Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of progenitor cell associated antigen CD34 was investigated in cells from 28 patients with chronic myeloid leukemia (CML). The CD34 positivity varied from 0-26% in patients with chronic phases CML (n = 17); from 6-64% in patients with accelerated phase CML (n = 4); and from 27-97% in the patients with blastic crisis of CML (n = 8). The difference in CD34 positivity between chronic (mean 10.1 +/- 2.3%), accelerated (37.7 +/- 13.3%) and blastic (58.0 +/- 7.3%) phases of CML is statistically significant (p less than 0.05), however, the number of patients studied, especially in accelerated and blastic phases is very small. There was no difference in the CD34 positivity of the cells in the peripheral blood and in the bone marrow. CD34 positivity was higher in patients with chronic phase CML at diagnosis (untreated patients) than in those who were studied during treatment. The possible importance of serially studying CD34 positivity in patients with CML is discussed in the paper.
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PMID:Expression of hematopoietic progenitor cell associated antigen CD34 in chronic myeloid leukemia. 171 38

A 39-year-old Japanese female who had been followed as chronic myelogenous leukemia (CML) since 1984 was admitted to our hospital because of dizziness. On admission, platelet count markedly increased (245 X 10(4)/microliters) in spite of daily administration of busulfan 2 mg. She was diagnosed as accelerated phase CML with thrombocytosis. So we tried to use interferon alpha (IFN-alpha) finally given in a dose of 9 X 10(6) U daily by subcutaneous injection. After that, platelet count decreased to 70 X 10(4)/microliters and megakaryocyte count in bone marrow decreased from 887.5/microliters to 395.7/microliters. But we had to stop IFN-alpha because of severe side effects.
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PMID:[Thrombocytosis in chronic myelogenous leukemia (CML) controlled by interferon alpha (IFN-alpha)]. 276 64

Three patients are described with late-stage myeloproliferative diseases, two with accelerated phase chronic myelogenous leukemia (CML) and one with refractory polycythemia vera (P vera), who achieved hematologic control after the addition of interferon (IFN) to hydroxyurea therapy. Both the CML patients continue to have a sustained clinical remission at 12 and 38 months. The patient with P vera had failed several previous treatments including busulfan, P32, hydroxyurea, and anagrelide, but became responsive after interferon use followed by reintroduction of hydroxyurea. Our observations support the efficacy of IFN alpha and hydroxyurea combination in late-phase myeloproliferative disease and warrants further clinical investigation.
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PMID:Efficacy of alpha interferon and hydroxyurea in late phase refractory myeloproliferative disease. 789 Feb 66

Thirty-two adults (median age 36 years) with leukemia (15 AML, eight CML, six ALL, three CLL) persisting or relapsing 1-40 months (median 4) after allogeneic BMT (20 matched siblings, eight unrelated, four family mismatch) underwent immunotherapy to elicit GVHD. This comprised one or more of: infusion of donor cells (n = 22), stopping cyclosporine (n = 14), and administration of interferon-alpha2b (n = 15) or interleukin-2 (n = 4). Eight acute leukemia patients received chemotherapy as well. The time from relapse to immunotherapy was 0-1344 days (median 4). Acute and/or chronic GVHD developed in 17 patients. Response was not evaluable in three patients due to early toxic death. There was no response in 10 patients, whereas 19 showed objective response. Nine patients died due to toxicity and 10 due to progressive disease. Thirteen patients are alive 4-58 months (median 14) after immunotherapy; 12 in remission (five AML, four chronic phase CML, one ALL, one accelerated phase CML, one CLL) and one with progressive disease (accelerated phase CML). Eleven of 13 patients who are alive had GVHD compared with six of 19 who died (P = 0.005, Fisher's exact test). We conclude that with the exception of CML in myeloid blast crisis, immunotherapy is active in most types of acute and chronic leukemia relapsing after allogeneic BMT. It is associated with considerable toxicity. Clinically obvious GVHD, especially chronic GVHD, results in a higher probability of survival.
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PMID:Induction of graft-versus-host disease as immunotherapy of leukemia relapsing after allogeneic transplantation: single-center experience of 32 adult patients. 924 16

