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)

Serum ferritin (SF) is elevated in adults with malignancies, chronic inflammatory disease, liver disease and iron overload. The purpose of this study was to determine whether the concentration of SF in children with a variety of malignancies correlated with the activity of their disease. Patients with acute lymphoblastic leukaemia (ALL) at initial diagnosis (n = 11) and relapse (n = 15) had a mean SF of 238 and 338 ng/ml, respectively, compared to the normal mean of 31 ng/ml and range of 7 to 140 ng/ml in children. In 30 patients with ALL in remission the mean SF was 109 ng/ml, less than the values in patients with active disease and greater than the normal mean (P less than 0.001). The concentration of SF was also increased in a group of 77 patients with a variety of solid tumors. The 28 cases with active disease had a mean SF of 242 ng/ml, significantly higher (P less than 0.001) that the value of 84 ng/ml in 49 patients with no evidence of residual tumor. The differences in SF concentration did reflect the activity of disease in the groups as a whole but it remains uncertain whether the assay will prove useful in following the response to treatment of patients with certain types of tumor.
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PMID:Elevated serum ferritin in children with malignancies. 19 90

Sera from 134 selected patients with various types of cancer were tested for soluble antigen-antibody complexes by the C1q binding method. Sera from 85 healthy blood bank donors served as normal controls. C1q binding activity (C1q BA) values above the 95th percentile for healthy subjects were found in 83% of sera from patients with neoplastic diseases. The incidence of abnormal C1q BA values among patients with malignant melanoma was 83%, with breast cancer 74%, with colon cancer 75%, with lung cancer 88%, with leukemia and lymphoma 85%, and with miscellaneous tumors 94%. High C1q BA values were found most frequently in sera of patients who had been diagnosed relatively recently (within 5 mo) and who had evident residual disease after surgical treatment. Recurrence or progression of tumor growth occurred significantly more frequently in lung cancer patients with high C1q BA. DNA was not detected in cancer patients' sera and treatment with DNase did not decrease in C1q BA. C1q BA in sera could not be explained by the presence of antiglobulin antibodies. Sucrose density gradient ultracentrifugation studies of the serum C1q BA in 4 cancer patients showed that the major binding activity was found between 19S and 7S.
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PMID:The C1q binding test for soluble immune complexes: clinical correlations obtained in patients with cancer. 32 5

1. BCG (1 mg/mouse) administered i.v. on day 5 after chemotherapy by cyclophosphamide (CPM), given itself at the dose of 80 or 134 or 403 mg/kg one day after the inoculation of L 1210 leukaemia 10(3) cells, increases the effect of the non-optimal doses: i.e. 80 mg/kg, which is insufficient to cure mice, and 403 mg/kg, which is toxic. It does not change the effect of the optimal dose of CPM (134 mg/kg) which cures most of the mice. 2. BCG (1 mg/mouse i.v.) given on day 15 before CPM decreases the effect of the latter at the dose of 134 mg/kg. These results suggest that: a. BCG given after chemotherapy is not only able to eradicate the residual disease, but can decrease chemotherapy toxicity; b BCG given before an optimal dose of chemotherapy may decrease its antileukaemic effect, via the enhancement of the chemotherapy immunodepressive action, as demonstrated by skin graft experiments; this deterioration of the effect of chemotherapy by immunodepression was also suggested when the combination of CPM and antithymocyte serum was used.
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PMID:[Immune manipulation of BCG administered before or after cyclophosphamide for chemo-immunotherapy of L1210 leukemia]. 81 77

The cancerolytic effect of active systemic immunotherapy, which has been shown experimentally able to eradicate a complete population of tumour cells provided they are not very numerous, has been confirmed in various forms of human leukemia and in a few solid tumours against which it was applied as treatment of the imperceptible residual disease which remains after chemotherapy or surgery. Its main indication is thus this residual disease composed of cells which are left behind after chemotherapy of systemic tumours, for this treatment obeys the laws of first degree kinetics, and surgery and/or radiotherapy which, even if they remove or completely sterilise a local tumour, often leave behind a few cells which have already migrated to the future sites of metastases. Active systemic immunotherapy of large volume tumours, especially when combined with chemotherapy, is of doubtful efficacy. Local immunotherapy has given interesting results but its clinical indications are not yet clear.
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PMID:The surgeon and the immunotherapy of cancer. 121 38

