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 increase in the serum levels of the IL-2 receptors is due to its release both in vivo and in vitro from activated cells or neoplastic cells expressing it constitutively. The diagnostic, prognostic and physiopathologic significance of the sIL-2R was investigated by testing the serum of 271 haemopathic patients in various stages of the disease. In HCL the elevated sIL-2R level has a diagnostic value. In HD the sIL-2R level appears to be directly correlated with the extent of the disease and is equally important in the follow up of patients with HCL, NHL, HD, AL and MDS, where the serum level of the soluble receptor is usually associated with the biological and clinical activity of the disease. Unlike other B lymphoproliferations, patients with Multiple Myeloma on average show only slightly elevated levels of soluble receptor with no significant differences related to the stage or evolution. As for the chronic myeloproliferative disorders, we found only slightly elevated values in ET and PV, with frankly pathological values in CML during a blastic crisis or in the accelerated phase and in MFI during the clinically active phase of the disease.
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PMID:[The soluble IL-2 receptor in malignant hemopathies]. 146 37

Diagnosis- and/or prognosis-related alterations of (proto) oncogenes may be detected in neuroblastoma (N-myc), carcinoma of breast and ovary (HER2/neu), NHL (c-myc, bcl-2), CML (c-abl/bcr), and some other neoplasias. A wide variety of methods for the detection of gene alterations can be applied. The methods of detection have to be chosen according to the expected mechanisms of oncogene activation, the availability of adequately prepared tissue, and the technical standard of the laboratory. The sensitivity, specificity, and quantitation of morphological techniques (immunohistochemistry and in situ hybridization) is restricted and their results have to be interpreted most carefully. Whenever possible, at least two different techniques should be used, preferably on two different levels, i.e. RNA/DNA and protein. Furthermore, the combination of morphological and non morphological methods should be aspired.
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PMID:[Oncogenes and oncogene products--possibilities and significance of their detection]. 170 8

The ability to deliver high-dose chemotherapy with or without radiotherapy followed by marrow rescue has made marrow transplantation the treatment of choice for children with AML in first remission, juvenile CML, and adult-type CML in chronic phase. For patients with ALL or NHL who relapse, transplantation in second remission represents a reasonable therapeutic option. The role of marrow transplantation for patients in the advanced stages of their disease will continue to be explored to develop promising new therapies, which may improve results of transplantation earlier in the disease course. Development of transplant preparative regimens that have the same or improved therapeutic efficacy with less late effects is especially important for growing and developing children. In the meantime, all children who have received a marrow transplant must be followed for development of delayed effects, which may not appear until years after the transplant procedure. Children who are cured of their leukemia continue to occasionally visit the pediatric hematologist/oncologist, but they do so less often with increasing time after curative therapy. Thus, it is necessary for the primary care pediatrician to be familiar with the details regarding the child's previous therapy in order to anticipate and to be prepared to treat the delayed effects. Attention to school performance is of particular importance for early identification of those children who may need special educational attention. Advances in the treatment of children with leukemia continue to be made both with chemotherapy and with marrow transplantation that should result in greater numbers of children being cured.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone marrow transplantation for pediatric leukemia. 176 98

Recently, several malignant cell types have been reported to express colony-stimulating factor-1 (CSF-1) transcripts; however, the clinical significance of CSF-1 in malignancy has not been investigated. Using a CSF-1 radioimmunoassay, we surveyed concentrations of biologically active CSF-1 in the peripheral blood of 316 patients with malignant and premalignant hematologic disorders; 75 had a myelodysplastic syndrome (MDS), 12 acute myelogenous leukemia (AML), 7 chronic myelogenous leukemia, 21 chronic lymphocytic leukemia (CLL), 106 non-Hodgkin's lymphoma (NHL; of low-, intermediate- and high-grade malignancy), 46 Hodgkin's disease (HD), 46 multiple myeloma (MM), and 3 monoclonal gammopathy of undetermined significance. Controls were 64 healthy subjects. The CSF-1 concentration was correlated with the type of disease, status of the disease, treatment status, and hematologic parameters. CSF-1 concentration was significantly elevated in 83.5% of the patients with active disease, and for each active disease group it was significantly greater (P less than .0001) than in the control. Thus, the high circulating CSF-1 concentration was not associated with a particular malignant phenotype or MDS subtype, but did correlate with the disease activity of both NHL and HD, and the tumor burden in MM, AML, and CLL. There was no correlation of the CSF-1 level with total counts of monocytes or neutrophils in patients with MDS or other malignancies. The cellular basis for the elevated circulating CSF-1 was not investigated. However, the results are consistent with the possibility that the premalignant or malignant cells themselves produce CSF-1 or regulate its production by normal cells.
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PMID:Increased circulating colony-stimulating factor-1 in patients with preleukemia, leukemia, and lymphoid malignancies. 201 2

