Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-seven adult patients with acute promyelocytic leukemia (APL) were treated between 1974 and 1984 with daunorubicin (DNR) or 4-(9-acridinylamino)methanesulfan-m-anisidide (AMSA) in combination with arabinosylcytosine (Ara-C) and 6-thioguanine (TG); they also received prophylactic heparin. Forty-one patients (72%) achieved complete remission (CR), including 11 of 12 patients who received the AMSA-containing regimen. The incidence of early fatal hemorrhage was 14%, lower than that of earlier studies or other published reports. Elevated WBC and serum lactate dehydrogenase levels at diagnosis were associated with an increased incidence of life-threatening hemorrhage and shorter remission duration. Advanced age was an unfavorable prognostic factor for male patients. Both DNR and AMSA in combination protocols are effective treatments for APL. The incidence of CR is similar to that achieved in other types of acute nonlymphoblastic leukemia (ANLL) with the same protocols, but the median duration of remission is significantly longer in APL (24 v 9 months) and the percentage of remissions longer than 60 months is also higher in APL (35% v 5%).
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PMID:Acute promyelocytic leukemia: treatment results during a decade at Memorial Hospital. 293 Aug 37

Leukemic cells from 89 (24%) of 369 children with newly diagnosed acute lymphoblastic leukemia (ALL) were found to have a pre-B immunophenotype. By comparison with blasts having the common ALL phenotype, the pre-B cells were more likely to have a DNA index less than 1.16 (P = 0.02), a pseudodiploid karyotype (P less than 0.001), and a chromosomal translocation (P = 0.001). Increased serum lactic dehydrogenase levels (P = 0.001) were also characteristic of pre-B ALL; otherwise, the clinical and laboratory features of the two groups were similar. A nonrandom chromosomal translocation, t(1;19)(q23;p13.3), was identified in blast cells from 16 (23%) of the 70 patients with pre-B ALL and adequate chromosome banding studies; different translocations were found in 11 of the remaining patients. The presence of any chromosomal translocation in the pre-B group was significantly related to a higher leukocyte count, an increased level of serum lactic dehydrogenase, an increased percentage of S-phase cells, black race, and a blast cell DNA index less than 1.16. Four presenting features were found to confer an increased risk of treatment failure among pre-B patients: pseudodiploidy, chromosomal translocation, black race, and higher serum lactic dehydrogenase level. In a multivariate analysis, pseudodiploidy emerged as the strongest factor for predicting relapse in pre-B ALL. The frequent association of chromosomal abnormalities of known adverse prognostic significance and high serum lactic dehydrogenase levels with pre-B-cell ALL explains, at least in part, the poor treatment outcome reported for children with this subtype of leukemia.
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PMID:Cytogenetic features and serum lactic dehydrogenase level predict a poor treatment outcome for children with pre-B-cell leukemia. 293 98

The human leukemia cell lines HL-60, KG-1, KLM-2, ML-3, THP-1, and U-937 were treated with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). TPA partially or completely inhibited the proliferative activity of the cell cultures. The number of cells with the ability to reduce nitroblue tetrazolium increased in the TPA-treated cell lines HL-60, ML-3, THP-1, and U-937, whereas the cell lines KG-1 and KLM-2 remained nitroblue tetrazolium negative. Except for KG-1 and KLM-2, all TPA-treated cell lines showed varying degrees of strong adherence to plastic surface. The carboxylic esterase, acid phosphatase, hexosaminidase, and lactate dehydrogenase isoenzyme profiles from these cell lines were analyzed by isoelectric focusing on horizontal polyacrylamide gels. The new or stronger expression of an esterase isoenzyme which is specific for monocytes-macrophages was induced in HL-60, ML-3, THP-1, and U-937 but not in KG-1 or KLM-2. The new expression of the tartrate-resistant acid phosphatase isoenzyme was induced in ML-3, THP-1, and U-937. The number of esterase and acid phosphatase isoenzymes and the staining intensity of isoenzymes characteristic for myeloid cells were increased by TPA in all cell lines. The loss of the hexosaminidase I isoenzyme which is a marker of immature hematopoietic cells was noted in KG-1, ML-3, THP-1, and U-937. TPA triggered an increase in number and staining intensity of the lactate dehydrogenase isoenzymes in all cell lines. Some isoenzymatic changes (e.g., monocyte-specific esterase, tartrate-resistant acid phosphatase, hexosaminidase I) appear to correlate with TPA-induced differentiation while other alterations in the isoenzyme patterns do not (e.g., lactate dehydrogenase, other esterase and acid phosphatase isoenzymes). Differentiation of nonmonocytoid cells appears, at the isoenzyme level, to be quite different from that of the monocytoid cell lines.
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PMID:Changes in isoenzyme profiles during induction of differentiation in human myelomonocytic leukemia cell lines. 294

