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At least 19 recordsLinked to original sources

PubMed1978

Spontaneous and induced preleukemia cells in C57BL/6 mice:brief communication.

A transplantation bioassay method was used to verify the presence of preleukemia cells in C57BL/6 mice shortly after leukemogenic treatment or in relation to age increase. Preleukemia cells were identified mainly among bone marrow cells of old C57BL/6 mice or within 10 to 30 days after leukemogenic treatment of young mice with radiation-induced leukemia virus variants, fractionated doses of irradiation, or 7,12-dimethylbenz[a]anthracene (DMBA), although the overt disease did not occur until many months later. Mice could carry preleukemia cells without necessarily developing overt leukemia. Since the leukemogenic agents used in the present studies induced T-leukemias, the role of the thymus in the induction of preleukemia cells was tested. Thymectomy affected viral transformation but did not diminish the number of preleukemia cells induced by DMBA or X-ray.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1978

Detection of cytochemical and morphological anomalies in 'preleukemia'.

The present investigations confirm and extend previous reports on the occurrence of cytochemical anomalies among the hemopoietic cells in preleukemia. The cytochemical patterns of the hemopietic cells obtained from 19 patients suffering from a preleukemic disorder have been studied. The diagnostic value of the cytochemical examination using a panel of 10 different tests is emphasized. In a prospective study in 17 out of 25 patients, preleukemia had been correctly diagnosed. In 4 patients leukemia developed within 2-4 months from the diagnosis ('imminent leukemia'), in 13 patients leukemia or smouldering leukemia developed between 4 and 25 months after the diagnosis ('true preleukemia'). The cytochemical profiles of the hemopoietic cells of the latter have been compared with those of 14 patients suffering from aplastic anemia. In preleukemia the blasts did not exceed 3% of the nucleated bone marrow cells. The clinical value of the diagnosis 'preleukemia' is discussed as well as the prognosis and the possible therapeutic approaches.

Adult↗

PubMed1980

Human preleukemia.

Preleukemia refers to the syndrome of hematopoietic dysfunction seen in some patients before typical features of acute myelogenous leukemia develop. Clinically, preleukemia is characterized by variable degrees of pancytopenia, with associated symptoms due to decreased circulating blood elements. The bone marrow is usually hypercellular, and there are prominent morphologic abnormalities in erythroid precursors and more subtle changes in megakaryocytes and granulocyte progenitors. During this phase of the leukemic process, the neoplastic clone is usually already established and predominant. A clear distinction should be made between the preleukemic syndrome and diseases that predispose to development of acute myelogenous leukemia. Preleukemia, like acute myelogenous leukemia, is a clonal hematopoietic stem cell neoplasm manifested functionally by abnormal hematopoietic cell maturation and ineffective hematopoiesis. During the course of preleukemia, precursor cell maturation becomes progressively impaired with termination in the severe maturational block characteristic of acute myelogenous leukemia. We favor the concept that preleukemia is an early phase of acute myelogenous leukemia.

Bone Marrow↗

PubMed1986

Effects of marrow grafting on preleukemia cells and thymic nurse cells in C57BL/Ka mice after a leukemogenic split-dose irradiation.

A split-dose regimen of whole-body irradiation (4 X 175 rad at weekly intervals) induced thymic lymphomas in C57BL/Ka mice after a latent period of 3-9 months. Meanwhile, preleukemia cells arose in the thymus and bone marrow and persisted until the onset of lymphomas. Simultaneously, thymic lymphopoiesis was impaired; thymocyte numbers were subnormal and thymic nurse cells disappeared in a progressive but irreversible fashion. The depletion of these lymphoepithelial complexes, which are normally involved in the early steps of thymic lymphopoiesis, was related to altered prothymocyte activity in bone marrow and to damaged thymic microenvironment, perhaps as a consequence of the presence of preleukemia cells. The grafting of normal bone marrow cells after irradiation prevented the development of lymphomas. However, marrow reconstitution did not inhibit the induction of preleukemia cells. They disappeared from the thymus during the second part of the latent period. At the same time, thymic lymphopoiesis was restored; thymocytes and nurse cell numbers returned to normal as a consequence of the proliferation of grafted marrow-derived cells within the thymus. The results thus demonstrated an intimate relationship between preleukemia cells and an alteration of thymic lymphopoiesis, which particularly involved the nurse cell microenvironment. Some preleukemia cells in marrow-reconstituted, irradiated mice derived from the unirradiated marrow inoculate. Thus these cells acquired neoplastic potential through a factor present in the irradiated tissues. The nature of this indirect mechanism was briefly discussed.