Since 1976 in Genoa, 291 TBI treatments were performed. Before allogeneic BMT, 1000 cGy/1 fx were prescribed in the first 22 patients, and then 990 cGy/3 fx/3 d in AML and CML, and the same or 1200 cGy/6 fx/3 d in ALL. Survival (S) and probability of remaining in remission (PRR) were 54% and 69% at 80 months in 80 AML; in 62 CML 45% and 60% at 60 months; in 69 ALL, 32% and 45% at 82 months. Differences in favour of higher doses and dose rates were observed and are presented. Before autologous BMT, 1000 cGy/1 fx were prescribed to AML and NHL, and 1200 cGy/3 fx/3 d to ALL patients. Disease free survival (DFS) was 71% and 13% at 82 months in 21 AML treated in first R and 9 ALL, respectively; 81% at 32 months in 11 NHL treated in R.
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PMID:Total body irradiation before allogeneic and autologous bone marrow transplantation: a ten year Genoa experience. 224 39

Sixteen children with refractory hematological malignancies were treated with a combination of BH.AC, aclacinomycin-A, 6-MP and predonisolone (BH-AC.AMP protocol). They were ALL(6), ANLL(8), CML(1) and NHL(1). The CR ratio was 17% in ALL, 50% in ANLL, and blast crisis of CML was treated successfully but NHL failed in the induction remission. Major complications were vomiting, nausea, gastrointestinal bleeding, hematuria and hemorrhagic cystitis. More than 10 days or 120 mg/m2 administration of aclacinomycin-A was thought to induce more severe side effects.
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PMID:[BH-AC.AMP protocol in the treatment of refractory childhood acute leukemia]. 317 40

We have previously reported the isolation of a monoclonal antibody (NHL-30.5) that reacts with an antigen expressed on a substantial proportion of marrow and blood cells of most patients with newly diagnosed or relapsing acute myeloid leukemia. This antigen is also found on several cell lines derived from myeloid malignancies of human origin. It is not present on mature hemopoietic cells or on the majority of differentiating bone marrow cells. In order to determine whether the NHL-30.5 antigen may, nevertheless, be expressed on low-frequency primitive normal hemopoietic cells, not detected in standard antibody screening procedures, its expression was studied on clonogenic erythropoietic and granulopoietic cells. Light-density (less than 1.077 g/mL) suspensions of normal or chronic myelogenous leukemia bone marrow and peripheral blood cells were stained with NHL-30.5 and fluorescein isothiocyanate labeled second antibody and then sorted into two fractions using the fluorescence-activated cell sorter. The first contained the top 5% of cells with the highest fluorescence intensity. The remainder were collected in the second fraction. Colony assays of both fractions showed the first to be enriched in CFU-E, BFU-E, and CFU-C content (fourfold to 17-fold). The second fraction was correspondingly depleted of these progenitors. These findings reveal NHL-30.5 antigen expression to be a transient event during normal hemopoiesis that characterizes primitive hemopoietic cells on several pathways. Subsequent experiments showed that the presence of up to 10 micrograms/mL of purified NHL-30.5 antibody in colony assay cultures neither inhibited nor stimulated colony formation. Marrow fibroblasts (subcultured marrow adherent cells) were NHL-30.5 negative. Immunoprecipitation studies showed that the antigen detected by NHL-30.5 is clearly distinct from that identified by My-10, another monoclonal antibody that has previously shown some similarities to NHL-30.5. It thus appears that the NHL-30.5 antibody reacts with a new myeloid differentiation antigen of as yet unidentified function that is normally restricted in its expression to early stages of hemopoiesis.
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PMID:Restricted expression of a new acute myelogenous leukemia-associated antigen (NHL-30.5) on normal hemopoietic progenitor cells. 345 4

