Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The data reviewed in this paper indicate that immunotherapy is effective in prolonging remission and survival in acute and chronic leukemia. The acute lymphocytic leukemias may or may not respond to immunotherapy and further work is needed in this area. No studies of immunotherapy in chronic lymphocytic leukemia have been done, but this will be an important area for investigation, since there is often profound immunodeficiency in this disease. The malignant lymphomas are another fertile area for this type of research, since they have a high response rate, tumor-associated immunodeficiency, and at least differentiation antigens if not tumor-specific antigens. The scientific basis for the use of immunotherapy in leukemia includes the demonstration of a relationship of rate and duration of remission and survival to immunocompetence, the demonstration of unique tumor-associated antigens on leukemia cells, and the demonstration of immune responses to these antigens which can be boosted by immunization. At the present time, active nonspecific immunotherapy with BCG and MER and active specific immunotherapy have been proved effective in acute myelogenous leukemia. Careful attention should be given to dose, schedule, route, and so forth. Other types of immunotherapy remain to be explored.
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PMID:Immunotherapy of leukemia. 78 12

The white blood cell count response was documented in various patients following transfusions of 500 ml of autologous or unrelated donor blood that had been subjected to 10 minutes of dialysis with 15 minutes of stagnation. Patients studied included 1 patient with acute nonlymphocytic (ANLL) and 2 patients with chronic lymphocytic leukemia (CLL). The control group consisted of 4 patients with renal failure. The ANLL patient showed a normal two-phase reaction after administration of donor's blood. It is possible that even under conditions of severe disturbance of hemopoiesis the general dependence on normal humoral regulation remains. The CLL patients showed a marked drop in circulating WBC in the first descending phase of the hemodialysis-induced reaction (HDIR). All blood cell types including lymphocytes and blast cells took part in this decrease of blood count; this suggests a cell-nonspecific effect. It is presumed that leukocytes that leave the circulation do not return into the blood and the procedure may be considered as a form of leukophoresis in vivo, with possible therapeutic value.
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PMID:The hemodialysis-induced reaction in patients with leukemia. 92 31

The effect of morphine and cocaine on the transport of hydrolyzed nitrogen mustard (NH2-OH) and choline by peripheral blood cells of normal subjects and patients with chronic lymphocytic leukemia, acute lymphoblastic leukemia, and acute myeloblastic leukemia was determined. Transport of HN2-OH by lymphocytes from normal individuals and patients with chronic lymphocytic leukemia was stimulated by morphine and cocaine and, in each case, the effect was statistically significant (P less than 0.05 or greater). However, choline transport by normal lymphocytes was not altered by cocaine and was only slightly stimulated by morphine; choline transport by lymphocytes from patients with chronic lymphocytic leukemia was not stimulated by either morphine or cocaine. HN2-OH and choline transport by cells from patients with either acute lymphoblastic or myeloblastic leukemia was stimulated to a comparable degree by both drugs. Stimulation of HN2-OH transport by morphine and cocaine was greater in normal lymphocytes than in acute leukemic cells and the differences were highly significant (p less than 0.001). Conversely, stimulation of choline transport was more marked in acute leukemic cells than in normal lymphocytes, and these differences were also highly significant (p less than 0.001). It was previously shown that transport of nitrogen mustard by normal and leukemic human cells was biphasic in nature, consisting of a choline-independent component at "high" drug concentrations and a choline-dependent system at "low" substrate concentrations. The preferential stimulation of the low-dose, choline-dependent system by morphine and cocaine in acute leukemic cells relative to that observed in normal lymphocytes suggests a possible mechanism of increasing the therapeutic index of nitrogen mustard.
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PMID:Drug-induced stimulation of transport of hydrolyzed nitrogen mustard and choline by normal and leukemic human cells in vitro. 106 33

Rabbit antisera to myelogenous leukemia (ML) cells were raised; ML cells from line K-562 that has the Philadelphia (Ph) chromosome were used as antigen. Antibodydependent, complement-mediated cytotoxicity was demonstrated by the trypan blue test and Cr release assay for cultured ML cells, whereas no cytotoxicity was demonstrated for cells from B (SB) and T (MOLT 4) lymphoblastoid cell lines. The antisera showed no cross-reactivity for normal human peripheral leukocytes or purified granulocytes. A low level (less than 8%) of cytotoxicity was directed against cell membrane associated fetal bovine serum proteins. Absorption of the immune serum with normal human bone marrow cells of first trimester human whole embryo cells reduced the cytotoxic titer to a similar extent; this suggested the possibility of crossreactivity between ML cells and fetal antigen(s). However, the ML antigen(s) was unrelated to carcinoembryonic antigen (CEA), since absorption with CEA had no effect on the serum cytotoxic titer. The anti-ML sera were cytotoxic for cells taken from 10 patients with chronic myelogenous leukemia and from 3 with acute myelogenous leukemia. In contrast, the leukocytes of 1 of 4 patients with acute lymphocytic leukemia, and 3 of 7 with chronic lymphocytic leukemia shared similar antigenic determinants as demonstrated by cytotoxicity tests. The significance of the cross-reactivity of some lymphatic and ML cells may be the result of the use of rabbit sera that did not distinguish antigens common to both granulocytic and lymphocytic cells, or it may reflect an "immature" or "blastic" antigen present on many leukemia cells.
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PMID:Cytotoxicity of antisera to a myelogenous leukemia cell line with the Philadelphia chromosome. 106 37