Animals↗

PubMed1976

Comparative electron-microscopic study of the erythrocytic line in refractory anemia (preleukemia) and myelomonocytic leukemia.

The bone marrow erythrocytic precursors of 12 patients with refractory anemia (preleukemia) or myelomonocytic leukemia were studied by transmission electron microscopy. The results were tabulated in a semiquantitative manner and a comparison was established between the two main diagnostic groups. The following results are reported. 1. Similar nuclear and cytoplasmic abnormalities of the normoblasts were observed in preleukemia and leukemia. 2. A nuclear lesion consisting of nuclear clefts and blebs was demonstrated in at least some of the normoblasts in all of the patients. Although not specific, this finding appears to be a new contribution in the field of preleukemia and myelomonocytic leukemia. 3. Iron overload, including the presence of pathologic sideroblasts, is common to both preleukemia and leukemia.

Bone Marrow↗

PubMed2000

[Study on clinical and laboratory features of preleukemia patients].

OBJECTIVE: To explore prospective diagnostic criteria for preleukemia. METHODS: A case control study of the discrepancies of clinical and laboratory features between patients with preleukemia and those with chronic aplastic anemia (CAA) or atypical paroxysmal nocturnal hemoglubinuria (a-PNH). RESULTS: There were eight variables of significance: (1) lymphocytoid micromegakaryocytes in marrow; (2) immature granulocytes in peripheral blood; (3) >or= 2% myeloblasts in marrow; (4) positive periodic acid schiff (PAS) staining of nucleated erythrocytes; (5) myeloid differentiation index >or= 1.8; (6) clonal karyotypic abnormalities; (7) negative sister chromatid differentiation; (8) > 4.0 cluster/colony ratio of granulocyte-macrophage colony-forming units (CFU-GM). The following criteria was assigned: A: To meet (1) and at least two of the other seven variables; B: To meet at least four of the eight variables. All of the patients with preleukemia met A or B and none of the patients with CAA or a-PNH did. CONCLUSION: Preleukemia is different from CAA or a-PNH. It has its own clinical and laboratory features, which may be useful for prospective diagnosis.

Adolescent↗

PubMed2002

Clinical and laboratory features of preleukemia patients.

OBJECTIVE: To explore prospective diagnostic criteria for preleukemia. METHODS: A case control study was done comparing the discrepancies on clinical and laboratory features between patients with preleukemia and those with chronic aplastic anemia (CAA) or atypical paroxysmal nocturnal hemoglubinuria (a-PNH). RESULTS: There were eight variables of significance: (1) lymphocytoid micromegakaryocytes in the bone marrow; (2) immature granulocytes in the peripheral blood; (3) > or = 2.0% myeloblasts in the bone marrow; (4) positive periodic acid schiff (PAS) stained nucleated erythrocytes; (5) myeloid differentiation index > or = 1.8; (6) typical colonal karyotypic abnormalities; (7) negative sister chromatid differentiation; (8) cluster/colony ratio of granulocyte-macrophage colony-forming units (CFU-GM) > 4.0. The following criteria were assigned: A: to meet variable one and at least two of the other seven variables and B: to meet at least four of the eight variables. All of the patients with preleukemia met either A or B and none of the patients with CAA or a-PNH did. CONCLUSIONS: Preleukemia is different from CAA or a-PNH. It has its own clinical and laboratory features, which may be useful for its prospective diagnosis.

Adolescent↗

PubMed1990

[Role of hemopoietic stem cells and progenitor cells in preleukemia].

Cases of myelodysplastic syndrome (MDS) that have evolved into overt leukemia may be retrospectively termed preleukemia. Studies with X-chromosomal markers in females strongly suggest that preleukemia originates from transformation of a very early hemopoietic stem cell. Growth characteristics of myeloblasts in preleukemia indicate that some of the cases already represent early stages of acute leukemia. In other preleukemias clonal evolution towards overt leukemia can be observed. This apparently involves neoplastic transformation of a granulocytic determined progenitor cell.

Colony-Forming Units Assay↗

PubMed1979

[Bone marrow culture in aplastic anemia and preleukemias].

After incubation of bone marrow cells obtained from normal subjects and patients with pancytopenia in the double layer agar culture (Robinson-Pike), the clusters of different size and the colonies were counted on days 2, 3, 5, 7 and 10. Aplastic anemia and two types of preleukemia could be distinguished by a different growth pattern. A high incidence of small clusters (4-12 cells) was found in patients with aplastic anemia on days 2 and 3, whereas these aggregates were markedly reduced in preleukemia of type B. In preleukemia of type A an excessive number of small clusters was obtained. The morphology of cells in clusters and colonies was studied by cytochemical staining and electronmicroscopy. In preleukemia marked defects of maturation were demonstrable in the cells.

