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PubMed1980

Chronic myelodysplastic syndrome (preleukemia) with the Philadelphia chromosome.

A patient with severe anemia, reticulocytopenia, and erythroid hyperplasia of the bone marrow developed fatal acute nonlymphocytic leukemia after 3 yr. A Philadelphia chromosome with the typical 9/22 translocation t(9q +;22q-) was identified by banding techniques in a small number of bone marrow cells throughout the preleukemic phase of the illness (14%--38% of metaphases) and during the acute transformation (50%). Granulocytic colony formation in vitro was abnormal in the preleukemic phase. The diagnosis of chronic granulocytic leukemia was excluded on the basis of clinical and laboratory findings. The identification of the Ph1 chromosome in this form of chronic myelodysplastic syndrome (preleukemia) provides a new example of a hematologic disorder predisposing to acute leukemia in which this chromosomal abnormality occurs.

Chromosomes, Human, 21-22 and Y↗

PubMed1982

Peripheral blood blast cell progenitors in human preleukemia.

Progenitors of blast cell colonies have been identified in acute leukemia. The peripheral blood of 18 of 25 patients with preleukemic states yielded low numbers of blast cell colonies, and the colony-forming cells were in an active proliferative state when assessed using short-term exposure to tritiated thymidine. The clinical significance of blast cell colonies is uncertain, but we suggest that further analysis of this cultural abnormality may lead to a better understanding of mechanisms and management in preleukemia.

Adolescent↗

PubMed1993

Human preleukemia: cellular, molecular and clinical aspects.

In a significant proportion of patients with acute myeloid leukemia (AML), a series of hematological alterations--including refractory anemia, neutropenia, thrombocytopenia, abnormal iron metabolism, and elevated levels of blast cells both in peripheral blood and bone marrow--are observed before the diagnosis of AML is made. This preleukemic state has called the attention of several investigators around the world, since it represents a way to study the origin and progression of leukemia in man. During the past 5 years, major advances in the molecular and cellular biology of this disease have been achieved. It is now known that preleukemia is a clonal disorder that arises from a malignant transformation at the level of primitive pluripotent hemopoietic stem cells. The hemopoietic progenitors in preleukemic patients have abnormal responses to hemopoietic regulators, thus, they do not seem to follow the controlled proliferation observed in the hemopoietic system under normal conditions. The mechanisms of cell differentiation and maturation are also altered, leading to the production of immature (blast) cells, instead of the development of fully mature erythrocytes, granulocytes, platelets and lymphocytes. Several oncogenes, such as C-FMS and RAS, have been found to be structurally altered in a significant proportion of preleukemic patients, suggesting that they may be involved in the pathogenesis of the disease. In spite of the advances made during the last few years, major questions regarding the biology of this hematological disorder are still unanswered.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

PubMed1976

Fever--a manifestation of preleukemia.

A patient had a preleukemic syndrome in which the major manifestation was a chronic relapsing fever over an 18-month period. A review of the literature shows that fever may be present in a considerable number of patients with preleukemia.

Agranulocytosis↗

PubMed1987

Chromosome characteristics of therapy-related acute non-lymphocytic leukemia and preleukemia: possible implications for pathogenesis of the disease.

Most cases of therapy-related acute nonlymphocytic leukemia or preleukemia show chromosome aberrations, primarily loss of whole chromosomes No. 5 and/or No. 7 or the long arms of these two chromosomes. Other abnormalities involve chromosome No. 21, often rearranged at band 21q22, and chromosome No. 17, in some cases rearranged at band 17p13. Important cellular genes have recently been localized to these regions, including the gene for one hematopoietic growth factor and the gene for the receptor for another hematopoietic growth factor. It is suggested that the total loss or change of structure or expression of some of these genes resulting from the various chromosome aberrations may be of pathogenetic significance in therapy-related acute nonlymphocytic leukemia.

Antineoplastic Agents↗

PubMed2000

Telomerase activity in preleukemia and acute myelogenous leukemia.