Different methods were used to detect minimal residual leukemic cells (LT 12 nl), which had been genetically marked with E. coli 1 acZ and neo-gene by retrovirus vector mediated gene transfer. The detection levels of flow cytometry based FDG staining and fluorophotometric method based MUG staining were 10(-3) to 10(-4) and 10(-2) to 10(-3), respectively. The method of G 418 selective agar culture was demonstrated as a 10(-4) to 10(-5) levels for the detection of LT 12 nl residual leukemic cells in bone marrow. The results indicated that the selective agar culture can be used as a sensitive method for the study of minimum residual disease in the BNML leukemia model. We have used the selective agar culture to study the distribution of clonal LT 12 nl cells in BNML during minimum residual disease (MRD). A heterogenous distribution pattern of the clonal leukemic cells was found in the genetically marked BNML leukemia model during the MRD phase.
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PMID:[Minimum residual leukemic cells in genetically marked brown Norway rat myelocytic leukemia model]. 130 72

The current study was designed to determine the nucleotide sequence of two distinct T-cell-receptor delta chain (TCR delta) rearrangements which account for 95% of all rearranged alleles in common non-T, non-B lymphoid precursor acute lymphoblastic leukemia (LP-ALL). The results presented demonstrate that TCR delta rearrangements in LP-ALL are incomplete, immature, and involve V delta 2 to D delta 3 or D delta 2 to D delta 3 joints. These rearrangements are found in most cases of ALL. These results are consistent with the hypothesis that these leukemias originate in multipotent lymphoid precursor cells. The remarkable diversity of the rearrangements detected by polymerase chain reaction, cloning and sequencing demonstrates the clonal specificity and potential for detection of leukemic residual disease. However, in some cases the number of nucleotide differences may not be sufficient for the discrimination of leukemic and non-leukemic cells carrying V delta 2-(D)-D delta 3 rearrangements. A novel inversional rearrangement was demonstrated in one leukemia. This novel inversional rearrangement potentially increases the degree of diversity of the junctional region which encodes the antigen binding domain of TCR delta.
Leukemia 1992 Oct
PMID:Rearrangement and diversification of T-cell receptor delta genes in acute lymphoblastic leukemia. 132 76

Minimal residual disease (MRD) in patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph1 ALL) who received allogeneic (n = 9) or autologous (n = 6) bone marrow transplantation (BMT) was evaluated by the polymerase chain reaction (PCR) for the bcr-abl transcript. Twelve patients received BMT at the time of hematologic and cytogenetic remission. However, MRD was detected in 8 of 10 patients evaluated. Seven patients, including three who had MRD before BMT, continue to have a disease-free survival 5 to 64 months after BMT. Twenty-one specimens obtained from these patients at various times after BMT did not show MRD. In three patients, MRD detected just before BMT seems to be eradicated by BMT protocol. The other eight patients developed cytogenetic or hematologic relapses 2 to 8 months after BMT. Seven of 14 samples from these patients demonstrated MRD, which preceded clinical relapse by 3 to 9 weeks. Thus, this technique for the detection of MRD appears to be useful for the more precise assessment of various antileukemia therapies and for early detection of leukemia recurrence.
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PMID:Detection of Philadelphia chromosome-positive acute lymphoblastic leukemia by polymerase chain reaction: possible eradication of minimal residual disease by marrow transplantation. 137 20