Clinical and cytogenetic findings were reevaluated in 941 consecutive patients with suspected neoplastic haematological conditions studied during 1973-1984. A total of 1652 attempts at cytogenetic analysis with banding technique were performed in 240 patients with acute nonlymphocytic leukaemia (ANLL), 177 with chronic myeloid leukaemia (CML), 157 with myelodysplasia (MDS), 82 with myeloproliferative disorders (MPD), 114 with acute lymphoblastic leukaemia (ALL), 42 with non-Hodgkin lymphoma or other lymphoproliferative disorders (NHL + LPD), and 120 patients with benign disorders. Only 1 patient with a benign disorder had an acquired clonal chromosomal abnormality (diagnostic specificity 0.99), whereas abnormalities were detected in 50.0% of patients with malignant haematologic disorders (diagnostic sensitivity 0.50). Success rate was 73-74.4% in ALL, MPD, and NHL + LPD, versus 87-94% in ANLL, MDS, CML, and benign disorders. The frequencies of detected abnormalities in diagnostic subgroups were within the limits of previous reports. Striking differences in cytogenetic pattern in relation to age were found in MDS and ANLL. Results from 1973-80 were compared to 1981-84. In spite of a marked reduction in failure rate of bone marrow (BM) analyses in the second time period, the fraction of patients with only inadequate cytogenetic analyses and the frequencies of detected chromosome abnormalities remained essentially unchanged. Peripheral blood samples had a high failure rate, and seldom provided additional information to BM analyses. Delay in transportation time of samples did not in general affect the outcome of cytogenetic analysis, with possible exceptions for a higher failure rate in ALL and lower frequency of detected abnormalities in ANLL.
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PMID:Cytogenetic analysis in 941 consecutive patients with haematologic disorders. 346 85

Primary and therapy-induced ocular manifestations of leukemia in 25 of 103 children suffering from the disease (60 patients with ALL, eight with AML, two with CML, 33 with NHL) were kept under observation for an average period of five years. The lens was involved in 10%, the retina in 9%, the optic nerve in 7%, and the orbit in 4% of these cases. The present authors' findings concurred with those published in the literature to date, in that they could not find a pathognomonic combination or a specific frequency of ocular symptoms related to one of the four types of leukemia.
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PMID:[Ocular findings in leukemia in childhood]. 348 Oct 1

The reactivity of a murine IgG1 monoclonal antibody, NHL-30.5, that detects a surface antigen expressed on acute myeloid leukemia (AML) cells has been studied. Initially raised against the HL-60 cell line, NHL-30.5 has subsequently reacted with blood and/or bone marrow cells from 15 of 19 AML patients studied at presentation or in relapse, 1 patient with chronic myelomonocytic leukemia (CMML), 1 patient with myelofibrosis (MF) who subsequently developed AML, and 1 of 5 patients with acute lymphoblastic leukemia (ALL). It has shown no detectable binding to cells from AML patients in remission (0/3), patients with chronic myelogenous leukemia in chronic phase (CML) (0/7), normal bone marrow (0/9), normal peripheral blood mononuclear cells, granulocytes, platelets, erythrocytes, monocytes, or splenocytes by radioimmunoassay or fluorescence analysis using flow cytometry. HL-60 cells induced to differentiate following incubation in the presence of dimethylsulfoxide (DMSO) lost their ability to bind NHL-30.5. Immunoprecipitation of iodinated HL-60 cell surface components showed the antigen to have an apparent mol./wt of 180,000 under reducing conditions. These results suggest that the antigen is different from any other myeloid antigens reported to date, and may be useful in further studies of leukemic cell phenotypes.
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PMID:NHL-30.5: a monoclonal antibody reactive with an acute myeloid leukemia (AML)-associated antigen. 385 4


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