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)

TNF alpha levels were determined by ELISA in serum from 112 BMT patients during pre-transplant conditioning. Patients who developed post-transplant complications had significantly higher TNF alpha levels than those without complications (mean 620 pg/ml vs 440 pg/ml, P = 0.04). In particular this effect is associated with patients who developed grade II-IV acute GVHD (mean 960 pg/ml, P < 0.001) and chronic GVHD (mean 724 pg/ml, P = 0.001). High TNF alpha levels were the only statistically significant risk factor for acute GVHD. IL-1 beta and IL-6 levels were not correlated with TNF alpha levels or posttransplantation complications. In multivariate analysis of chronic GVHD, patient age > 17 years and CMV disease were the only statistically significant risk factors. Relapse was associated with low levels of TNF alpha during conditioning (mean 318 pg/ml, P = 0.02). In multivariate analysis, high risk disease was the only factor that correlated with relapse. Low risk patients had significantly higher levels than high risk patients (551 vs 377, P= 0.04). CML and MDS patients had higher TNF alpha levels than acute leukemia patients. There was no difference in TNF alpha levels between patients conditioned with BU/CY and CY/TBI. We conclude that determination of TNF alpha levels during conditioning may be useful in the prediction of acute GVHD.
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PMID:TNF alpha levels are increased during bone marrow transplantation conditioning in patients who develop acute GVHD. 774 64

We looked for MDM2 gene amplification and over-expression by Southern and Northern blot analysis in 135 and 66 cases of haematological malignancies, including ALL, AML, CML in chronic phase, CLL, MDS, PLL, non-Hodgkin's lymphoma (NHL) and myeloma. No amplification of the gene was found. An over-expression of MDM2 RNA was seen in 9/66 (14%) patients tested, including 3/9 ALL, 3/24 AML, 2/4 myelomas, 1/1 PLL, but 0/2 CML, 0/2 NHL and 0/21 MDS. None of the patients over-expressing MDM2 had modifications of P53 gene transcript or p53 mutations. Most of the patients over-expressing MDM2 gene had poor prognostic features (including 'unfavourable' cytogenetic abnormalities), poor response to chemotherapy and short survival. Our findings suggest that over-expression of MDM2 is seen in a relatively small number of haematological malignancies, and is associated with poor prognosis.
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PMID:Over-expression of the MDM2 gene is found in some cases of haematological malignancies. 780 95

We evaluated the in vitro proliferative response to exogenous IL-1 beta in terms of tritiated thymidine (3H-TdR) incorporation in leukemic cells obtained from 119 patients with various types of acute leukemia. The content of IL-1 beta in leukemic cells was measured by enzyme-amplified sensitivity immunoassay. We observed a significant proliferative response to exogenous IL-1 beta in leukemic cells from 27/66 patients with de novo AML, 1/29 patients with ALL, 2/3 patients with AUL, 8/12 patients with AML arising from MDS, 4/7 patients with myeloid crisis of CML, and 0/4 patients with lymphoid crisis of CML. Proliferation was marked in myeloid leukemic cells of a more premature stem cell origin. There were no significant differences in proliferative responses among the different FAB classes of de novo AML. The IL-1 beta content of leukemic cells was low in patients with lymphoid leukemia, but there was no significant difference among the various types of myeloid leukemia. There was no correlation between the proliferative response to exogenous IL-1 beta and the IL-1 beta content of leukemic cells. When we correlated the proliferative response to exogenous IL-1 beta with treatment outcome in patients with de novo AML, we found the rate of complete remission (CR) to be lower in those with a high proliferative response. We noted a longer duration of CR (p = 0.07) and of survival (p < 0.05) in patients with a low proliferative response. Thus, a high proliferative response to IL-1 beta in the cells of AML patients may indicate a poor prognosis.
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PMID:Interleukin-1 beta (IL-1 beta) and acute leukemia: in vitro proliferative response to IL-1 beta, IL-1 beta content of leukemic cells and treatment outcome. 783 16

