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PubMed1992

[Gene diagnosis and successful reversion in a patient with preleukemia].

According to the FAB classification, a patient (case 1) could not be diagnosed as MDS-RA, although she had clinical features of MDS, as compared with another patient (case 2) who was diagnosed as RAS and had abnormal karyotype (20q- and 5q-) of bone marrow (BM) cells. BM cells of the two patients were SCD (sister chromatid differentiation) negative. Rearrangement of c-erbB and c-erbA was found in the genome of the BM cells in both patients, when southern blot hybridization was performed with probe v-erbB+A. Therefore, case 1 could be diagnosed as preleukemia. During a period about 3 years of treatment with the drug stanozolol in case 1 there was good effect and successful reversion was obtained. She had then normal hematologic and cytogenetic patterns of BM and PB and the rearrangement of c-erbB of BM cells also disappeared. She has worked for two years since then. The mechanism of effective treatment and successful reversion was discussed briefly. Probe v-erbB was shown to be useful in investigation of gene diagnosis of preleukemia or MDS (shown elsewhere).

Adult↗
PubMed1992

Leukemia: stem cells, preleukemia and cure.

Several new or evolving concepts of leukemia biology and treatment are considered including: most leukèmias result from transformation of a stem cell, their phenotype reflecting the site of clonal expansion rather than transformation; most leukemias are preceded by one or more preleukemia phases; and cure may be possible by re-establishing preleukemia or forcing maturation of leukemia cells.

Cell Transformation, Neoplastic↗
PubMed1989

[Childhood hypoplastic preleukemia].

Aplastic anemia preceeding acute leukemia is known as hypoplastic preleukemia, which tends to be more frequently evolved into acute lymphoblastic leukemia, whereas myelodysplastic preleukemia are specific for acute myelocytic leukemia. More than forty cases had been reported in the literatures. Here we report a 11-year-old boy who was initially diagnosed as aplastic anemia and treated with prednisolone and androgen with prompt response terminated into overt acute lymphoblastic leukemia.

Anemia, Aplastic↗
PubMed1988

Point mutation of the ras protooncogenes and chromosome aberrations in acute nonlymphocytic leukemia and preleukemia related to therapy with alkylating agents.

Nine cases of overt acute nonlymphocytic leukemia and four cases of preleukemia or a myelodysplastic syndrome, all related to intensive treatment with alkylating agents, were studied cytogenetically and investigated using a rapid and sensitive dot blot screening procedure for point mutations in the Ha-ras, Ki-ras, and N-ras protooncogenes within codons 12, 13, and 61. The technique involves a selective amplification of genomic DNA sequences containing the codon sequence of interest, in combination with oligonucleotide hybridization. Examining fractionated mononuclear cells from bone marrow or peripheral blood, an N-ras mutation at position 13 was observed in one patient with overt leukemia, resulting in a base change from GGT to TGT thus converting glycine to cysteine. The other cases exhibited no ras gene mutations. It is surprising that c-ras mutations are only occasionally observed in overt acute nonlymphocytic leukemia related to treatment with alkylating agents, as such abnormalities have often been observed in acute nonlymphocytic leukemia de novo, and as many alkylating agents are known to produce DNA adducts leading to point mutations and substitution of single amino acids. The fact that deletions of varying parts of the long arms of chromosomes 5 and 7 are observed in most cases of therapy-related acute nonlymphocytic leukemia and preleukemia, as confirmed by our own series of 71 patients, suggests that loss of heterozygosity for specific alleles on the two chromosomes, rather than activation of a protooncogene, could be an important step in leukemogenesis.

Acute Disease↗
PubMed1988

[Induction of myelogenous differentiation: a therapeutic possibility for preleukemia and acute leukemia?].

Human acute myelogenous leukemia often arises from a transformation at the stem cell level leading to a block in differentiation. The malignant cell, therefore, remains in the proliferative pool and rapidly accumulates. In preleukemia, also known as myelodysplastic syndromes, the malignant clone is already established, leading to disturbed hematopoiesis. One therapeutic approach, therefore, might be to overcome this block in differentiation and thus shift the cell from the proliferative into the differentiating pool. For several years now research in leukemia has focused on study of the proliferation and differentiation of normal and leukemic hematopoietic cells. Numerous substances have been identified which are able to trigger differentiation in myeloid cells, including the retinoids, vitamin D, tumor necrosis factor and hematopoietic hormones. The possible role of these agents in the treatment of preleukemia and acute myelogenous leukemias is discussed.