Eight cases of Hodgkin's disease and acute leukemia are reported. An additional 74 cases of acute myelocytic leukemia or one of its variants, 11 cases of acute lymphocytic leukemia, 12 cases of chronic myelocytic leukemia and 37 cases of chronic lymphocytic leukemia associated with Hodgkin's disease are reviewed from the literature. In 3 of the 82 patients with acute myelocytic leukemia and Hodgkin's disease, the two diseases occurred simultaneously. Of the remaining 79 patients, 76 had received radiation therapy for their Hodgkin's disease and acute myelocytic leukemia had developed 1.2 to 19 years later (mean 6.5 years). Thirty-four of these patients also received antineoplastic chemotherapy. Only three patients with Hodgkin's disease were treated with multiple chemotherapy alone; in these, Hodgkin's disease developed 1.2, 1.5 and 3.2 years later. In 4 of 11 patients with acute lymphocytic leukemia and Hodgkin's disease, the two disorders occurred simultaneously. The other seven patients were all treated with radiation for their Hodgkin's disease, and acute lymphocytic leukemia developed 2 to 8 years later (mean 4.5 years). Three of the 7 patients also received alkylating agents. It is concluded that the development of acute leukemia, mostly acute myelocytic leukemia but also acute lymphocytic leukemia, during the course of Hodgkin's disease, is most likely related to radiation therapy. There is as yet insufficient evidence to implicate intensive chemotherapy in the causation of acute leukemia since in only three patients with Hodgkin's disease treated with chemotherapy alone has the development of acute leukemia been reported. It is possible, however, that chemotherapy potentiates the effect of radiotherapy. 2t is also possible that acute leukemia is part of the natural history of Hodgkin's disease and is occurring with greater frequency because of improved survival in Hodgkin's disease since the introduction of better radiotherapeutic and chemotherapeutic treatment regimens.
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PMID:Hodgkin's disease and acute leukemia. Report of eight cases and review of the literature. 109 Jan 58

Acute myelocytic leukemia occurring many years after intensive radiotherapy and/or chemotherapy has been reported in 82 patients with Hodgkin's disease, 58 patients with multiple myeloma, and 40 patients with chronic lymphocytic leukemia. The precise incidence of this occurrence is uncertain, since the total number of patients at risk is unknown. Most patients with Hodgkin's disease had received intensive radiation therapy. Many also received chemotherapy. One-third of the patients with myeloma were treated only with melphalan. Acute leukemia may occur as part of the natural history of Hodgkin's disease and multiple myeloma; it has been seen with increasing frequency in recent years due to improved survival secondary to better treatment. It is also possible that radiotherapy and/or chemotherapy may be causally related to the development of acute leukemia.
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PMID:Acute leukemia as a delayed consequence of cancer chemotherapy. 125 23

The progressive accumulation of leukemic cells in acute myeloblastic leukemia (AML) results from the self-renewal capacity of leukemic blast progenitors. The growth of leukemic blast progenitors is supported by growth factors and colony-stimulating factors (CSFs) have been shown to stimulate this phenomenon in vitro. After repeated subculture of leukemic cells obtained from a patient with AML M4 in the presence of recombinant G-CSF, a cell line dependent on G-CSF was established. This cell line, designated OCI/AML1a, does not respond to GM-CSF, interleukin-3 (IL-3), IL-1 or stem cell factor as well as G-CSF. The stimulatory effect of G-CSF on OCI/AML1a cells is almost completely blocked by monoclonal anti-G-CSF antibody. With G-CSF added in the culture, the OCI/AML1a cell line has been growing exponentially for over 5 years now. Another cell line, with growth dependent on IL-3, has also been established from a patient with chronic lymphocytic leukemia in the acute phase. This cell line TMD2 does not respond to G-CSF, GM-CSF, IL-1, or stem cell factor and anti-IL-3-antibody blocks the stimulatory effect of IL-3 on these cells. Receptors for IL-3 have been found on the surface of TMD2 cells. Although the TMD2 cell line is not derived from AML, the novel character of IL-3-dependency provides useful information for the study of the role of growth factor(s) in leukemic cell proliferation. These two CSF-dependent cell lines are expected to be excellent models for the investigation of the precise mechanism by which G-CSF and IL-3 stimulate the growth of leukemic cells.
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PMID:Colony-stimulating factor (CSF)-dependent growth of two leukemia cell lines. 128 44

