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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cellular or proto-oncogenes are normal cellular genes important in normal cell growth and development. In some instances abnormal expression of these genes is associated with altered cell growth or with malignant transformation. Abnormalities of cellular oncogenes are common in human leukemias. These arise by multiple mechanisms such as mutation, translocation, amplification, and others. Sometimes more than one abnormality is present within a single oncogene. In other instances, a leukemia cell may contain abnormalities of several different oncogenes. Some oncogene abnormalities are relatively specific for certain leukemias and occur in almost all cases; examples include ABL in chronic myelogenous leukemia or MYC in Burkitt leukemia/lymphoma. Other abnormalities are also relatively specific but occur in only some cases such as NRAS in acute myelogenous leukemia or BCL2 in B-cell acute lymphoblastic leukemia. In other leukemias, such as most cases of acute lymphoblastic leukemia and chronic lymphocytic leukemia, oncogene abnormalities are uncommon. The precise role of oncogenes in the pathogenesis of human leukemia is unknown. Retrovirus transduced versions of some of the oncogenes modified in human leukemias cause leukemia in animals. Other oncogenes, modified or unmodified, transform animal and human hematopoietic cells in vitro. Some oncogene products are hematopoietic growth factors or growth factor receptors while others regulate cell proliferation or differentiation by diverse mechanisms. Disruption of the balance between these processes seems the most likely mechanism of oncogene related leukemogenesis. If the role of oncogenes in human leukemias can be defined, innovative diagnostic and therapeutic strategies may be forthcoming.
Leukemia 1990 Feb
PMID:Oncogenes and leukemia. 240 17

The cellular ets-1 gene homologous to the 5' region of the v-ets sequence of the E26 retrovirus codes for a 6.8-kb mRNA that is translated into a 51-kDa protein in human cells. A survey of mRNA from human tissues showed the thymus as the tissue with the highest level of ets-1 transcription, within other hematopoietic organs and tissues, including spleen, fetal liver, lymph nodes, bone marrow, and peripheral lymphocytes exhibiting low or undetectable levels of hybridization. A high level of ets-1 expression was found in murine thymocyte mRNA as well. Investigation of the ets-1 expression levels in human leukemic samples showed that primary malignant T cells (T-ALLs), corresponding to intrathymic stages of maturation, have a much higher level of ets-1 mRNA than malignant T lymphoid cells with a mature phenotype, such as adult T cell leukemias (ATLs). T-ALLs were also higher in ets-1 expression than the other lymphoid (pre-T-ALL, c-ALL, pre-B-ALL) malignant cells analyzed. Insignificant amounts of the specific ets-1 mRNA were detected in several acute myeloid leukemias representing various degrees of maturation. The elevated ets-1 mRNA in thymocytes suggests a biological role for the ets-1 product in these cells that could be explored to investigate ets-1 function. Finally, the exhibited expression of ets-1 in lymphoid cells and absence from malignant myeloid cells makes it a candidate marker for phenotyping human hematopoietic tumors.
Leukemia 1988 Jan
PMID:High expression of ets-1 gene in human thymocytes and immature T leukemic cells. 244 55

The presence of glucocorticoid receptors on the leukemic cells of 33 patients affected with acute lymphatic leukemia (ALL) and 6 patients affected with acute myeloic leukemia (AML) was investigated by dexamethasone-induced cytolysis and [3H] dexamethasone binding. The tests undertaken proved that after 20 hours of incubation 9 of 26 non-T-non-B-ALL (c-ALL and unclassified ALL) and 2 of AML were lysed with dexamethasone; blood lymphocytes and bone marrow leukocytes of healthy donors, however, were not affected. Non-T-non-B-ALL and AML were able to bind essentially more [3H] dexamethasone than T-ALL. There existed no correlation between dexamethasone binding and dexamethasone-induced cytolysis.
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PMID:[Detection of glucocorticoid receptors in leukemia cells by dexamethasone-induced cytolysis and [3H]-dexamethasone binding]. 245 4