Allogeneic bone marrow transplantation (BMT) is potentially curative therapy for leukemia, lymphoma, and marrow failure. Ninety-two patients have received allogeneic BMT at Oklahoma Memorial Hospital in the past 10 years. Patients with acute myelogenous leukemia (AML; N = 30), chronic myelogenous leukemia (CML; N = 27), acute lymphoblastic leukemia (ALL; N = 12), myelodysplastic syndromes (MDS; N = 8), lymphomas (N = 8), and aplastic anemia (N = 7) were treated with a variety of myeloablative preparative regimens. The major causes of mortality were bacterial, viral, and fungal infections, or disease relapse. Standard and high risk (refractory or multiply-relapsed disease) AML, CML, and ALL patients had median survivals of 14.5 months vs. 3 months, > 18 months vs. 9 months, and 10 months vs. 4.5 months (p = 0.01), respectively. At 7.5 years median follow-up, 71% of the aplastic anemia patients are disease-free. Guidelines for the optimal time for BMT have been developed that encourage transplantation earlier in the course of the disease, thus facilitating better outcomes with these otherwise fatal disorders.
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PMID:Allogeneic bone marrow transplantation: experience with 92 patients. 812 87

In 67 cases of newly diagnosed blood malignancies, NonT-ALL, T-ALL, AMLL, AML, CML, CLL, HCL, PLL, MDS, B splenic lymphoma, AUL, as well as in 9 cell lines (U937, HEL, Jurkat, HL60, UHKT2, KG1, Raji, K562, REH), we have analysed the expression and distribution of 2 relatively incompletely studied antigenic markers from the CD nomenclature: CDw12 and CD17, individually and in combination with well characterized ones. We present our data for the usefulness of these molecules in immunodiagnosis of leukemias and lymphomas.
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PMID:Expression of CDw12 and CD17 cell surface antigens on leukemic cells from patients with blood malignancies. 815 32

Two genes have been implicated in leukemias of patients with abnormalities of chromosome 3, band q26: EVI1, which can be activated over long distances by chromosomal rearrangements involving 3q26, and EAP, a ribosomal gene that fuses with AML1 in a therapy-related myelodysplasia patient with a t(3;21)(q26.2;q22). AML1 was identified by its involvement in the t(8;21)(q22;q22) of acute myeloid leukemia. Here we report the consistent identification of fusion transcripts between AML1 and EAP or between AML1 and previously unidentified sequences that we named MDS1 (MDS-associated sequences) in the leukemic cells of four patients with therapy-related myelodysplasia/acute myeloid leukemia and in one patient with chronic myelogenous leukemia in blast crisis, all of whom had a t(3;21). In addition, we have identified a third chimeric transcript, AML1/EVI1, in one of the therapy-related acute myeloid leukemia patients. Pulsed-field gel electrophoresis established the order of the genes as EAP, the most telomeric, and EVI1, the most centromeric, gene. The results indicate that translocations could involve multiple genes and affect gene expression over long distances.
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PMID:Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and unrelated genes at 3q26 in (3;21)(q26;q22) translocations. 817 Oct 26

p53 overexpression was studied immunohistochemically in paraffin-embedded bone marrow biopsies using a recently described technique for antigen retrieval based on microwave oven heating of paraffin sections. Using a monoclonal antibody (PAb1801) that reacts with human cellular p53, nuclear staining was detected in 7/11 (63%) therapy-related myelodysplastic syndromes and in 3/4 (75%) therapy-related acute myeloid leukemias. Conversely, staining for p53 was seen only in 9/40 (22%) cases of "primary" hematologic conditions (P < 0.007); these included myelodysplastic syndromes [#2], acute myeloid leukemia [#4], and chronic granulocytic leukemia in accelerated phase or blast crisis [#3]. Biopsies of normal controls and of chronic granulocytic leukemia in stable phase were consistently p53(-). Nine of the 10 karyotyped p53(+) acute myeloid leukemia/myelodysplastic syndrome cases showed complex cytogenetic findings with frequent involvement of chromosome 5 and/or 7. Only four of the 33 karyotyped p53(-) cases showed similar cytogenetic changes. Chromosome 17 involvement was present in four of 13 (31%) cytogenetically assessed p53+ cases, but in none of the p53(-). In univariate analysis, p53 expression in both MDS and AML was significantly associated with shorter survival. The frequent overexpression of p53 in therapy-related myelodysplastic syndromes, therapy-related acute myeloid leukemias and in accelerated phase/blast crisis, chronic granulocytic leukemia and its strong association with complex karyotypes suggests an important role of this gene in the pathogenesis of these leukemic conditions.
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PMID:Frequent p53 overexpression in therapy related myelodysplastic syndromes and acute myeloid leukemias: an immunohistochemical study of bone marrow biopsies. 824 7

