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)

Terminal deoxynucleotidyl transferase activity was investigated by enzyme assay and (or) an indirect immunofluorescence method with specimens from 151 patients who had a variety of neoplastic and nonneoplastic conditions: leukemia, 62; non-Hodgkin's lymphoma, 36; Hodgkin's disease, seven; lymph nodes without neoplasms, 21; normal peripheral blood, 15; normal bone marrow, ten. Immunologic studies were done on samples from 82 of these patients. Increased terminal deoxynucleotidyl transferase activity was found by both methods in patients who had acute lymphoblastic leukemia and the lymphoid blast crisis of chronic myelocytic leukemia and by the immunofluorescence method in patients who had lymphoblastic lymphoma. A single patient with acute monoblastic leukemia was found by both technics to have increased enzyme activity. Three B-cell proliferations were positive by the enzyme assay; none was positive with the immunofluorescence method. In the remaining 42 B-cell proliferations, the levels of terminal deoxynucleotidyl transferase activity were found to be normal by both the enzyme assay and the immunofluorescence method. Cytoplasmic positivity was observed in as much as 10% of the cells in 13 specimens that were otherwise negative and in eight samples in association with nuclear positivity. A comparison of terminal deoxynucleotidyl transferase activity in microunits/mg protein (enzyme assay) with the percentage of positive cells (immunofluorescence method) yielded a correlation coefficient of 0.62 (P less than 0.01).
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PMID:Terminal deoxynucleotidyl transferase activity in neoplastic and nonneoplastic hematopoietic cells. 702 Mar 99

Intracellular activities of total lactic dehydrogenase (LDH) and phosphohexose isomerase (PHI) were investigated in the leukaemic cells of 14 patients with acute myeloid leukaemia (AML), five with chronic myeloid leukaemia (CML), seven with acute lymphoblastic leukaemia (ALL), 19 with chronic lymphocytic leukaemia (CLL), 16 with leukaemic non-Hodgkin's lymphoma (NHL) and in the lymphocytes of 14 normal persons. Intracellular total LDH-activity of the blasts of AML and ALL was in the same range as the normal lymphocytes. Patients with CLL and NHL had significantly lower levels (P less than 0.01) of total intracellular LDH than the controls. Intracellular PHI activity was consistently lower in the lymphoid malignancies (ALL, CLL, NHL) than in normal lymphocytes (P less than 0.05), or in leukaemic myeloblasts (P less than 0.01). The intracellular LDH/PHI index of the leukaemic lymphoblasts was significantly elevated as compared to lymphocytes from normal subjects (P less than 0.0001) or to leukaemic cells from patients with AML (P less than 0.001), with CLL (P less than 0.0001) or with NHL (P less than 0.001). The patients with CLL and NHL, on the other hand, had significantly lower levels of LDH/PHI ratio than the normal subjects (P less than 0.0001 and P less than 0.025 respectively).
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PMID:Intracellular lactic dehydrogenase and phosphohexose isomerase activity in leukaemia and malignant lymphoma. 706 11

The incidence of elevated serum levels of immunoreactive calcitonin (CT) in human myeloproliferative and lymphoproliferative disorders was investigated. On the basis of twice the normal range, about 45% of patients with acute leukemia and blast crisis of chronic myelocytic leukemia (CML) showed elevated serum levels of CT. Markedly elevated levels (greater than 1,000 pg/ml) were only found in this group. Since immunoreactive CT dropped to normal or only slightly elevated levels in remission and increased again before or during relapse, serum CT levels seem to reflect the activity of the disease. However, in patients with chronic leukemia, Hodgkin's and non-Hodgkin's lymphoma, a lower incidence and only slightly elevated serum levels were found. In addition, the molecular weight of the proteohormone in serum specimen and cell extracts was investigated by gel chromatography. Besides physiological CT, different high-molecular weight forms of the hormone could be demonstrated in serum and in cell extracts. Extracts of leukemic cells revealed higher molecular forms only. It is suggested that the proteohormone is ectopically produced by leukemic cells.
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PMID:Ectopically produced calcitonin in human hemoblastoses. 712 Aug 75