This clinical trial was designed to evaluate the role of high-dose cytarabine (ara-C) in the treatment of adults with acute myeloid leukaemia (AML) in first relapse. We also tested the hypothesis that the selective use of AMSA (100 mg/m2/d on days 7, 8 and 9) would increase the complete remission (CR) rate when leukaemia cells remained in the bone marrow immediately following 6 d of Ara-C (2-3 g/m2/12 h) alone. Of 155 patients evaluable for response, 115 (74%) experienced marked cytoreduction by day 6 and received no further induction chemotherapy; 53 (45%) of these patients achieved CR after one course and 45 (38%) had resistant disease. The 36 patients (23%) with inadequate cytoreduction after the 6 d of ara-C alone were randomly assigned either to no further chemotherapy (21 patients) or to 3 d of AMSA (15 patients). The CR rates after one course were 14% and 53%, respectively (P = 0.01), and the fractions with resistant disease were 76% and 40%, respectively. The fractional reduction of leukaemia cells in the day 6 bone marrow aspirate specimen (P < 0.0001) and the reduction in the leukaemia cell mass measured in the day 6 marrow biopsy (P = 0.001) were the strongest predictors for achieving CR versus having residual disease in univariate analyses. The median duration of remission was 5 months, but seven patients (10%) remain in CR after 30-92 + months. Among the 140 patients who received only the 6 d of ara-C, the pretreatment albumin (P = 0.002) and lactate dehydrogenase (P = 0.01) levels were the strongest predictors of response in univariate analyses, but only the albumin remained significant (P = 0.01) in a stepwise logistic regression analysis. Those patients with albumin > 4.0 mg/dl and LDH < 125% of normal had a 71% CR rate, and only 16% had resistant disease. Thus, pretreatment characteristics and rapid cytoreductin in the day 6 bone marrow sample identified a favourable subset of patients with AML in first relapse, some of whom responded quite well to 6 d of ara-C alone and have had long disease-free remissions.
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PMID:The selective use of AMSA following high-dose cytarabine in patients with acute myeloid leukaemia in relapse: a Leukemia Intergroup study. 141 16

Acute myeloid leukemia (AML) blast cells (BC) express antigens that are commonly found on their normal counterparts. The leukemia colony-forming cell (L-CFC) subpopulation, identified by its ability to form leukemia colonies in vitro, is thought to be the stem cell population that produces BC. To ascertain the association between myeloid antigens on the BC and the L-CFC from the same patient, we compared the expression of CD14, CD15, CD33, p124 and HLA class I from 17 cases of AML. These particular myeloid antigens were studied because they are suitable targets in purging bone marrow for autotransplantation. We found no significant difference in the expression of CD14, CD15, CD33, and HLA class I on the BC and L-CFC from the same patient, although we observed considerable heterogeneity among different AML cases. Analysis of the progenitor cell antigen p124 revealed significant within-patient differences on the BC and L-CFC (p = 0.007), with a greater tendency for expression on the L-CFC. This heterogeneity may be due to differences in maturation stage of the L-CFC and BC. This information is important when L-CFC phenotype is used to determine the appropriate selection of antibodies for purging of residual disease in the context of auto-transplantation.
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PMID:Predictive value of flow cytometric analyses of blast cells in assessing the phenotype of the leukemia colony-forming cell (L-CFC) population in acute myeloid leukemia. 142 80

The genetic sequence of the third complementarity determining region (CDR III) of the immunoglobulin heavy chain (IgH) gene was analysed in 55 rearranged alleles from 36 children presenting with B-lineage acute lymphoblastic leukaemia (ALL). This confirmed the unique nature of these rearrangements. However, contrary to the hypothesis that the CDR III is produced by a random process of rearrangement, biased utilisation of diversity (D) segments and of joining (J) regions 4, 5 and 6 was demonstrated. Moreover, preferred sequence boundaries were seen in J regions 1 to 5 and were suggested at the 3'-end of certain D regions, notably D21/9 and DK1. Similar patterns of rearrangement have been noted in normal B-lymphocyte clones. Together with relatively limited N nucleotide addition, these factors may restrict the potential sequence variability at the D-N-J junction. The occurrence of clonal progression by secondary gene rearrangements, such as V-V replacement, favours the use of this site when designing clone-specific oligonucleotide probes for use in monitoring minimal residual disease (MRD). In cases where biased features of D-J rearrangement are shared by both the leukaemic and normal B-lymphocyte clones this could reduce the sensitivity of these probes in detecting low levels of residual disease.
Leukemia 1992 Nov
PMID:Third complementarity determining region (CDR III) sequence analysis in childhood B-lineage acute lymphoblastic leukaemia: implications for the design of oligonucleotide probes for use in monitoring minimal residual disease. 143 6


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