Owing to recent technical developments in automated hematology analyzers, identification of 5-part differential counts in white blood cells and also of abnormal leukocytes has become possible. Blood specimens from 200 patients with leukemic hematologic conditions were processed through a Coulter STKS which gives a favorable white cell differential count utilizing the following parameters: volumetric impedance (V), electric conductivity/cell volume (C), and a monochromatic laser beam which provides collectively white cell scatterplot (S). To analyze the presented figures of a pathologic scatterplot (SP) on the visual display unit, the standard scale derived from 220 normal SP patterns which was composed of four kinds of cell SP scales (neutrophil: N, monocyte: Mo, eosinophil: Eo, lymphocyte: Ly) was applied. Leukemic SP figures were variable depending upon both the type of FAB classification and their therapeutic processes. SP forms of M0-blasts were semi-round and located in the central area surrounded by N-, Mo-, and Ly-SP scale. Blast SP of M1 and M2 was shown as a developing process to the SP field containing immature myeloid cells extending from the central area. It was reasonable that immature neutrophilic SP expression was obtained in M3 and Ph1 positive CML. However, the SP of M3v and Ph1 negative CML showed myelomonocytic features as CMMoL does. Typical myelomonocytic SP patterns were obtained in M4 patients. SP figures of MDS were characterized by deformability, dislocation and another abnormality, and these changes, especially in lymphocytes are very useful for diagnosis of MDS. Therefore, the FAB subtype of AML including MDS and CML could be distinguished from each other on the basis of SP pattern. In lymphoproliferative disorders, limited conductivity in ALL-SP was characteristic, while irregular and deformed SP was peculiar in leukemic malignant lymphoma. It would be a valuable process to analyze the SP pattern obtained from an automated hematology analyzer for identification of leukemic diseases.
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PMID:[Hematological analysis of leukemic diseases using an automated hematology analyzer]. 829 37

The recovery of colony-forming cell numbers after curative treatment for leukemia and severe aplastic anemia (SAA) was studied. We examined 191 patients (85 acute myeloid leukemia [AML], 48 acute lymphocytic leukemia [ALL], 32 chronic myeloid leukemia [CML], 17 SAA, and nine myelodysplastic syndrome [MDS]) who were in hematologic remission 6 months to 13 years after either curative chemotherapy (n = 69) or allogeneic bone marrow transplantation (BMT) (n = 122) by culturing their precursor cells from bone marrow (BM) (n = 548) and peripheral blood (PB) (n = 529) in methylcellulose. Thirty-six BM donors and 25 PB donors served as controls. BM colony-forming cell numbers were abnormally low in all patients (p < 0.002) irrespective of underlying disorder and type of treatment (chemotherapy or irradiation). These numbers did not normalize with time--colony-forming cells were still strongly reduced up to 10 years after therapy, whether or not the patient had received an allogeneic bone marrow graft (p < 0.002). We also compared patients who remained in stable hematologic remission with those who later relapsed (6 months to 2 years after treatment). BM colony-forming cell numbers were significantly lower in patients who subsequently relapsed (p = 0.004). In contrast to BM cultures, we found normal colony-forming capacity by PB precursors in all patients. We conclude that (1) after chemotherapy or BMT, colony-forming cell numbers of BM in culture are permanently reduced; (2) this defect is probably due to a dysfunction of the BM environment rather than to a numerical reduction of the precursor cell pool; and (3) very low colony-forming capacity may be related to relapse.
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PMID:Colony growth in cultures from bone marrow and peripheral blood after curative treatment for leukemia and severe aplastic anemia. 840 33

In 1991, 4,961 bone marrow transplants (BMT) were performed in Europe by 171 teams in 21 countries. 217 were from an unrelated donor. Two years ago, this number was 99, five years ago less than ten. Main indications for unrelated BMT were CML (115), AML (32), ALL (24), SAA (19), MDS (10). Major differences exist in the European countries with regard to the number of BMT performed per number of inhabitants and with regard to indications. The present study documents the marked increased in the use of unrelated BMT in Europe. It illustrates the need for health care strategies and for clearer definitions of indications.
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PMID:Frequency and indication of unrelated bone marrow transplants in Europe. European Group of Bone Marrow Transplantation (EBMT). 844 51


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