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)

Current views about the origin of acute lymphoid leukemia (ALL) emphasize the importance of maturation arrest at a precursor cell level. Recently, the CD22 antigen has been identified in the cytoplasm of normal bone marrow-borne immature B lineage cells, while the CD3 antigen (epsilon chain) has been detected within normal immature thymic blasts. In the first part our study performed on 100 cases of known acute leukemias, the expression of such cytoplasmic molecules, referred to as cCD22 and cCD3, was analyzed together with their appearance in the leukemic cells' membrane (mCD22 and mCD3). The presence of cCD22 in B-lineage ALL and that of cCD3 in T-ALL has indeed fully confirmed the diagnosis reached by other markers, and mCD22 and mCD3 were expressed on only a few cases of B- and T-lineage ALL, also revealing a degree of developmental asynchrony within leukemic blasts. In the subsequent analysis both cCD22 and cCD3 have been included in a standard panel of diagnostic reagents applied on 500 consecutive cases of acute leukemia. Here the aim was to analyze both the diagnostic precision of individual markers and the heterogeneity of various leukemic types in terms of the expression of membrane and intracellular antigens and their cytochemical features (Sudan Black B and esterases). It has been found that cCD22 and cCD3 are exquisitely specific for B-precursor ALL (TdT+, CD19+) and T-ALL (TdT+, CD7+), respectively, while both markers are absent in acute myeloblastic leukemia (AML) and acute myelomonocytic and monocytic leukemia (AMML/AMoL). These observations contrast the findings which demonstrate that 31% of cases among nonlymphoid acute leukemia (including AML and AMML) express CD7 and/or TdT. The study of myeloid antigens detected by CD13, CD33, and CD14 is also informative and complementary, both in diagnosing and subdividing the AML and AMML/AMoL groups. The peculiar main observation of this study is that only with the combined use of these markers in a microplate assay for membrane antigens, followed by double staining for intracellular antigens such as terminal deoxynucleotidyl transferase, cCD3, cCD22, c mu heavy chain, and T cell receptor beta, it is possible to safely establish the lineage affiliation and subgrouping of virtually all acute leukemias. Among these cases are those with aberrant combinations of markers, including 14% of B-lineage ALL (cCD22+,CD19+,TdT+) and a single case T-ALL (cCD3+,CD7+,TdT+), which exhibit CD13 and/or CD33 antigens, cases with mixtures of ALL and AML blasts, and 1.2% of acute leukemias which lack lineage affiliation and can be regarded as acute undifferentiated leukemia.
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PMID:The reliability of cytoplasmic CD3 and CD22 antigen expression in the immunodiagnosis of acute leukemia: a study of 500 cases. 246 63

The micronucleus test was applied in a group of 36 patients with malignant disease of the blood (acute lymphoblastic leukemia, ALL, and acute non-lymphocytic leukemia, ANLL) in order to evaluate to what extent it may be relevant for the efficiency of the cytostatic treatment. To this end, the test was applied at the onset of the disease (when diagnosed) and at different intervals after initiating the cytostatic therapy. Determination of the incidence of micronucleated cells and immature cells (blasts) at the two moments of the study established a correlation between the frequency of micronucleated cells and blast cells, the response to the anticancerous treatment and survival duration, the data obtained reflecting the prognostic value of the test in some malignant hemopathies.
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PMID:Micronucleus test applied in patients with acute leukemia, before and at different intervals during the cytostatic treatment. 253 Apr 46

Both S-100 antigen and calmodulin were shown in normal lymphocytes with S-100 being decreased in lymphocytic leukemia cells. Although small amounts of S-100 antigen and calmodulin were shown in acute myeloblastic leukemia cells, they could not be detected in normal granulocytes. In lymphoblastic leukemia, S-100 antigen levels in T-cell leukemia cells were higher than in B-cell leukemia cells, while calmodulin was decreased in chronic leukemia cells. In mitogen-stimulated lymphocytes, the levels of S-100 antigen were decreased, while those of calmodulin were either increased or unchanged. Calcium-dependent cyclic nucleotide phosphodiesterase was highest in acute lymphoblastic leukemia. These data suggest, therefore, that calcium ions may play a role in the proliferation, differentiation or leukemic change in lymphocytes and, hence, that measurement of calcium binding proteins may be useful in the investigation of leukemia cells or lymphocytes.
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PMID:S-100 antigen and calmodulin in human leukemic cells. 253 71