54 patients affected with acute lymphatic leukaemia (ALL) in the period from 1978-1984 were examined concerning the frequency of pre-B-ALL in comparison with other immunological subtypes of ALL. For this purpose the following markers were tested: 1. Cytoplasmatic IgM 2. Rosette formation with sheep erythrocytes 3. T-cell specific antigen 4. C-ALL antigen 5. Surface immunoglobulin By means of these markers the patients were divided into 5 immunological subtypes of ALL, viz. 1. Pre-B-ALL (16.6%) 2. O-ALL (37.1%) 3. C-ALL (27.9%) 4. T-ALL (16.6%) 5. B-ALL (1.8%) The immunological subtypes of ALL were compared by means of clinical parameters (age, initial leukocyte number, mediastinal tumor, initial CNS involvement). No difference could be detected between O-ALL, pre-B-ALL and C-ALL, whereas T-ALL showed a distinctly worse prognosis.
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PMID:[Acute lymphatic leukemia with pre-B-cell characteristics]. 247

The interactions of five different lectins: peanut (PNA), lentil (LEN), wheat germ (WGA), soybean (SBA), Asparagus pea (FBP) with leukaemic cells obtained from 31 children: 25 with acute lymphoblastic leukaemia (ALL) and 6 with acute myeloblastic leukaemia (AML) were examined in this study. The relationship of lectin-binding ability to cells cytomorphological, cytochemical and immunological features and its potential clinical application were investigated. It has been shown that PNA and LEN receptors were found in the majority of blast cells. The SBA reacting cells were found only in few patients and FBP binding was not found in studied ALL and AML cells. There was a clear difference in the WGA binding capacity in ALL cells with L1 and L2 characteristics respectively. No differences were found in PNA. WGA and LEN reactivity between PAS negative and PAS positive leukaemic cells. Only PNA of all studied lectins seemed to differentiate T- from B-ALL blast cells. Only WGA binding of ALL cells showed the positive correlation to the risk index value.
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PMID:Binding of lectins to human leukaemic cells. 247 5

It has been found that kinetic parameters of proliferation in a dominating clone of bone marrow blast cells with Ia-positive and Ia-negative phenotype, as well as with expression of myeloid differentiating antigens (ICO-GM1 and ICO-G2), or in the absence of these antigens, do not significantly differ in children with subvariants MO-M4 of acute nonlymphoblastic leukemia, sensitive and resistant to the therapy. A higher rate of the bone marrow blast cell population growth and a lower effectiveness of the combined chemotherapy have been recorded in children with T-cell and pre-B-cell acute lymphoblastic leukemia as compared to acute lymphoblastic leukemia with the phenotype of blast cells that have only Ia-like or "common" antigens.
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PMID:[Comparative evaluation of blast cell proliferation and effectiveness of combined chemotherapy in children with different immunocytological subvariants of acute lymphoblastic and nonlymphoblastic leukemia]. 258 57

Ninety-four consecutive patients with acute leukaemia were analysed using cytochemical stains and, in selected individuals, a panel of monoclonal antibodies combined with measurement of the enzyme terminal deoxynucleotidyl transferase. These results were correlated with the French-American-British morphological classification. Acute non-lymphoblastic leukaemia was diagnosed in 55 individuals on the basis of morphology and cytochemical criteria; 6 of this group were further studied with antibodies directed against specific myelomonocytic antigens, but no further clinically useful information was obtained. Blasts from 36 patients did not stain with either Sudan black or myeloperoxidase. These individuals were considered to have acute lymphoblastic leukaemia (ALL) and were further assessed with monoclonal antibodies directed against epitopes expressed on cells of lymphoid lineage; 10 were classified as arising from T precursors; 23 were of B lineage, of which 13 marked as common, 6 as null, 1 as pre-B, 2 as B-ALL and 1 to have a pattern characteristic of lymphoblastic lymphoma. Two cases could not be classified and 1 was found to have megakaryoblastic features. In a further 3 patients who had undergone lymphoblastic transformation as a terminal event in the course of chronic granulocytic leukaemia, 2 were immunophenotypically common and 1 was marked as a null cell. This study confirms the value of monoclonal antibodies for accurately assigning lineage to the acute leukaemias and particularly in those situations where conventional morphological criteria and cytochemical markers are inconclusive.
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PMID:Immunophenotyping in the diagnosis and classification of acute leukaemia. 259 3