Serum concentrations of CD8 antigen were measured at diagnosis with an enzyme-linked immunoassay in children with acute lymphoblastic leukemia (n = 344) or non-Hodgkin's lymphoma (n = 65). All patients had detectable levels of the serum antigen, which in its soluble nonreduced form appeared to be a 52-Kd homodimer as compared with the 66-Kd surface membrane component on most thymocytes and on a subset of functionally distinct T cells (suppressor/cytotoxic). Increased serum levels of CD8 in leukemia patients were significantly related to recognized high-risk prognostic features: high leukocyte count, large liver and spleen size, high serum lactic dehydrogenase level, T-cell immunophenotype, presence of a mediastinal mass, pseudodiploid karyotype, DNA index less than 1.16, and chromosomal translocation. Children with serum CD8 levels greater than or equal to 450 U/mL were more likely to fail treatment than were those with lower levels (P = .002), even in the group with non-T-cell leukemia (P = .003). In a multivariate analysis, serum CD8 antigen contributed independent prognostic information beyond that conveyed by age, leukocyte count, and race (P = .02). High serum CD8 antigen levels also correlated with advanced stages of disease in children with non-Hodgkin's lymphoma or B-cell leukemia. Children with higher serum CD8 antigen levels (greater than or equal to 700 U/mL) had a poorer treatment outcome (P = .003), even after results were adjusted for disease stage and serum lactic dehydrogenase level (P = .05). Measurement of serum levels of CD8 antigen not only has important prognostic value in childhood lymphoid malignancies but also could be useful in assessing the immunoregulatory role of T cells in patients with cancer.
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PMID:Serum levels of CD8 antigen in childhood lymphoid malignancies: a possible indicator of increased suppressor cell activity in poor-risk patients. 297 Aug 71

The clinical and pathological features of T-cell type malignant lymphoma related to human T-cell leukemia virus (HTLV) were investigated in eight patients presenting lymphadenopathy. Biopsy of lymph nodes showed an histology of diffuse non-Hodgkin's lymphoma. All patients were positive for anti-ATLA antibody and HTLV proviral DNA in the lymph node cells. Most patients showed pronounced hypercalcemia and high serum levels of lactic dehydrogenase. All patients died between 3 and 17 months (mean 8 months) after the onset of disease. HTLV-related malignant lymphoma should be added to the spectrum of ATL, being classified as a lymphoma type ATL.
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PMID:Lymphoma type adult T-cell leukemia--a clinicopathologic study of HTLV related T-cell type malignant lymphoma. 300 98

We describe five patients with adult T-cell leukemia/lymphoma (ATL) with neither integration of human T-cell leukemia virus type I (HTLV-I) into their leukemia cells nor anti-HTLV-I antibody in their sera. These findings indicate that HTLV-I may not have been involved in leukemogenesis in these patients. The clinicohematological, cytopathological, and immunological features of HTLV-I-negative ATL were exactly the same as those of HTLV-I-associated ATL. Leukemia cells with pleomorphic nuclei, generalized lymphadenopathy, hepatosplenomegaly, skin lesions, hypercalcemia, and elevated lactate dehydrogenase levels, all of which are characteristic features of typical ATL, were also seen in these patients with HTLV-I-negative ATL. Leukemia cells expressed T3, T4, and pan-T-cell antigens in three cases, and T3 and pan-T-cell antigens in two. All five patients had lived in ATL-nonendemic areas. The finding of HTLV-I-negative ATL suggests that factor(s) other than HTLV-I infection may be involved in ATL leukemogenesis.
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PMID:Adult T-cell leukemia/lymphoma not associated with human T-cell leukemia virus type I. 301 71

The risk of development of CNS leukemia was investigated in 153 adults with acute lymphocytic leukemia (ALL) who received systemic combination chemotherapy without CNS prophylaxis. Overall, 31 patients (20%) developed CNS leukemia after a median of 6 months of therapy; the estimated 1-year incidence of CNS leukemia was 21% (SE, 3.9%). Characteristics significantly associated with CNS involvement included the presence of elevated hemoglobin creatinine, alkaline phosphatase, fibrinogen, and lactic dehydrogenase levels; B-cell leukemia; and high leukemic cell proliferative activity. Multivariate analysis identified lactic dehydrogenase levels of greater than or equal to 600 U/L and greater than or equal to 14% of cells in the S + G2M compartment to have independent additive poor prognostic significance. Patients were categorized into different risk groups for CNS leukemia with 1-year incidences ranging from 4% to 55%. While related to a high occurrence of CNS leukemia at diagnosis (33%) and subsequently (100%), the low incidence of B-cell disease excluded it from the multivariate analysis. The use of systemic chemotherapy containing multiple agents with good CNS penetration and in high doses (VAD regimen) in 90 patients was associated with a trend for lower CNS leukemia at 1 year (15% v 31%), especially in the low-risk category. We propose to develop future therapies for adults with ALL that include risk-oriented CNS prophylactic approaches.
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PMID:Identification of risk groups for development of central nervous system leukemia in adults with acute lymphocytic leukemia. 305 30