The treatment results of 96 patients with Philadelphia-positive chronic myeloid leukemia (CML) in accelerated phase (AP) were reviewed retrospectively. Treatment of AP consisted of allogeneic bone marrow transplantation in 20 (14 related and 6 unrelated donors) or conventional chemotherapy (CC) in 76 patients. Three main treatment strategies were followed in the CC group: continuation (group A) or dose escalation (group B) of chronic phase therapy or change of chronic phase therapy to hydroxyurea (group C). Median survival was 7.0 months in group A (range 1.8-110), in group B 8.3 months (range 0.9-40) and in group C 9.6 months (range 1.5-47.6), p=0.89. Survival in CC was dependent on response to therapy as the achievement of a second chronic phase was significantly associated (p<0.001) with a longer median survival (21 months) compared with stable accelerated phase disease (11 months) or treatment failure (5 months). Median survival in the BMT group was 16.7 months (range 5-77), the 5-yr probability of relapse was 25% and the 5-yr disease-free survival was 36%. For patients <55 yr median survival after BMT was significantly prolonged compared with median survival after CC (n=45, 8.3 months, p=0.008). After developing criteria of AP, median survival in our analysis has been less than 1 yr. The results of conventional chemotherapy in the treatment of accelerated phase CML are disappointing. If a suitable donor is available allogeneic BMT should be performed without delay in patients with AP.
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PMID:Chronic myeloid leukemia in accelerated phase: treatment results with conventional chemotherapy and allogeneic bone marrow transplantation in 96 patients. 968 86

Fitness landscapes, which provide a unique perspective for viewing co-evolving cell populations, were used to study the evolution of CML and MDS. This led to several conclusions: (1) accelerated phase CML and RAEB/RAEBt are not specific disease entities. They represent the time when AML cells are replacing preleukemia cells; (2) monoclonal hemopoiesis and RA/RARS represent a variety of clinical syndromes with a common appearance but with different evolutionary potential; (3) malignant cells alter the fitness landscape enhancing their proliferative advantage. These studies provide the basis for new approaches to treatment.
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PMID:Fitness landscapes and the myeloid leukemias. 1007 Nov 32

Neurological side effects and complications of cryoglobulinemia were observed during interferon-alpha (IFN-alpha) therapy in a patient with chronic myeloid leukemia (CML). A 50-year-old man was hospitalized because of leukocytosis and extramedullary tumors in the lumbar spine. In addition, the patient complained of dysesthesia in his feet. A diagnosis of accelerated phase CML was made. Administration of prednisolone, vincristine, hydroxyurea, and Ara-C and irradiation of the lumbar spine were started. Two months later, the patients achieved hematologic response and the size of his tumors decreased. Thereafter, we started IFN-alpha treatment (3-6 x 10(6) units daily) by intramuscular injection. After 8 weeks of this treatment, the patient complained of worsening dysesthesia in his feet. An axonal form of peripheral neuropathy was diagnosed by electrophysiological examination. Immunological studies revealed decreased complement levels and type III mixed cryoglobulinemia. Methylprednisolone pulse therapy alleviated the neurological symptoms and lowered the cryoglobulin levels. The clinical course suggested that mixed cryoglobulinemia was associated with CML and that the increase in cryoglobulin levels was caused by IFN-alpha and played a causative role in the worsening peripheral neuropathy. Therefore, to prevent these side effects, careful clinical assessment is necessary before starting IFN-alpha therapy.
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PMID:[Development of cyroglobulinemia and polyneuropathy in a chronic myeloid leukemia patient during interferon-alpha treatment]. 1035 42