A phase II evaluation of vindesine (VDS) was carried out in 46 patients with hematologic malignancies refractory to conventional chemotherapy. Two VDS schedules were employed (at random): (A) a weekly bolus (5 mg/m2 i.v. X 4); (B) fractionated daily injections (0.5 mg/m2 i.v. q.12 h X 10, course to be repeated after 10-15 days). Complete and partial remissions were observed in acute lymphocytic leukemia (3/14 patients), acute non-lymphocytic leukemia (2/12 patients), chronic myelocytic leukemia in blastic crisis (4/12 patients) and non-Hodgkin's lymphoma (4/8 patients). Responses were seen with higher frequency in patients treated with the weekly bolus (42.8 vs 16%). Myelosuppression was the most relevant side effect in both schedules. Neurotoxicity occurred infrequently and was generally mild in degree. Further trials with VDS in combination with other drugs are recommended in hematologic malignancies.
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PMID:Vindesine in the treatment of refractory hematologic malignancies: a phase II study. 715 7

Despite the difficulty in establishing human hematopoietic tumors in nude mice, four human lymphomas were successfully heterotransplanted and passaged serially in our laboratory. Additional immunosuppression with chemotherapy, whole-body radiation or splenectomy was not required for establishment of these tumors. All four of these tumors were of the non-Hodgkin's lymphoma type. In each case the tumors in the nude mice were histologically identical to the biopsy specimens from the patient in whom they were derived. Attempts to transplant tumor from 17 patients with Hodgkin's disease or 4 patients with immunoblastic lymphadenopathy were unsuccessful. Tumors from 2 patients with chronic myelogenous leukemia and 1 with hairy cell leukemia could be grown in nude mice conditioned with whole-body radiation or cytosine arabinoside, but these tumors could not be passaged to other nude mice. Cell surface markers were determined on the four serially passaged lymphomas. These surface markers were similar to the markers on the original tumors, even after long periods of mouse-to-mouse passage. In 1 patient with fevers, night sweats and mediastinal mass in whom a diagnosis had not been made after several biopsies, examination of tumor tissue that had been transplanted from the patient to the nude mouse clearly established the diagnosis of lymphoma.
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PMID:Human hematopoietic tumors in nude mice. 728 69

In an attempt to sustain potentially cytotoxic concentrations of vincristine in man, a five-day continuous infusion of vincristine after an initial intravenous bolus injection was administered to 30 patients with refractory malignancies. Three dosage levels were explored (0.5 mg/m2, 0.75 mg/m2, and 1.0 mg/m2 daily for five days). Neurologic and hematologic toxicity were severe at the high dose level, whereas mild to moderate toxicity occurred at the 0.5 and 0.75 mg/m2 dose levels. Objective responses were noted in 11 patients (37%) with the following malignancies: non-Hodgkin's lymphoma (4), acute non-lymphoblastic leukemia (2), chronic granulocytic leukemia in blast crisis (1), carcinoma of the breast (3), and small cell carcinoma of the lung (1). Responses were observed at each infusion dose level. Nine of the 11 responders had previously progressed while receiving conventional intravenous bolus injection of vincristine. These data suggest that the clinical usefulness of vincristine may be enhanced by the use of infusion techniques. A maximum daily dose of 0.5 mg/m2 given for five days is recommended for future trials of intravenous vincristine infusion.
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PMID:Intravenous vincristine infusion: phase I trial. 730 14

