth, and differentiation features, which seemingly accounted for early refractoriness to therapy and disease progression.

Adult↗
PubMed1985

In vivo differentiation of blast-phase chronic granulocytic leukemia. Expression of c-myc and c-abl protooncogenes.

A patient with chronic granulocytic leukemia in acute blastic transformation was treated with mithramycin, an RNA synthesis inhibitor, after in vitro exposure of her leukemic cells to mithramycin showed differentiation to normal appearing granulocytes. Mithramycin therapy in vivo resulted in a prompt and dramatic hematologic response. Before therapy, the patient's leukemic cells had high levels of transcription of the cellular myc and abl protooncogenes. After initiation of therapy, protooncogene mRNA decreased rapidly. These observations indicate that mithramycin can induce differentiation both in vitro and in vivo and suggest that such changes may be associated with altered oncogene expression.

Adolescent↗
PubMed1987

Chronic myelogenous leukemia: amplification of a rearranged c-abl oncogene in both chronic phase and blast crisis.

The specific genetic events that distinguish the blast crisis from the chronic phase cells of chronic myelogenous leukemia (CML) are unknown. The most common karyotypic change that occurs as CML evolves from chronic phase to blast crisis is the development of multiple Philadelphia (Ph1) chromosomes, each of which is presumably harboring a translocated c-abl oncogene. We describe here a patient with CML who presented in lymphoid blast crisis with three Ph1 chromosomes/metaphase associated with an amplified, rearranged c-abl oncogene fragment and high levels of the aberrant 8-kilobase bcr-abl transcript. This rearranged c-abl fragment was amplified to a similar degree in both the patient's blast crisis cells and in his terminally differentiated granulocytes, but the level of the aberrant CML-specific bcr-abl transcript was some eight- to 16-fold higher in the blast crisis cells v the granulocytes. This analysis indicates that genomic amplification of a translocated c-abl oncogene, although perhaps important in the evolution of CML, nevertheless cannot, by itself, be the sole genetic event giving rise to blast crisis.

Adult↗
PubMed1990

Rearrangement and expression of p53 in the chronic phase and blast crisis of chronic myelogenous leukemia.

We tested a population of over 60 patients with chronic myelogenous leukemia (CML) for changes in the structure and expression of the p53 gene, which is located on chromosome 17. Six of 27 (22%) blast crisis samples and 3 of 5 (60%) accelerated phase samples had rearrangements of chromosome 17, whereas only 3 of 42 (7%) chronic phase patients had cytogenetic changes in chromosome 17. There was no loss of heterozygosity during the transition to blastic crisis among seven individuals who were informative for polymorphic probes for regions in or around the p53 gene on 17p. One patient in the chronic phase and one patient in the blastic phase of the 61 CML patients studied exhibited rearrangements of the p53 gene that were detectable by Southern analysis. One p53 allele was rearranged in the chronic phase patient and both p53 alleles were rearranged in the blastic phase patient. The p53 messenger RNA (mRNA) was of normal size (2.8 kb) in chronic phase and blast crisis, and the expression of the p53 gene was at least as high or higher in blast crisis as in the chronic phase of CML. The high incidence of abnormalities of chromosome 17 in blast-crisis CML found in our studies and the discovery of rearrangements of the p53 gene in two CML patients studied suggest that further study with probes for the p53 gene and anonymous polymorphic sites in chromosome 17 should be conducted in CML.

Blast Crisis↗