Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596978 (Leukemia)
 15,069 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In nine patients with CLL treated with chlorambucil followed by alpha-2b-interferon (alpha 2b-IFN), T, B and natural killer (NK) cells and NK activity were studied before entering the study, after chlorambucil treatment, and after administration of alpha 2b-IFN. When considered as a whole, basal NK activity was lower in CLL patients than in controls (21.0% +/- 10.9 versus 40.2% +/- 17.4, p less than 0.001); however, when considered individually, four out of nine patients had normal NK activity at diagnosis. Chlorambucil did not increase global NK activity (21.7% +/- 7.1), whereas alpha 2b-IFN did so (44.3% +/- 19.1). After alpha 2b-IFN only one of seven patients studied had low NK activity. Previously increased absolute counts of CD2+, CD4+, CD8+, CD16+, CD57+ lymphocytes were reversed with chlorambucil treatment to normal levels, while after this therapy CD11b+ and CD19+ cells decreased without reaching normal values. During alpha 2b-IFN therapy, an increase up to normal levels in the percentage of CD16+ (2.7% +/- 3.4 versus 7.7% +/- 6.5, p = 0.04) and CD57+ (3.0% +/- 3.0 versus 8.1% +/- 6.2, p = 0.020) lymphocytes was observed whereas the absolute number of CD19+ B-cells further decreased (5.2 x 10(9)/l +/- 2.5 vs 3.8 x 10(9)/l +/- 2.3), albeit not significantly.
Leukemia 1992 Jun
PMID:Recombinant alpha-2b-interferon may restore natural-killer activity in patients with B-chronic lymphocytic leukemia. 137 76

The soluble Interleukin-2 Receptor (sIL-2R) serum levels were assessed in 42 patients with Hairy-Cell Leukemia (HCL) at diagnosis and after alpha-Interferon therapy and correlated with spleen size, peripheral hematological values, hairy cell index (HCI) and clinical response. Serum sIL-2R levels were significantly increased in all HCL patients, particularly in those with a higher HCI (> 0.50) and in non-splenectomized patients. Among the 26 HCL patients who were studied before and after 12 months of alpha-IFN treatment, 16 normalized the sIL-2R level and 10 did not. Our findings suggest that sIL-2R levels in HCL patients correlate with the splenic and bone marrow tumor burden as assessed by HCI. In addition patients with low levels of sIL-2R at diagnosis appear to have a better chance of achieving a good clinical response.
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PMID:Serum soluble interleukin-2 receptor levels in hairy cell leukemia: correlation with clinical and hematological parameters and with alpha-interferon treatment. 147 20

Twenty six patients with Philadelphia chromosome (Ph1) positive chronic myelogenous leukemia (CML) treated with IFN-alpha were classified on the basis of the fusion pattern of BCR/ABL chimeric mRNA determined by a reverse-transcriptase-polymerase chain reaction (RT-PCR) method. The relationship between the fusion pattern of BCR/ABL mRNA and the clinical outcome was also analysed. Twelve patients showed M-bcr exon 3/ABL exon 2 (B3/A2) chimeric mRNA and nine had M-bcr exon 2/ABL exon 2 (B2/A2) mRNA. Eleven of the 12 patients with B3/A2 achieved complete hematological response with IFN-alpha therapy, as did three of the nine patients with B2/A2. The mean duration to blastic crisis was significantly longer in the B3/A2 patients (mean 52.4 months) than in the B2/A2 patients (mean 26.2 months) (p less than 0.01). These results suggest that the fusion pattern of BCR/ABL mRNA may affect the therapeutic response to IFN-alpha and clinical outcome in CML patients.
Leukemia 1992 Sep
PMID:Possible correlation between fusion pattern of BCR/ABL mRNA and clinical response to alpha-interferon in chronic myelogenous leukemia. 151 6