Cell Differentiation↗
PubMed1986

Marrow transplantation in preleukemia.

Preleukemia has generally been treated by palliative measures. Several reports have indicated that cytarabine given as low-dose infusion results in responses, albeit short lived, in a fraction of patients. We have shown recently that marrow transplantation offers a useful alternative. Twelve patients have been treated and followed for a minimum of 1 year. Three were conditioned with cyclophosphamide (CY) only, and all died with recurrent or persistent disease. Nine were conditioned with CY and total-body irradiation; all but 1 had lasting engraftment, and 7 are surviving, free of disease, 16-36 (median 27) months after transplantation. These data show that marrow transplantation can provide successful therapy for preleukemia.

Adolescent↗
PubMed1982

Abnormal erythroid progenitor cells in human preleukemia.

Ten patients with preleukemia were studied by the erythroid cell clonal culture technique. In nine of these patients, erythroid colonies derived from peripheral blood BFU-E were not observed, while the other patient had markedly decreased peripheral blood BFU-E-derived erythroid colonies in vitro. In three patients, marrow cells were also cultured and no BFU-E-derived erythroid colonies were detected. These studies indicate that immature erythroid progenitor cells, BFU-E, in patients with preleukemia are either markedly decreased in number or grossly defective in their proliferative or differentiative capacities.

Adult↗
PubMedDate not supplied

Recognition of preleukemia.

Preleukemia, which can only be diagnosed retrospectively with certainty, presents multiple findings and clinical data which contribute to a pattern recognition process. The development of cytogenetic and marrow culture studies has not only provided additional criteria for diagnosis but also better indices of prognosis. Preleukemia can be considered to be an early expression of neoplastic disease that merges into smoldering leukemia and progresses to acute leukemia. However, in the prospective evaluation of a patient, the term hemopoietic dysplasia should be used since there are no criteria to predict the outcome in an individual case.

Acute Disease↗
PubMed1976

Myelopoietic cell proliferation in granulocytopenia of refractory anaemia and preleukemia states with hyper-plastic bone marrow.

Myelopoiesis in healthy subjects and in 8 cases of refractory anaemia or preleukemia states was studied by the combined cytophotometric-autoradirgraphic method. Granulocytopenia was present in 7 of 8 cases. The results can be summarized as follows: 1. Mature myelocytes of healthy persons are a mainly differentiating cell population with a low labelling index (3-10%) and a high incidence in G1-Phase. 2. The proliferating immature granulopoietic cells of the patients with neutropenia showed a reduced labelling index with 3H-thymidine as a result of an arrest of these cells in G1 (6 of 8 cases). 3. A similar result was obtained in the study of the hyperplastic myelopoiesis of an other patient with preleukemia and normal granulocyte count in peripheral blood, with the disturbance of cell proliferation preceding the symptom neutropenia. 4. Finally in only one case an increased frequency of myelopoietic cells in G2-phase was found suggesting an arrest of cell proliferation in the premitotic phase.

Adult↗
PubMed2005

Myelodysplastic/myeloproliferative disease with erythropoietic hyperplasia (erythroid preleukemia) and the unique translocation (8;9)(p23;p24): first description of a case.

We report on a patient fulfilling the diagnostic criteria of unclassifiable myelodysplastic/myeloproliferative diseases with prominent erythropoietic hyperplasia/dysplasia (erythroid preleukemia) and the unique translocation (8;9)(p23;p24). The patient presented with B-symptoms, erythroblastemia, thrombopenia, marked eosinophilia, presence of myeloid precursors in the peripheral blood, and decreased erythropoietin level. Nodular peritrabecular polymorphous blasts, dysplastic megakaryocytes, and a diffuse argyrophilic fibrosis were detected in the trephine bone marrow biopsy. Immunohistochemically, the blasts stained positively for glycophorin C and hemoglobin A; the proliferation fraction was nearly 90% in the Ki-67 stain. Expression of the phosphorylated Janus kinase 2 was detected in almost all megakaryocytes and in isolated erythroblast islets, suggesting a probable activation of Janus kinase 2, the jak-2 gene being mapped on 9p24. Ten months after initial diagnosis, the disease progressed to frank acute erythroid leukemia. We report for the first time a myelodysplastic/myeloproliferative disease (erythroid preleukemia) accompanied by the specific chromosomal aberration t(8;9)(p23;p24), distinct histopathology, and clinical and laboratory symptoms, and progress to acute erythroid leukemia.