The acute lymphoblastic cell lines designated BAL-KHc and BAL-KHs were established from the peripheral blood of a Japanese female patient with a B-cell acute lymphoblastic leukemia. The BAL-KHc and BAL-KHs exhibited B-cell characteristics with positive cell markers for CD19, CD20, CD21 and HLA-DR antigens. Immunoglobulin with gamma and kappa chains was demonstrated on the cultured and fresh leukemia cells respectively. The cells lacked the Epstein-Barr virus genome and expressed abnormal chromosome constitutions including a t(8;14)(q24;q32). These results suggested that the cell lines present B-cell characteristics. The BAL-KHc cells showed different cell growth characteristics and cell surface marker profile compared to those of the BAL-KHs. These variations suggest that the BAL-KHc cells were probably frozen at a different stage of B-cell maturation from those of BAL-KHs, although both cell lines originated from the cells in the same peripheral blood sample of the patient.
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PMID:Human acute lymphoblastic leukemia cell lines with characteristics of intraclonal variation in B-cell differentiation stage. 270 74

A total of 25 evaluable adult patients with acute lymphoblastic leukaemia (ALL) were treated with an intensive chemotherapy regime modified from the L17/L17M protocol of the Sloan-Kettering Hospital. There were 18 men and 7 women; their median age was 36 years (range, 13-78). Seven cases had L1 morphology and 18, L2. The immunophenotype was common-ALL in 10, null-ALL in 9, T-ALL in 4 and B-ALL in 1. Of the 25 patients, 14 (56%) achieved a complete remission (CR). The causes of induction failure were partial remission (PR) only in 7 (28%) and hypoplastic death in 4 (16%). Of the 14 CR patients, 11 (78.6%) relapsed. Five patients developed CNS disease. The median disease-free survival and overall survival were only 9 and 13 months, respectively. As the follow-up periods of the surviving patients were short, late relapses may still occur and the overall treatment result is likely to be worse on longer follow-up. The possible causes of this disappointing result are discussed.
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PMID:Treatment of adult acute lymphoblastic leukaemia using an intensive chemotherapy protocol. 271 59

The incidence of childhood leukaemia in The Netherlands in the period 1973-1986 was studied by means of the DCLSG nationwide register, which lists all patients according to bone marrow slides classified in the DCLSG central laboratory. Acute lymphocytic leukaemia (ALL) accounted for 81% of cases, acute non-lymphocytic leukaemia (ANLL) for 13%, chronic myelocytic leukaemia (CML) for 2.5%, and acute unclassifiable leukaemia (AUL) for 3%. The peak incidence of ALL was at age 3, common-ALL and pre B-ALL comprising about 95% of the immunophenotypes at this age. Incidence rates for ALL remained stable between 1973 and 1978 at 2.85 cases per 10(5) children per year, exhibited a temporary increase between 1979 and 1984 to 3.60 and dropped back to the lower, previous level in 1985 and 1986. This rise was seen mainly among children in the 1-4 year age group, especially at age 3, and those with common-ALL and an initial WBC less than 5.0 x 10(9) l-1. Cumulative incidence rates per year of birth were fairly homogeneous up to age 6, except for the 1978 birth cohort which exhibited higher rates. Incidence rates for ANLL, CML and AUL remained stable over time. Changes in ascertainment, declining birth rates and a 50% decrease in childhood mortality, e.g. from infectious diseases, could not explain this temporary variation. Moreover, incidence rates in this survey appeared to be similar to those reported in various developed countries for the same period. As far as the aetiology of childhood common-ALL is concerned, therefore, the Dutch data appear to support the hypothesis of 'random mutation' as well as that of a limited role of environmental factors.
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PMID:Childhood leukaemia in The Netherlands, 1973-1986: temporary variation of the incidence of acute lymphocytic leukaemia in young children. 278 5


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