Relapse of chronic myeloid leukemia (CML) in chronic phase after allogeneic stem cell transplantation (SCT) can be successfully treated by donor lymphocyte infusion (DLI). However, relapse of accelerated phase CML, blast crisis, or acute leukemia after allogeneic SCT are resistant to DLI in the majority of cases. In vitro-selected and expanded leukemia-reactive T-cell lines may be more effective in inducing an antileukemic response in vivo. To treat a patient with accelerated phase CML after allogeneic SCT, leukemia-reactive cytotoxic T-lymphocyte (CTL) lines were generated from her HLA-identical donor. Using a modification of a limiting dilution assay, T cells were isolated from the donor, selected based on their ability to inhibit the in vitro growth of CML progenitor cells, and subsequently expanded in vitro to generate CTL lines. Three CTL lines were generated that lysed the leukemic cells from the patient and inhibited the growth of leukemic progenitor cells. The CTL did not react with lymphocytes from donor or recipient and did not affect donor hematopoietic progenitor cells. The 3 leukemia-reactive CTL lines were infused at 5-week intervals at a cumulative dose of 3.2 x 10(9) CTL. Shortly after the third infusion, complete eradication of the leukemic cells was observed, as shown by cytogenetic analysis, fluorescence in situ hybridization, molecular analysis of BCR/ABL-mRNA, and chimerism studies. These results show that in vitro cultured leukemia-reactive CTL lines selected on their ability to inhibit the proliferation of leukemic progenitor cells in vitro can be successfully applied to treat accelerated phase CML after allogeneic SCT.
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PMID:Complete remission of accelerated phase chronic myeloid leukemia by treatment with leukemia-reactive cytotoxic T lymphocytes. 1043 7

Imatinib inhibits the BCR-ABL tyrosine kinase created by the Philadelphia chromosome (Ph+) in chronic myeloid leukaemia (CML). Complete haematological responses were achieved in 88% of patients and major cytogenetic responses were detected in 49% of patients with chronic phase CML treated with oral imatinib 400 mg/day in a multicentre noncomparative study of 532 patients. Administration of oral imatinib 400 or 600 mg/day to 235 patients with accelerated phase CML in a multicentre noncomparative study resulted in haematological responses in 63% of patients and major cytogenetic responses in 21% of patients. 26% of the 260 patients with blast crisis CML receiving imatinib 400 or 600 mg/day in a multicentre noncomparative trial sustained a haematological response and 13.5% of patients had a major cytogenetic response. Imatinib 400 or 600 mg/day orally achieved ahaematological response in 19 of 32 patients with Ph+ acute lymphoblastic leukaemia in a pilot study. Clinical improvement was demonstrated in 89% of 36 patients with gastrointestinal stromal tumours unresponsive to standard chemotherapy during treatment with 400 or 600 mg/day oral imatinib in a noncomparative phase II trial. Adverse events were frequent in clinical trials of imatinib but most events were mild or moderate in severity. Serious adverse events reported include severe fluid retention, cytopenias and hepatotoxicity.
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PMID:Imatinib. 1169 65

Arsenic has a long history of use in Chinese and Western medicine but fell out of use in the mid-20th century because of the unacceptable side effects that occurred at the doses that were thought to be necessary. The re-emergence of arsenic trioxide (ATO) in clinical use is due largely to purification of this compound from traditional mixtures, and the definition of effective, low-dose regimens for the treatment of acute promyelocytic leukemia (APL). ATO was first purified and used in controlled studies in patients with APL in China in the 1970s. Studies have subsequently also been performed in the United States. Complete response (CR) rates reported in patients with relapsed or refractory APL have varied from 52% to 92%, with similar rates reported in patients with newly diagnosed disease. The mechanism of action of ATO suggests it may be active against other malignancies, and ATO has shown some activity in patients with accelerated phase chronic myelogenous leukemia (CML) and multiple myeloma (MM). Clinical trials are ongoing and planned to define the optimal use of this compound in hematologic malignancies. Preliminary results from studies in patients with primary hepatocellular and gallbladder tumors indicate that ATO may also prove active against some solid tumors.
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PMID:Expanding the use of arsenic trioxide: leukemias and beyond. 1201 19


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