Anemia, Aplastic↗

PubMed1976

Proliferative behavior of hemopoietic cells in preleukemia and overt leukemia observed in one patient.

Hemopoietic cell proliferation was studied in a patient suffering from preleukemia characterized by peripheral pancytopenia and hypercellular bone marrow with ineffective erythropoiesis. Two years later when overt acute myelogenous leukemia had developed the study was repeated. The kinetics of proliferation were investigated by a new method which allows evaluation of the rate and time of DNA synthesis in individual morphologically defined cells. Erythropoiesis was found ineffective to the same degree in both stages of disease. The rate of erythroid cell proliferation, however, was reduced in overt leukemia only. The myeloid system showed a grossly reduced production rate of myeloblasts in preleukemia whilst the same parameter was strongly increased in leukemia. This high production rate of myeloblasts in overt leukemia was interpreted as indication of a far-reaching self-maintenance of the myeloblast pool in this stage of disease. The proliferative activity of the individual myeloblasts was reduced already in preleukemia, and even more so in leukemia. In order to explain the amplification of the myeloblast pool with the onset of overt leukemia a change in the mode of myeloblast divisions is assumed. For this a transition from steady state to some degree of exponential growth gives the most plausible explanation.

Aged↗

PubMed1983

Partial myeloperoxidase deficiency in preleukemia.

In seven subjects with partial and apparently acquired form of myeloperoxidase (MPO) deficiency, some functional properties of neutrophils (PMNs) were studied. Five patients suffered from preleukemia, one from diabetes mellitus and one from carcinoma of the breast with bone marrow metastases. Intracellular bactericidal activity, oxygen consumption and superoxide radical production were within normal limits. In three patients with preleukemia, the serum opsonic activity was markedly reduced (less than m-3SD) in an autologous system, but normal in the presence of pooled normal serum. Decreased opsonic activity was also found when these patient's sera were assayed in the presence of normal PMNs. Since the levels of IgG and C3 were comparable in the patients' sera and the pooled serum, a deficiency of another unknown opsonin or the presence of an opsonization inhibitor has to be postulated. The partial MPO defect apparently doesn't decrease the intracellular killing of Staphylococcus aureus by PMNs. The known susceptibility to bacterial infections in preleukemia may be explained by the reduction of serum opsonization conducing to a secondary decrease of the ingestion and killing of bacteria by the PMNs.

Blood Bactericidal Activity↗

PubMed1979

[A prospective study on course and prognostic criteria in "preleukemia" (author's transl)].

The natural course of disease was followed in 33 patients with so-called preleukemia by a prospective multicentric protocol. Patients with the following criteria were included: Anaemia with granulocytopenia and/or thrombocytopenia, normal or increased cellularity of the bone marrow and exclusion of a known diagnosis of underlying disease. Follow up after assumption of "preleukemia" was 3 years or more. Median survival was 26 months after diagnosis of preleukemia and 36 months after the first unequivocal symptoms of the blood dyscrasia. 40% of the patients changed to the picture of leukemia within 2 years. The most important parameters suggesting subsequent transition to overt leukemia where chromosomal abberations and an increased blast count of the bone marrow.

Acute Disease↗

PubMed1984

A complicated but nonrandom karyotype in preleukemia.

A patient with preleukemia who possessed a complicated hypodiploid karyotype in 100% of bone marrow cells is described. The clinical, hematologic, and cytogenetic features showed a marked similarity to a patient with preleukemia described by Watt et al. [1]. Both patients terminated their disease in acute nonlymphocytic leukemia. Another patient with similar cytogenetic features, but who presented in the acute leukemic phase of polycythemia rubra vera, also is described. All three patients possessed a translocation involving chromosome #11 at band p15. This, together with many numerical and structural abnormalities, particularly those involving chromosomes #5, #7, and #17, may prove useful in defining a variety of preleukemia with a poor prognosis.

Aged↗

PubMed1985

Deletion of chromosome band 13q14: a primary event in preleukemia and leukemia.

Chromosome abnormalities were analyzed in 200 consecutive patients with preleukemia and leukemia, and four patients were found with a deletion of 13q14 for an incidence of 2%. Together with data on chromosome aberrations in cancer from the literature, our results indicate clearly that deletion of band 13q14 is a nonrandom chromosome anomaly in premalignant and malignant blood disorders. Deletion of 13q14 appears specifically to constitute a primary event in the initiation of preleukemia. An additional rearrangement involving another chromosome must occur for progression of the preleukemia to acute nonlymphocytic leukemia.