Increased numbers of bone marrow mast cells were found in 45 (2.2%) of 2,000 bone marrow specimens obtained from patients who had hematologic disorders. Mast cells were most frequently seen in the marrows of patients who had preleukemic syndromes, lymphoproliferative disorders, and acute leukemia. The 16 patients who had preleukemic syndromes included those with refractory sideroblastic and megaloblastic anemia (with or without an excess of blasts), idiopathic pancytopenia or pure erythrocytic aplasia, paroxysmal nocturnal hemoglobinuria, idiopathic refractory neutropenia, agranulocytosis or thrombocytopenia, and persistent eosinophilia. Five of the seven patients who had acute leukemia had nonlymphoblastic leukemia; two had blastic crisis of chronic granulocytic leukemia. Of the 13 patients who had lymphoproliferative disorders, eight had chronic lymphocytic leukemia, three had macroglobulinemia, and two had non-Hodgkin's lymphoma. Three patients who had chronic renal failure associated with severe anemia and two who had chronic liver disease, splenomegaly, or hypersplenism were also encountered. In this study there appeared to be a consistent relationship between the presence of increased numbers of mast cells and the lymphocyte and plasma cell counts in the bone marrow. The significance of the presence of secondary mastocytosis in premalignant lesions, neoplasia, and, in particular, lympho- and myeloproliferative disorders, is still unclear.
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PMID:Increased bone marrow mast cells in preleukemic syndromes, acute leukemia, and lymphoproliferative disorders. 745 27

The present study investigated the peripheral blood mononuclear cells (PBMC) blastic responses to PHA, PHA plus recombinant IL-2 (rIL-2) and rIL-2 alone; the expression of membrane-bound IL-2R on PHA-stimulated PBMC; and the levels of IL-1 alpha, IL-2, IL-6, and sIL-2R in serum and in culture supernatants from PHA-stimulated PBMC in 17 patients with with non-Hodgkin's lymphoma (NHL), 4 with Hodgkin's lymphoma (HL), 5 with Hairy cell leukemia, 1 with chronic myelogenous leukemia, and 1 with chronic lymphocytic leukemia. The patients with HL and NHL with active disease (AD) were separated from those in clinical remission. The patients with AD were studied at diagnosis (obviously before therapy) and the patients in clinical remission were out of therapy since at least 6 mo. The lymphocyte blastogenic response to PHA was significantly lower in patients with HL and NHL with AD than in the control group. The response to rIL-2 alone was in the same range in the control group and in HL and NHL AD patients. By adding rIL-2 to PHA there was an increase of the blastogenic response of the same patients. The percentage of CD25 expressed on PHA-stimulated lymphocytes from patients with HL and NHL AD and from normal subjects is in the same range. Serum levels of IL-2, IL-6, and sIL-2R were significantly higher in HL and NHL AD patients than in controls as well as in all other hematological malignancies. Supernatants derived from PHA-stimulated PBMC were assessed for the presence of cytokines and sIL-2R by ELISA. The levels of IL-2, IL-6, and sIL-2R were significantly lower in HL and NHL AD patients than in controls as well as in all other hematological malignancies.
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PMID:Membrane-bound/soluble IL-2 receptor (IL-2R) and levels of IL-1 alpha, IL-2, and IL-6 in the serum and in the PBMC culture supernatants from 17 patients with hematological malignancies. 749 95

Initially discovered as antiviral agents, the interferons (IFNs) proved to be a class of cytokines with multifunctional properties, including inhibition of cell growth and modulation of immune functions. A number of clinical trials were thus carried out in cancer and viral diseases, and IFN-alpha therapy was shown to have a wide range of indications in hematology and dermatology: B-cell malignancies (hairy cell leukemia, non-Hodgkin's lymphoma, multiple myeloma), myeloproliferations (chronic myeloid leukemia, thrombocytosis), cutaneous T lymphoma, basal-cell carcinoma, cutaneous squamous cell carcinoma, Kaposi's sarcoma. IFN therapy also showed efficacy in viral tumors (condyloma acuminatum and laryngeal papillomatosis) and chronic hepatitis B and C. The antitumoral action of IFN-alpha mainly involves its capacity to inhibit cell proliferation, partly via antagonistic effects on growth factors. The elucidation of IFN-alpha signalling pathway(s) leading to gene activation, a better understanding of the interactions between IFN-alpha and cytokine network, and the development of combination therapy with other biological treatments or chemotherapy should greatly improve the clinical use of IFNs.
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PMID:[Interferons, a class of cytokines with a large therapeutic activity range]. 751 33

Analysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology-antibody-chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML-M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML-M2 and t(15;17) in AML-M3 were seen in granulocytic lineages only; t(14;18) in non-Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B-CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T-CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL-EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30-positive Reed-Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages.
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PMID:Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms. 752 Feb 72


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