The development of acute leukemia from preleukemia involves the appearance of clones with increasing proliferative potential. The studies described here demonstrate that telomerase activity progressively increases as the bone marrow cells acquire increasing proliferative potential. This was demonstrated by measuring telomerase activity in normal bone marrow, in post-treatment lymphoma marrows with skewed Lyonization, and in MDS and AML marrows. The greater telomerase activity in myelodysplastic marrow than in normal marrow is not due to a higher proportion of blast cells or to a higher proliferative rate of the MDS marrow. These data demonstrate that the increasing proliferative potential of the marrow which occurs during the development of AML is associated with a simultaneous increase in telomerase activity.

Adolescent↗

PubMed1975

The platelets in preleukemia and myelomonocytic leukemia. Ultrastructural cytochemistry and cytogenetics.

Light and electron microscopic studies of platelets from 16 patients with myelomonocytic leukemia or "preleukemia" revealed major morphologic alterations in 15 and minor ones in 1. Although variable in severity from case to case, the changes present followed a distinct pattern. In most cases there were two platelet populations, one morphologically normal and one morpholigically abnormal. The most salient changes pertained to size (giant forms), shape (the platelets being rounded and probably spheroidal), decrease or absence of the microtubules, and increase in immature elements. A striking feature was the variation in size and shape of the granules, with truly giant forms (up to 2.5 mum) being present. In cytogenetic studies in 14 cases, there was no correlation between the chromosomal changes and the various types of platelet anomalies.

Adult↗

PubMed1976

Platelet granulopathy: a new morphologic feature in preleukemia and myelomonocytic leukemia: light microscopy and ultrastructural morphology and cytochemistry.

We have previously reported on the ultrastructure of platelets in preleukemia and myelomonocytic leukemia. We referred to an unusual and distinct anomaly of the platelet granules found in 15 of 16 patients. In the present communication we wish to describe and illustrate the light microscopic appearance of giant anomalous granules. Close scrutiny of the platelet morphology and a search for the aforementioned platelet granulopathy are important in the evaluation of patients with myeloproliferative diseases. In this paper we describe and illustrate in more detail the ultrastructure and ultrastructural histochemistry of the abnormal granules. In those patients with the platelet granulopathy, we have conducted in vitro platelet aggregation studies and carried out an electron microscopic evaluation of the aggregates. At least some of the giant granules remained morphologically intact in advanced stages of the aggregation phenomenon, and thus they are probably composed of elements that were not released during aggregation.

Acid Phosphatase↗

PubMed1976

The erythrocytic line in refractory anemia (preleukemia or hemopoietic dysplasia) and myelomonocytic leukemia. II. Some unusual morphologic variants of the polychromatic normoblasts and reticulocytes.

In a combined scanning and transmission electron microscopic study of the red blood cell line in patients with refractory anemia (preleukemia) and myelomonocytic leukemia, certain elements with abundant, convoluted membranes that formed projections over the cell surface were observed. These cells were both normoblasts (nucleated) and reticulocytes (anucleated) and constituted what appeared to be a distinct subpopulation of the red blood cell line. It is possible that in these erythrocytes there is a nucleocytoplasmic asynchronism. We are not certain, however, that they are linked to the leukemic process.

Anemia, Aplastic↗

PubMed1976

Preferential involvement of chromosomes no. 8 and no. 21 in acute leukemia and preleukemia.

Chromosome analyses were performed by a direct method on bone marrow cells of 147 patients with acute leukemia and preleukemia; in 53 chromosomally abnormal cell lines were found. Chromosome abnormalities due to structural alterations were observed in 48% of the aneuploid patients. Using the ASG banding technique, the exact identification of the abnormal chromosomes was successfully made in 22 aneuploid patients. Even though variability between patients existed in the chromosome changes; the nonrandom occurrence of some chromosome abnormalities was revealed, involving most frequently chromosomes No. 8 and No. 21. Abnormalities of chromosome No. 22 were not encountered, contrasting sharply with the frequent involvement of this chromosome in chronic myelogenous leukemia. The significance of the preferential involvement of No. 8 and No. 21 chromosomes is discussed in relation to leukemogenesis.

Acute Disease↗

PubMed1988

Vitamin C in leukemia and preleukemia cell growth.