Biopsy↗
PubMed1984

Acute nonlymphocytic leukemia, preleukemia, and acute myeloproliferative syndrome secondary to treatment of other malignant diseases. II. Bone marrow cytology, cytogenetics, results of HLA typing, response to antileukemic chemotherapy, and survival in a total series of 55 patients.

Secondary acute nonlymphocytic leukemia or its earlier stages, preleukemia or an acute myeloproliferative syndrome with refractory cytopenia and clonal cytogenetic abnormalities of the bone marrow, was diagnosed in 55 patients previously treated for other malignant diseases. In patients with overt leukemia, cytologic, and cytochemical studies showed predominance of the French-American-British (FAB) type M2. Cytogenetic examination demonstrated a normal karyotype in 11 cases, whereas clonal abnormalities were observed in 44 patients. Defects of chromosome 7 were observed in 24 cases, most often -7, and defects of chromosome 5 in 14 cases, most often 5q-. In addition, chromosomes 3 and 17 were possibly nonrandomly involved. Other abnormalities commonly observed in de novo acute nonlymphocytic leukemia as t(8;21) and t(15;17) were not observed and +8 rarely seen in secondary leukemia. The survival from the leukemic complication was short for the whole group of 55 patients (median, 7 months). However, a significantly longer survival was observed in a subgroup of 11 patients with a normal karyotype (P less than 0.01), due to a favorable response to antileukemic chemotherapy, and in a subgroup of 11 patients with -7 or -C as the only cytogenetic abnormality (P less than 0.01), due to a prolonged preleukemic phase, compared with the remaining 33 cases with mostly multiple karyotypic abnormalities. Three preleukemic patients with -7 who were studied during transformation to overt leukemia all developed additional cytogenetic abnormalities. According to the two-step or multistep hypothesis for malignant transformation, the prolonged preleukemic course in patients with -7 as the only abnormality could represent a premalignant stage, in which further evolution is required for development of overt leukemia. The patients showed a random distribution of blood groups and HLA types.

Acute Disease↗
PubMed1976

Preleukemia: does it exist?

In acute myeloid leukemia (AML), many of the remaining normal-appearing cells exhibit various abnormalities. An interpretation is that these cells are descendants of leukemic cells which have succeeded in overcoming the major final differentiation block that exists in AML. Direct evidence is quoted that red cell precursors in AML are of leukemic descent and it is claimed that the target cell of AML is the pluripotent stem cell. Next, evidence has been compiled that all three cell lines (red cell, n. granulocytes, platelets) exhibit qualitative defects in "prelukemia." Hence it is postulated that preleukemia per se doses not exist but that preleukemic states which with a rather high frequency sooner or later end in overt AML are actually true leukemias that, however, differentiate reasonably well. Another way of phrasing it is that preleukemic states are AMLs that present in partial and sometimes long-lasting remission, which only after months to years lose their differentiation ability and then are classified as AML.

Aneuploidy↗
PubMed1989

Risk of secondary acute leukemia and preleukemia after Hodgkin's disease: the Institut Gustave-Roussy experience.

From 1960 to 1984, 871 patients were treated for Hodgkin's disease at the Institut Gustave-Roussy. Twenty-six percent of the cohort were treated with radiotherapy (RT) alone, 6% with chemotherapy (CT) alone, and 68% with a combination of RT and CT, either at first line or for salvage treatment. MOPP chemotherapy was given to 42% of the patients. Overall, 19 secondary acute leukemias or preleukemias were observed, 3 of them after extended RT alone, the other 16 after a combination of RT and MOPP. Among the alkylating agents used, only nitrogen mustard (mechloretamine) was shown in a multivariate analysis to be significantly associated (P less than 0.001) with an increased risk of secondary leukemia. A dose response was observed, with the risk relative to general population incidence rates being 45 in patients having been treated with 1-59 mg (total dose) of nitrogen mustard, 211 in those treated with 60-119 mg, and 636 in those treated with greater than or equal to 120 mg. No other factors were found to be associated with leukemia risk. The 10-year cumulative incidence of leukemia was zero in patients treated with limited RT alone, 2.4% in those treated with extended RT alone, 0% in those treated with a combination of RT and CT without nitrogen mustard, and 12.4% in those treated with RT + nitrogen mustard. Whether other alkylating agents give a similar result remains to be determined; these data suggest that the use of nitrogen mustard at a higher total dose than 60 mg is questionable in the treatment of Hodgkin's disease.