Since autocrine stimulation by tumor necrosis factor-alpha (TNF alpha) may be implicated in the proliferation of normal and malignant B cells, we measured the production of TNF alpha protein by these cells in response to various B-cell stimulatory agents. Purified malignant and non-malignant B lymphocytes were incubated with interleukin-4 (IL4), interferon-alpha (IFN alpha) and IFN gamma, and the supernatants were tested for the production of TNF alpha using an enzyme-linked immunosorbent assay (ELISA). Chronic lymphocytic (CLL) and prolymphocytic (PLL) leukemia cells produced low amounts of TNF alpha, irrespectively of the addition of inducers. Normal B lymphocytes (tonsillar and blood) produced TNF alpha, but the level was not influenced by any of the inducers tested. Hairy cell leukemia (HCL) cells produced TNF alpha in the absence of stimuli and this production was markedly enhanced by addition of IFN alpha or, to a lesser extent, by IFN gamma and IL4. These results contradict the hypothesis that IFN alpha exerts its therapeutic action in HCL by inhibition of autocrine TNF alpha production.
Leukemia 1992 Feb
PMID:Production of tumor necrosis factor-alpha by normal and malignant B lymphocytes in response to interferon-alpha, interferon-gamma and interleukin-4. 842 86

The authors analyzed twelve patients with symptomatic essential throthrombocythemia (E.T.) diagnosed from 1983 to 1991. Haemorrhagic and thrombotic phenomena were the main presenting features. Treatment consisted mostly of alpha-interferon (IFN-alpha 2b) subcutaneously in dosage ranging from 3 to 5 MU/m2 and hydroxyurea (HU) in conventional dosage. A clinical response was seen in seven patients treated with IFN-alpha 2b (4 CR and 2 PR), and in four patients treated with HU (3 CR and 1 PR). No significant side effects were observed. Our findings indicate that IFN-alpha 2b offers a non-leukaemogenic and very promising therapeutic alternative for E.T.
Leukemia 1992
PMID:Essential thrombocythemia--clinical features, therapy and follow-up of 12 cases. 160 10

Thuja polysaccharide g fraction (TPSg) was shown to be an inducer of the CD4+ fraction of the human peripheral blood T-cell subset (1,2). Furthermore, it could be demonstrated that TPSg is a potent inhibitor of the expression of HIV-1-specific antigens and of the HIV-1-specific reverse transcriptase (3). This report deals with the cytokine pattern induced by TPSg in human peripheral blood lymphocyte (PBL) and purified monocyte/macrophage cultures. In addition, a further characterization of the CD4+ T-cell fraction stimulated by TPSg was performed by FACS analysis. TPSg is induces IL-1 beta, IL-2, IL-3, IL-6, gamma-IFN, G-CSF, GM-CSF, and TNF-beta production in PBL cultures; and IL-1 beta and IL-6 in monocyte/macrophage cultures. Enzyme-linked immunosorbent assays (ELISAs) demonstrated that no IL-4 was produced by PBL cultures under TPSg influence.
Leukemia 1992
PMID:Mitogenic activity of high molecular polysaccharide fractions isolated from the cuppressaceae Thuja occidentalis L. enhanced cytokine-production by thyapolysaccharide, g-fraction (TPSg). 160 22

Expression of differentiation and activation antigens on peripheral blood mononuclear cells of four chronic lymphocytic leukaemia (CLL) patients was studied before and during interferon-alpha 2b therapy. Patients had clinical stage B(II) disease, a lymphocyte count of over 60 G/l and a lymphocyte doubling time shorter than 12 months. One of the patients unresponsive to previous chemotherapy experienced a substantial decrease of the lymphocyte count during interferon-alpha 2b (IFN-alpha 2b) therapy, with a nadir at one fifth of the initial value while on this therapy. The lymphocyte count decreased slightly in a further patient, while it increased in two patients. Treatment with IFN-alpha 2b left the phenotype of CLL lymphocytes essentially unchanged. The elevated serum beta-2 microglobulin values increased further during treatment with the exception of the CLL patient responsive to IFN-alpha 2b therapy. The clinical stage of the disease did not change in any of the patients when evaluated according to the criteria of the International Workshop on CLL. Further studies are necessary to determine which of the CLL patients benefit from therapy with interferon-alpha 2b.
Leukemia 1992
PMID:Differentiation and activation antigens on blood mononuclear cells in lymphocytic leukemia before and during IFN-alpha 2B therapy. 160 26