Acute Disease↗

PubMed1987

Translocations and deletions with breakpoint on 21q are nonrandomly associated with treatment-related acute nonlymphocytic leukemia and preleukemia.

Six of 70 (8.6%) consecutive cases with therapy-related acute nonlymphocytic leukemia (ANLL) or preleukemia had a translocation or deletion with a breakpoint on 21q. Such aberrations were seen in only one of 200 (0.5%) consecutive cases of de novo ANLL examined at our laboratory. The figures reflect a 17.1-fold increased incidence of 21q aberrations in therapy-related ANLL or preleukemia, compared with ANLL de novo. The difference is highly significant (p = 0.003). The increased incidence of 21q aberrations in therapy-related myelodysplastic syndromes was confirmed by literature studies. Band 21q22 was most often involved. Cases with t(8;21), which is strongly associated with the M2 variant of ANLL, or cases with i(21q), which is supposedly due to a centromeric misdivision, were not included in the count. It is concluded that the 21q aberrations are associated with treatment-related ANLL or preleukemia with at least the same degree of specificity as aberrations of #5 and #7.

Acute Disease↗

PubMed1981

Preleukemias.

A chromosomally abnormal clone is demonstrable in the bone marrow of a significant number of patients with hemic disorders that carry an increased risk for the subsequent development of leukemia. These "preleukemia" states include a variety of cytopenias, myeloproliferative disorders, and childhood syndromes. The cytogenetic alterations that occur nonrandomly in these dyscrasias are often similar to those observed in acute nonlymphocytic leukemia and in the accelerated phase of chronic granulocytic leukemia: monosomy for chromosome 7; trisomy for 8,9,21, and the long arm of 1(1q); deletions of 5 and 20 (5q-, 20q-); and an isochromosome derived from 17 (iso 17q). These findings support the view that despite clinical differences, these various preleukemic disorders are all characterized by the presence in the hematopoietic tissues of a clone of cells derived from an altered hemic stem cell. Furthermore, the data suggest that preleukemia, chronic leukemia, and acute leukemia may be fundamentally similar diseases, differing primarily in the rate at which the aberrant clone is expanding. Chromosome studies may be of prognostic value in the cytopenic preleukemias. Patients with abnormalities show a decreased survival and are at increased risk for progression to acute nonlymphocytic leukemia. In the myeloproliferative disorders and the preleukemic childhood disorders, cytogenetic alterations are not clearly predictive, and aberrant clones may persist for years without clinical progression.

Blood Cells↗

PubMed1992

Genetic lesions in preleukemia.

Preleukemia is thought to be a clonal disorder of hemopoietic stem cells. The conversion of a normal cell into a preleukemic and ultimately leukemic state is a multistep process requiring the accumulation of a number of genetic lesions. The myelodysplastic syndromes have become a paradigm for human preleukemia, where nonrandom chromosomal abnormalities, including complete or partial deletions of chromosomes five and seven, trisomy eight and Y chromosome loss suggest specific changes. Of particular significance are 5q deletions, as many genes important in hemopoiesis are located in this region, including the proto-oncogene FMS, which encodes the receptor for the macrophage colony-stimulating factor, CSF-1. Genetic damage such as point mutations in the RAS and FMS genes has been detected in preleukemia patients. The RAS gene family (N, K and H) encodes membrane-bound G proteins, which, like other proto-oncogenes, are components of the intracellular signal transduction pathways controlling mitogenesis and differentiation. The characterization of such lesions may ultimately identify those patients at greatest risk of leukemic transformation.

Chromosome Aberrations↗

PubMedDate not supplied

Feline preleukemia: an animal model of human disease.

In man, hematologic abnormalities precede the development of acute myeloblastic leukemia in about one-third of individuals. This preleukemic state may represent a stage of adult leukemia wherein small numbers of leukemic cells are present and the normal marrow stem cell compartment has not been seriously compromised. A syndrome resembling human preleukemia occurs in cats infected with feline leukemia virus (FeLV). This disorder is characterized by anemia, leukopenia or thrombocytopenia occurring weeks or months prior to the development of feline acute leukemia. The natural occurrence of this syndrome in this domestic animal population makes it a potential model of human preleukemia. Initial poor results of therapy of human preleukemia presently prohibit one from carrying out controlled trials with chemotherapeutic agents in such a group of patients. Preliminary trials with chemo- and/or immunotherapy may be more easily attempted with FeLV infected preleukemic cats.

Animals↗