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)

Treatment of elderly patients with hematological malignancies is difficult and a matter of controversy. Low responsiveness to therapy and high risk of mortality have been reported. The risk of chemotherapeutic death increases after age 60, and an age-adjusted chemotherapy schedule is needed. In stage III and IV Hodgkin's disease, for example, an age-adjusted COPP regimen may be adopted. Many non-Hodgkin lymphomas (NHL) of elderly patients have a slow course. However, for intermediate to high grade aggressive NHL, dose-reduced CHOP regimen, or non- or low-dose methotrexate-containing programs like BECALM, CNOP, and low dose-ACOP-B are acceptable. MACOP-B regimen with G-CSF may be used for patients under age 65. For the treatment of elderly patients with AML, it is reported that a reduced-dose DAT regimen is better than the standard dose for inducing CR in patients older than 60. In elderly AML patients over 60, the dose-adjustment reported by Mori, or low-dose cytarabine with G-CSF, is recommended. Information about elderly patients with acute lymphoblastic leukemia is scarce. Aggressive treatments like L-17 M regimen are not tolerable by elderly patients, and a combination chemotherapy consisting of vincristine and prednisolone is recommended.
Gan To Kagaku Ryoho 1992 Sep
PMID:[Treatment of elderly patients with hematological malignancies]. 138 69

The t(8;21)(q22;q22) is a nonrandom cytogenetic abnormality associated with acute myelogenous leukemia of the M2 subtype (FAB classification). The 8q- and 21q+ derivative chromosomes have previously been isolated in somatic cell hybrids and used to map the anonymous sequences D21S65 and D21S17, which were proximal and distal, respectively, to the breakpoint on chromosome 21. DNA from a series of 12 t(8;21) patients and 7 controls was analyzed by pulsed field gel electrophoresis. Physical linkage of probes D21S65 and D21S17 on a 2100 kb NruI fragment was established by partial digestion experiments. In all the patients, the translocation generated a rearranged D21S65 NruI fragment of 650 to 750 kb, suggesting heterogeneity in the breakpoints. This heterogeneity was confirmed by using BssHII, SacII, and EagI enzymes. Our results are consistent with the presence of a 100 Kb breakpoint cluster region on chromosome 21 encompassing the AML1 gene. Interestingly, in half of the patients, demethylation of an NruI site located 7 kb proximal to the last exon of the AML1 gene occurred on the nontranslocated chromosome 21.
Genes Chromosomes Cancer 1992 Sep
PMID:Molecular analysis of 12 patients with the t(8;21) translocation and M2 acute myelogenous leukemia. 138 53

A 13-year-old boy with Down syndrome (DS) had a brainstem glioma confirmed at autopsy, 10 years after receiving prophylactic cranial irradiation for acute myeloblastic leukemia. There is no clear association of brain tumors with DS; despite a reported link between leukemia and glioma, a causal association with radiation therapy is more likely.
Cancer 1992 Sep 01
PMID:Brainstem glioma after radiation therapy for acute myeloblastic leukemia in a child with Down syndrome. Possible pathogenetic mechanisms. 138 83

Acute myeloid leukaemia (AML) blast cells express haemopoietic growth factor receptors. However, their presence does not predict response to the cognate ligand in vitro. This suggests that haemopoietic growth factor receptor structure or function may be abnormal in some cases of acute myeloid leukaemia. The granulocyte-macrophage colony-stimulating factor receptor alpha-chain gene (GM-CSF-R) has recently been localised to the pseudoautosomal region of the sex chromosomes. A sex chromosome is lost in 25% of cases of AML FAB subtype M2. The loss of one allele of this gene may have some aetiological significance in AML if the other allele is altered leading to abnormal receptor structure, function or number. In this initial study, we have examined DNA from leukaemic cells of 29 patients with AML, including three with FAB subtype M2 with deletion of an X or Y chromosome for evidence of gross rearrangement of this gene. We report that although the gene is highly polymorphic for a number of restriction enzymes, we have found no evidence of gross rearrangement in AML.
Leukemia 1992 Sep
PMID:Human GM-CSF receptor alpha-chain gene is highly polymorphic but not rearranged in AML. 138 92

The effect of an interleukin 1 receptor antagonist (IL-1ra) on the proliferation of acute myelogenous leukemia (AML) cells was investigated. The antagonist reduced the spontaneous clonogenicity of these cells as well as the clonogenicity of these cells subsequent to exposure to the antagonist. The effects of the IL-1ra on the clonogenicity of leukemia cells was observed even when the antagonist failed to inhibit DNA synthesis by the leukemia cell population as a whole. The data are consistent with the concept that the administration of IL-1ra subsequent to cytotoxic therapy has the potential of slowing the regrowth of leukemia cells thereby potentiating the effects of chemotherapy.
Leukemia 1992 Sep
PMID:Effects of an IL-1 receptor antagonist on acute myeloid leukemia cells. 138 93