The induction of poliomyelitis by lactate dehydrogenase-elevating virus (LDV) in C58 mice is dependent upon several host factors including old age, loss of immune competence and genetic predisposition. Two genetic components segregate with susceptibility to this neurological disease: the presence of multiple proviral copies of N-tropic endogenous murine leukemia viruses (MuLV) and homozygosity of the permissive allele for N-tropic viral replication (Fv-1n/n). We have quantified the levels of RNA for several endogenous retroviruses, using virus specific oligonucleotide probes, in various tissues of C58 mice in relation to age and immunosuppression. A tissue specific increase in expression of 3.0 kb AKR MuLV RNA in the spinal cords of mice occurred with increasing age of the mice and was enhanced several-fold by immunosuppression in old mice. Susceptibility to LDV-induced poliomyelitis occurs in the same age dependent manner as AKR MuLV expression and is also enhanced by immunosuppression. In contrast, the mink cell focus forming virus (MCF) RNA levels in the spinal cord remained constant despite apparent variations in MCF RNA expression in other tissues, and no xenotropic retrovirus RNA was detectable in spinal cords or brains of the C58 mice. The increased AKR MuLV RNA in the spinal cord was shown by in situ hybridization to be mainly located in the same motor neurons that become infected with LDV in these mice and are destroyed as paralysis develops. These results support a novel dual virus virus hypothesis for LDV-induced poliomyelitis in which increased endogenous retroviral expression in motor neurons renders these cells susceptible to cytocidal replication of LDV and hence to the development of LDV-induced poliomyelitis.
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PMID:Susceptibility of C58 mice to paralytic disease induced by lactate dehydrogenase-elevating virus correlates with increased expression of endogenous retrovirus in motor neurons. 323 56

The phorbolester 12-0-tetradecanoylphorbol 13-acetate (TPA) was used for the induction of differentiation in cells of the human leukemia cell line SPI-802. The cellular morphology, surface marker antigen expression, and isoenzyme profiles of four enzymes (carboxylic esterase, acid phosphatase, hexosaminidase, and lactate dehydrogenase) served as parameters for monitoring the induced phenotypical changes. TPA led to distinct alterations of the morphology and significantly affected the growth rate with cessation of cell proliferation. No major increase in the number of nitro blue tetrazolium-positive cells or aggregation of cells, phagocytosis of latex beads, adherence to plastic surface, or development of pseudopodia were observed. As TPA-treated SPI-802 cells remained negative for these markers of the monocyte-macrophage complex, it can be concluded that the cells did not differentiate into monocytes and macrophages. The immunological marker profile based on testing of 55 monoclonal antibodies, terminal deoxynucleotidyl transferase and two erythrocyte rosette tests indicated a differentiation of SPI-802 cells along the granulocytic cell lineage. This was confirmed by isoenzyme analysis, especially that of carboxylic esterase. An isoenzyme specific for monocytes and macrophages was not detected. In earlier studies it was found that SPI-802 cells produce hemoglobin upon exposure to TPA or hemin. This latter observation and the present results suggested a comparison with the two erythroleukemia cell lines K-562 and HEL. SPI-802 cells appear to have the potential to differentiate along several cell lineages.
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PMID:Induction of differentiation in the human leukemia cell line SPI-802: morphological, immunological, and isoenzymatic changes. 345 1

The human leukemia cell line CTV-1 was established from a case of acute monoblastic leukemia (AMoL). We analyzed the phenotypic marker profile of the CTV-1 cells in their original, untreated state and during induction of differentiation with the phorbolester 12-0-tetradecanoylphorbol 13-acetate (TPA). TPA led to morphological changes with signs of differentiation. Cell proliferation decreased in a dose-dependent fashion during exposure to TPA. In the surface marker analysis using a panel of 45 monoclonal antibodies (MoAbs) and several polyclonal antisera, CTV-1 cells were negative for markers of the T- and B-cell lineages, and were positive for several, but not all, myelomonocytic markers. Although the cells were reactive with the MoAb Leu-7 which identifies natural killer (NK) T-cells, no NK activity was detected. In the isoenzyme analysis of the four enzymes carboxylic esterase, acid phosphatase, hexosaminidase and lactate dehydrogenase (LDH) performed by isoelectric focusing on polyacrylamide gels, CTV-1 cells displayed isoenzyme profiles of immature myeloid cells. The overall marker profile of CTV-1 cells demonstrated cells of monocytoid origin arrested at a very early stage of differentiation, possibly close to the stage of precursor cells. As compared to other myelomonocytic cell lines, CTV-1 cells showed unusual morphological, immunological, functional and biochemical features and appeared to be relatively insensitive to treatment with TPA, although some alterations of the phenotype could be induced.
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PMID:Monocytoid leukemia cell line CTV-1: morphological, immunological and isoenzymatic characteristics. 345 74


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