Leukocyte acid phosphatase and its isoenzyme composition was studied in leukemic patients to determine the specificity of different isoenzymes in leukemic leukocytes. It was found that leukocyte acid phosphatase content is significantly increased in ALL, AML, and CML patients, while CLL patients had decreased levels of acid phosphatase. The distribution and intensity of leukocyte ACP isoenzymes vary in respective leukemic condition. Thus isoenzyme 'O' was predominant in AML and CML, while isoenzymes 1, 2 and 3 predominated in ALL. The lack of predominance of isoenzyme 3 was a feature in CLL patients. It was concluded that the isoenzyme patterns, though promising, presented inconclusive picture for diagnosis purpose and further studies on immunochemical characteristics of these isoenzymes are warranted to ascertain their cell specificity.
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PMID:Total leukocyte acid phosphatase and its isoenzymes in patients with leukemia. 129 3

Since the translocation breakpoint t(15;17) (q22;q21) in acute promyelocytic leukemia (APL) occurs within the retinoic acid receptor-alpha (RARA) gene, the expression of many genes normally regulated by RARA may be affected by this translocation. To identify genes that may be aberrantly expressed in APL, a subtraction cDNA library of an APL patient with t(15;17) was constructed. A cDNA, pRD1, specifically expressed in APL was identified. DNA sequence analysis of pRD1 showed that this gene is similar to the DNA sequence of annexin VIII, a gene which encodes a vascular anticoagulant. The annexin VIII gene was assigned to chromosome 10, which indicates that specific expression of this gene in APL is not directly involved in the t(15;17) breakpoint region. We have analyzed the expression of annexin VIII gene in nine t(15;17)-positive APL patients and one APL patient with a chromosome 17q-abnormality. We found that all APL samples expressed high levels of the annexin VIII gene. Expression of the annexin VIII gene in all other leukemias, including acute myelogenous leukemia, chronic myelogenous leukemia, chronic lymphocytic leukemia, and acute lymphoblastic leukemia, was undetectable, except in one patient with acute myelogenous leukemia in which a very low level of expression was detected. Annexin VIII is highly expressed in the APL cell line, NB4. Its expression was significantly reduced after 8 hours of all-trans retinoic acid (ATRA) treatment, whereas the expression of RARA increased several-fold within 4 hours postinduction. Thus, increased expression of RARA preceded the downregulation of annexin VIII after ATRA induction, suggesting an inverse relationship between RARA and annexin VIII expression. Since increased expression of the fusion transcript was seen after ATRA induction and an APL without a t(15;17) translocation expressed high levels of annexin VIII, it appears that increased expression of annexin VIII in APL is not related to the fusion transcript. Therefore, dysregulation of the RARA gene may be related to the overexpression of annexin VIII in APL.
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PMID:Specific expression of the annexin VIII gene in acute promyelocytic leukemia. 131 14

The anti-proliferative effects of selenium were studied both in vivo and in vitro. At a selenium concentration of 0.6 micrograms/ml, cells from patients with ALL-L1, L2 and AML-M1, M3 and M5 were more sensitive than cells from patients with CML. Cells from patients with AML-M2, CLL and leukaemic lymphoma were least sensitive. Normal bone marrow or peripheral blood cells were not sensitive to selenium at this concentration. In the mouse leukaemia models (L797, L615, L7712), the sensitivity of leukaemic cells were: L797 (93% cytotoxicity) greater than L615 (49.7% cytotoxicity) greater than L7712 (4.4% cytotoxicity). Sodium selenite injected i.p. increased the longevity of L797-inoculated mice. Administration of 40 micrograms selenium daily for 7 days resulted in a significant increase in the longevity of mice inoculated with 10(5) L797 cells. However, no remarkable increase of the longevity was observed in either L615- or L7712-inoculated mice after treatment with sodium selenite for 7 days. Treatment of the HL-60 leukaemic cell line with selenium caused a dose- and time-related decrease in DNA, RNA and protein syntheses as measured by [3H]-thymidine, [3H]-uridine and [3H]-leucine uptake respectively. The inhibitory effect of selenium on DNA synthesis was reversed when selenium was removed from the medium, demonstrating that selenium-induced inhibition of DNA synthesis was due to interference with DNA biosynthesis rather than DNA template damage. These results suggest that the anti-leukaemic effect of sodium selenite is associated with inhibition of DNA replication, transcription and translation.
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PMID:The anti-leukaemic effects and the mechanism of sodium selenite. 131 17


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