Adult↗
PubMed1982

Impaired T-cell and NK-cell function in patients with preleukemia.

The responses to the T-cell mitogens Phythemagglutinin (PHA) and Concanavalin A (Con A) and the natural killer (NK) cell activity are tested in patients with preleukemia (PL). The results are compared with those of healthy controls. The PL patients show low responses to T-cell mitogens and low NK cell activities. It is discussed that the data are not of prognostic value in PL as to development of overt leukemia. However, the results suggest that PL impaired cell functions are not limited to erythropoiesis, granulopoiesis, and thrombopoiesis but are also found in the immune system.

Adolescent↗
PubMed1987

Progressive preleukemia presenting amegakaryocytic thrombocytopenic purpura: association of the 5q- syndrome with a decreased megakaryocytic colony formation and a defective production of Meg-CSF.

The authors present a patient with the typical clinical picture of an acquired amegakaryocytic thrombocytopenic purpura. After 16 months of observation, the patient developed acute myelomonocytic leukemia. During the preleukemic phase and after progression to overt leukemia, serial in-vitro analyses of megakaryocytic, granulocytic, erythrocytic and T-lymphocytic colony growth were carried out in a microagar culture system. At presentation, a marked diminution of CFU-M was observed, whereas CFU-E, BFU-E, CFU-C and CFU-TL were in the normal range. The CFU-M number remained at its low level during the whole observation period. The CFU-C number declined steadily during the preleukemic period, while BFU-E, CFU-E and CFU-TL remained constant until January 1985 when the patient developed AML. After progression to overt leukemia, a distinct reduction became evident in all colony-forming cells. Cytogenetic studies performed during the preleukemic phase indicated the presence of a 5q- chromosome. The authors submit evidence here that the patient was not only characterized by defective megakaryocytic colony formation but also by a deficiency of functional megakaryocyte colony-stimulating activity. No humoral or cellular inhibitors of CFU-M colony formation were found. It is concluded that in preleukemia with a 5q- chromosome the megakaryocytic cell lineage may be involved in the process that precedes overt leukemia at an earlier time than cells of granulocytic and erythrocytic lineages. In addition, it is shown here that megakaryocytopoiesis during the preleukemic period can be characterized by two different defects: first, an intrinsic megakaryocytic stem cell defect and, second, a deficiency of functional megakaryocytic colony-stimulating activity.

Adult↗
PubMed1982

An unusual karyotype in preleukemia.

A case of a myeloproliferative disorder classified as preleukemia is described in which the patient developed a single, complicated, abnormal karyotype in 100% of the bone marrow cells (45, XY, -2, -5, -7, -8, -11, -12, -13, -14, + t(2;5), +t(11;12), +t(16;17), +17, plus three or four dicentric markers). The possible significance of these unusual, if not unique, chromosome changes is discussed in relation to hematologic and clinical findings and with particular reference to the existing nonrandom patterns of chromosome changes in myeloproliferative disorders and acute nonlymphoblastic leukemias.

Aged↗
PubMed1985

Preleukemia and leukemia with 12p- and 19q+ chromosome alterations following Alkeran therapy.

Among 20 patients with acute nonlymphocytic leukemia or dysmyelopoietic preleukemia secondary to Alkeran therapy for another tumor, four had a del(12)(p11-p12) and four had a translocation to 19q13 among multiple karyotypic alterations in their neoplastic hematopoetic clones. It is suggested that these two cytogenetic abnormalities may occur nonrandomly in such hemic disorders and may play a limited role in their pathogenesis.

Chromosome Deletion↗
PubMed1985

A 2p;11q chromosome translocation in dysmyelopoietic preleukemia.

Three patients with dysmyelopoietic preleukemia had a marrow clone with translocation t(2;11)(p21;q23) as the only chromosome change. In one patient, the cytogenetically altered cells disappeared following treatment with 13-cis-retinoic acid. Although these patients did not constitute a homogeneous clinical subgroup, the 2p;11q translocation should probably be added to the short list of nonrandom karyotypic alterations involving 11q23 that have been described in various hematopoietic disorders.

Aged↗