Retinoic acid receptor (RAR)-alpha mRNA expression was studied in a variety of myeloid leukemia cells with variable responsiveness to the induction of terminal differentiation by retinoic acid (RA). Cells from both the wild-type (wt), RA-responsive HL-60 promyelocytic leukemia cell line and a selected greater than or equal to 300-fold RA-resistant subline expressed approximately equal amounts of two RAR-alpha transcripts, 4.0 and 3.1 kb in size. In wt cells, the RAR-alpha did not change during induction of granulocyte differentiation by RA or macrophagic differentiation by 12-0-tetradecanoylphorbol-13-acetate (TPA). Relative to HL-60 cells, other cultured and fresh myeloid leukemia cells expressed 2.5-fold less to equal amounts of the RAR-alpha transcripts. The relative expression in six cases of acute promyelocytic leukemia (APL; two RA-responsive; one, previously treated with 13-cis-RA in vivo, equivocally RA-responsive) and one case of acute myelogenous leukemia (AML) with promyelocytosis (RA unresponsive) was 0.91 +/- 0.14 versus 0.53 +/- 0.14 for eight cases of nonpromyelocytic AML (p congruent to 0.001). Lymphoid leukemia cells expressed 2- to 5-fold less RAR-alpha mRNA. No qualitative variations in the mRNA transcripts were observed, although the 3.1 kb transcript was relatively decreased in three cases. The RAR-alpha gene was not amplified or detectably rearranged in any DNA source, although an apparent EcoRI restriction fragment length polymorphism was observed. It is concluded (a) that the steady-state level of RAR-alpha mRNA is not tightly correlated with natural responsiveness/unresponsiveness or, in some instances, acquired resistance to RA-induced differentiation and (b) that further studies are needed to determine if the mean 1.7-fold higher RAR-alpha mRNA level in APL cells could be an essential factor in the RA-responsiveness of APL cells, as primarily regulated at a different molecular level.
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PMID:Expression of retinoic acid receptor-alpha mRNA in human leukemia cells with variable responsiveness to retinoic acid. 255 72

We examined activities of procoagulant and fibrinolysis in homogenate of leukemic cells. Procoagulant activity (PCA) was increased in patients with acute myelocytic leukemia (AML) and acute promyelocytic leukemia (APL), but it was significantly decreased in patients with chronic myelocytic leukemia (CML) and adult T cell leukemia. In CML, PCA was increased in the blastic phase. Plasminogen activator activity (PLGAA) was also increased in patients with AML, APL and acute lymphocytic leukemia (ALL) associated with disseminated intravascular coagulation (DIC). Elastase-like activity, trypsin-like activity and chymotrypsin-like activity (CTLA) were increased in those with myelocytic leukemia, but they were low in those with lymphocytic leukemia. PCA, PLGAA and CTLA were significantly higher in patients with DIC than in those without DIC. Measurement of procoagulant and fibrinolytic activity in leukemic cells homogenate may be useful not only for studying hemostatic abnormalities but also for classification of leukemic cells.
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PMID:[Activity of procoagulant and fibrinolysis in homogenate of leukemic cells]. 259 44

The cytogenetic data of 77 patients (47 adults and 30 children) with myelodysplastic syndromes and acute non-lymphoid leukemia are evaluated with regard to the morphological types of leukemia and prognosis. The groups of the adult patients were found to be different in the frequency and types of non-random chromosome aberrations. In patients with secondary leukemias and mutagen-related leukemias the incidence of chromosomal abnormalities was higher than in those with the idiopathic form of the disease. Specific abnormalities were total or partial loss of chromosome 5 and/or 7, and an additional chromosome 8. In contradistinction to these the patients with primary leukemias had specific translocations associated with pseudodiploidy. We found the frequency of aberrations in adults exposed to mutagen agents similar to that in children with ANLL, but the types of aberrations were similar to those of adults without any exposition. Comparing the median duration of remission and survival of patients' groups with different cytogenetic findings we found the chromosome aberrations to be of prognostic value. The present data demonstrate the usefullness of cytogenetic investigations in the diagnosis of the disease and in morphological and etiological classification of patients.
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PMID:[Clinical significance of chromosome number deviations in myelodysplastic syndromes and in acute non-lymphoid leukemia]. 265 51

The distribution of acute leukemia according to type was examined in Japanese children by three surveys: (1) a review of bone marrow slides of 81 cases diagnosed as acute myelogenous leukemia between 1964 and 1976; (2) a prospective study of 97 cases observed since 1977, and (3) a study of 8108 cases registered with the Children's Cancer Registry of Japan from 1969 to 1984. The results indicate that the ratio of acute lymphocytic leukemia to non-lymphocytic leukemia in Japan is not different from that in other countries.
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PMID:Acute non-lymphocytic leukemia is not a major type of childhood leukemia in Japan. 271 49