We report two cases of secondary acute lymphoblastic leukemia (ALL) with t (4;11) (q21;q23) translocation occurring after chemotherapy and radiotherapy for a prior cancer. Seven previously published cases of secondary ALL with t (4;11) (q21;q23) are also reviewed. Most patients had received a combination of topoisomerase II inhibitors (anthracyclines, mitoxantrone, or the epipodophillotoxin derivatives VP16 or VM26) and cyclophosphamide, which have also been implicated in the pathogenesis of secondary acute myeloid leukemia (AML) with 11q23 rearrangements. These observations give further support to the existence of a subgroup of secondary acute leukemias with cytogenetic findings "specific" for de novo ALL and AML, especially those with translocations involving the 11q23 region.
Ann Hematol 1992 Sep
PMID:Secondary acute lymphoblastic leukemia with t (4;11): report on two cases and review of the literature. 139 Nov 25

We report a case of idic(X)(q13),r(X)(p22q13), and del(X)(:p11-->cen-->q11:) in a 71-year-old female patient with de novo acute nonlymphocytic leukemia (ANLL), FAB-M4. The abnormal X chromosomes of this patient were identified cytogenetically by G-banding technique and were further confirmed by fluorescence in situ hybridization (FISH) using an alpha-satellite probe to chromosome X centromere. The features of this are compared with other cases reported in the literature.
Cancer Genet Cytogenet 1992 Sep
PMID:Cytogenetic and FISH studies of abnormal X chromosomes in a patient with ANLL. 139 97

The karyotypes of 98 patients between the ages of 8 and 81 years with acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloid leukemia (CML) are presented. Although the well-described cytogenetic abnormalities associated with particular FAB subtypes in the West were observed, certain important local differences were noted. In ALL, hyperdiploidy was rarely observed, whereas the Philadelphia chromosome was observed in 50% of abnormal karyotypes. In AML, the t(8;21) was infrequently observed in M2 case, whereas trisomy 4 and 6, rarely reported elsewhere, formed 12% of the abnormal cases. In MDS, the incidence of -5/5q- and/or -7/7q- was 83% of cases with aberrant cytogenetic findings. Neither i(17q) nor an extra Ph was seen in 26 cases of CML including 9 cases of accelerated phase/blast crisis. In addition, previously unreported cytogenetic abnormalities occurring as single cases are presented. These findings are discussed in the context of geographical heterogeneity of chromosomal abnormalities in leukemia and emphasize the importance of continued epidemiologic studies of cytogenetics in hematologic malignancies.
Cancer Genet Cytogenet 1992 Sep
PMID:Cytogenetic analysis of hematologic malignancies in Hong Kong. A study of 98 cases. 139 2

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.
Bone Marrow Transplant 1992 Sep
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

Urinary excretion of parathyroid hormone-related protein (PTH-rP) was measured by radioimmunoassay in 25 patients with adult T-cell leukemia (ATL), in 68 patients with other hematologic disorders and in 13 asymptomatic individuals seropositive for human T-cell leukemia virus type I (HTLV-I). The mean levels of urinary PTH-rP in ATL patients with hypercalcemia (11.01 micrograms/g.Cr) were higher than in ATL patients with normocalcemia (5.16 micrograms/g.Cr). The mean levels in patients with acute type (8.84 micrograms/g.Cr), lymphoma type (4.18 micrograms/g.Cr) and crisis ATL (18.20 micrograms/g.Cr) were significantly higher than in urine of healthy controls. However, all asymptomatic carriers of HTLV-I and patients with chronic and smoldering ATL had normal urinary PTH-rP levels. In 7 patients with acute myelogenous leukemia, 1 patient with blastic crisis of chronic myelogenous leukemia and 3 patients with malignant lymphoma, the urinary levels of PTH-rP were above the normal range. Urinary levels of PTH-rP of the ATL patients with hypercalcemia correlated with the serum calcium levels. Urinary levels of PTH-rP of the all ATL correlated with serum lactic dehydrogenase level. These findings suggest that the measurement of urinary levels of PTH-rP is useful for evaluation of ATL and that some tumor cells of other hematologic diseases may produce PTH-rP.
Rinsho Ketsueki 1992 Sep
PMID:[Urinary excretion of parathyroid hormone-related protein in patients with adult T-cell leukemia and other hematologic disorders]. 143 36


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