Therapy with alpha-interferon (IFN alpha) can suppress the Ph1-positive hemopoiesis in a percentage of patients with chronic myelogenous leukemia (CML). We used IFN alpha to treat a 30-year-old CML patient, characterized by favourable prognostic signs (such as low leukocytosis, absence of splenomegaly and no increase in bone marrow blasts) at diagnosis, and obtained a complete remission, as evaluated by Southern blot and cytogenetic analysis, after one year of treatment. However, the polymerase chain reaction (PCR) revealed the persistence of a minimal residual disease. The IFN alpha therapy was stopped and the hematological status remained stable until eighteen months later, when a cytogenetic analysis revealed the appearance of a clone characterized by t(9;22) and trisomy 8, accounting for 30% of bone marrow metaphases. This cell population spontaneously regressed in the following months, before any cytotoxic treatment. However, as leukemic cells, detected by PCR, were still present, the patient received a high dose chemotherapy, which induced the complete eradication of the Ph1-positive clone, as demonstrated by the absence of bcr-abl transcript at the PCR reaction. Molecular and cytogenetic remission persist one year later, without any further therapy.
Leukemia 1992 Jul
PMID:Transient cytogenetic relapse in a Ph1-positive chronic myelogenous leukemia patient previously treated with alpha-interferon. 162 97

The possible synergistic interaction between azidothymidine (AZT) and interferon alpha (rIFN-alpha 2a) in the treatment of chronic myelogenous leukemia (CML) was studied in vitro using marrow or peripheral blood hematopoietic progenitors from 10 patients with CML in the mixed (CFU-GEMM) colony culture assay. Used singly, either agent inhibited erythroid (BFU-E) and granulocyte-macrophage (CFU-GM) CML hematopoietic progenitor proliferation in a dose-dependent fashion, with the inhibitory effect being more pronounced on BFU-E than on CFU-GM colony-forming cells. The combination of both drugs in therapeutic concentrations exerted a significant synergistic inhibition on CML stem cells as assessed by the median-effect principle and isobologram equation analysis. A suboptimal dose of AZT (0.5 mumol/l) synergistically augmented the effect of rIFN-alpha 2a whereas an inactive dose of 10 U/ml rIFN-alpha 2a similarly enhanced the CML stem cell growth inhibition exerted by AZT. Our data indicate that AZT may augment the already established therapeutic benefits of IFN-alpha in CML.
Leukemia 1991 Feb
PMID:Synergistic antiproliferative effect of interferon alpha and azidothymidine in chronic myelogenous leukemia. 202 Jan 93

The breakpoint localization was analyzed in 61 patients with Philadelphia chromosome (Ph) positive chronic myelogenous leukemia to compare the breakpoint localization and clinical course. All patients were treated with interferon alfa (IFN alpha) or IFN alpha plus IFN gamma at the time of the study. Thirty-three of the patients had been pretreated with other cytostatic drugs. Sixty-nine per cent of the breakpoints were located in the 5' region of the major breakpoint cluster region (M-bcr), 29% in the 3' part. There was no significant difference between these two groups with respect to response to IFN(s), clinical course or conversion to blast crisis, nor survival.
Leukemia 1991 Jun
PMID:Breakpoint localization within the M-bcr and clinical course do not correlate in patients with chronic myelogenous leukemia undergoing alfa interferon therapy. 205 69


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