Fibrinopeptide A (FPA) was systematically investigated in 74 patients with acute leukaemia at different stages of the disease (50 with non-lymphocytic leukaemia, ANLL; 24 with lymphocytic leukaemia, ALL). At diagnosis, 75% of the cases had high FPA levels (86% in ANLL and 54% in ALL) with significantly higher levels in ANLL than in ALL (13.4 vs 4.4 ng/ml; p less than 0.001). Patients with DIC (20 cases in ANLL and 1 case in ALL) had significantly higher levels (p less than 0.001). FPA levels were neither correlated with fibrinogen or FDP levels nor with blast cell count. During chemotherapy, median FPA did not show significant changes whereas, at the end of therapy, a return toward normality was generally observed both in ALL and ANLL apart from the group of patients with acute promyelocytic leukaemia. Among the 24 patients who entered post-remission follow-up (13 ANLL and 11 ALL), 10 cases out of the 11 relapsing (6/6 with ANLL and 4/5 with ALL) had increased FPA 1 to 2 months before the ascertainment of the relapse. However, 16% and 9% of the samples obtained on different occasions, respectively from ANLL and ALL cases in maintained first remission, showed FPA above the normal limit. This study demonstrates that subclinical activation of blood coagulation, as indicated by high FPA level, is common both in lymphocytic and non-lymphocytic leukemia and suggests that this phenomenon is related to disease activity.
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PMID:Clinical significance of fibrinopeptide A in acute lymphocytic and non-lymphocytic leukaemia. 276 77

We studied the risk of the development of acute myeloid leukemia (AML) during initial remission in 733 consecutive children with acute lymphoid leukemia (ALL) who were treated with intensive chemotherapy. This complication was identified according to standard morphologic and cytochemical criteria in 13 patients 1.2 to 6 years (median, 3.0) after the diagnosis of ALL. At three years of follow-up, the cumulative risk of secondary AML during the first bone marrow remission was 1.6 percent (95 percent confidence limits, 0.7 and 3.5 percent); at six years, it was 4.7 percent (2 and 10 percent). The development of secondary AML was much more likely among patients with a T-cell than a non-T-cell immunophenotype (cumulative risk, 19.1 percent [6 and 47 percent] at six years). Sequential cytogenetic studies in 10 patients revealed entirely different karyotypes in 9, suggesting the induction of a second neoplasm. In eight of these patients, the blast cells had abnormalities of the 11q23 chromosomal region, which has been associated with malignant transformation of a pluripotential stem cell. There was no evidence of loss of DNA from chromosome 5 or 7, a karyotypic change commonly observed in cases of AML secondary to treatment with alkylating agents, irradiation, or both. We conclude that there is a substantial risk of AML in patients who receive intensive treatment for ALL, especially in those with a T-cell immunophenotype, and that 11q23 chromosomal abnormalities may be important in the pathogenesis of this complication.
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PMID:Secondary acute myeloid leukemia in children treated for acute lymphoid leukemia. 274 49

Sweet's syndrome is known often to associate with non-lymphocytic leukemia (ANLL); however, there have been very few reports of Sweet's syndrome associated with myelodysplastic syndrome (MDS). It was reported that improvement and exacerbation of these two syndromes occurred simultaneously. We present here a 49-year-old male with Sweet's syndrome developed in RAEB in T. He complained of fever and infiltrative eruptions on the trunk and legs. At the time of admission to Tsukuba University Hospital, the peripheral blood showed leukocytopenia (WBC 2,000/microliter: Blast 9%, PMN 51%) and anemia (Hb 6.5 g/dl). Pseudo-Pelger anomaly of neutrophils was found on the blood smear. From the hematological findings and the result of skin biopsy, the patient was diagnosed as having MDS (RAEB in T) complicated by Sweet's syndrome. Prednisolone was effective to improve his fever and eruptions. However, when treated with low-dose Ara-C and when transformed into acute myelogenous leukemia, there was no correlation between the condition of Sweet's syndrome and the percentages of blasts in the marrow. We suggest that eruptions of Sweet's syndrome associated with MDS are not always a good index of exacerbation of MDS.
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PMID:[Appearance of Sweet's syndrome in a patient with myelodysplastic syndrome (MDS) without relation to the hematological findings of MDS]. 279 96


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