Vitamin C was shown to be an essential requirement for the growth of mouse myeloma cells in an in vitro colony assay. Human leukemia (acute nonlymphocytic leukemia) cell colonies grow well in a similar in vitro culture system, and vitamin C has been shown to enhance the growth of leukemic cell colonies in 77 (35%) of 219 leukemic patients while none of 34 normal bone marrows tested simultaneously shows growth enhancement by this vitamin. This vitamin C effect is reproducible in repeated experiments in same patients, specific to this vitamin, selective for leukemic cells, and is proven to be biological in nature. Further, leukemic cells are mobilized back and forth between cycling and resting states with vitamin C supplementation/depletion. Our more recent study indicates that the preleukemia (myelodysplastic syndrome), generally known to be related to acute nonlymphocytic leukemia, has similar pattern in terms of vitamin C sensitivity, with 8 of 25 patients (32%) showing the growth enhancement with this vitamin.

Ascorbic Acid↗

PubMed1975

The ultrastructure of the platelets in refractory anemia ("preleukemia") and myelomonocytic leukemia.

We have conducted extensive morphologic studies of the platelets in 16 patients with preleukemia or myelomonocytic leukemia. Although the degree and frequency of the changes varied in the different cases, it was evident that the platelets in these two pathologic states often were structurally abnormal. The abnormalities include changes in size (mainly giant forms), shape (frequent presence of round cells), and quantitative (particularly decreases) as well as qualitative changes in the platelet granules. Quite remarkable has been the finding of giant granules of irregular contour and heterogeneous composition, perhaps the result of fusion of several single granules. Other changes have included overabundance of the membranous systems of the platelet.

Adenosine Diphosphate↗

PubMed1984

Progressive preleukemia with a chromosomally abnormal clone in a kindred with the Estren-Dameshek variant of Fanconi's anemia.

One of two sisters with hypoplastic anemia and increased chromosomal fragility, but no clinical stigmata of Fanconi's anemia (FA), progressed to preleukemia (with a clone of chromosomally abnormal cells in the bone marrow), and then to acute nonlymphocytic leukemia. The findings indicate that constitutional genetic instability can lead to karyotypically aberrant neoplastic clones in the Estren-Dameshek variant of FA as well as in the more typical chromosomal fragility syndromes.

Adolescent↗

PubMed1978

Acute megakaryocytic leukemia. Description of a case initially seen as preleukemia syndrome.

A 52-year-old man had aregenerative anemia unresponsive to pyridoxine hydrochloride. Acute leukemia developed, and he died four months after diagnosis. At autopsy he had acute megakaryocytic leukemia with involvement of bone marrow, liver, spleen, adrenals, kidneys, and thyroid. Chromosomal analysis revealed absence of both diploid and Ph1 chromosomes. A mode of 45 chromosomes and aneuploidy were present. This is similar to the only other case with chromosomal studies. Of the 15 acceptable documented cases, eight were men and seven were women. Their age varied from 28 to 76 (mean, 55) years. Only two were less than 40 years of age. Most had pancytopenia, and all were dead within six months of diagnosis.

Autopsy↗

PubMed1998

Preleukemia in long-term plasmacytoma-regressor mice.

Our previous results have indicated that mice whose plasmacytoma regressed following curative melphalan chemotherapy manifested various persistent immunohematological abnormalities including immunosuppression, myeloproliferation, as well as excessive production of and response to growth factors. Mice not bearing plasmacytoma treated with an identical dose of melphalan chemotherapy did not exhibit such abnormalities. In the present study we show that plasmacytoma-regressor mice (PRM) contain preleukemic cells which do not progress to leukemia in these mice. However, adoptive transfer of splenocytes originating in PRM to preirradiated but otherwise untreated syngeneic recipients resulted in the development of overt leukemia in these recipients. The presence of leukemia in the primary recipient mice was ascertained by blood counts as well as by spleen histology. Furthermore, splenocytes from the irradiated primary recipients adoptively transferred to non-irradiated secondary recipients caused leukemia formation in 100% of the secondary recipients. Sex chromosome analysis of the leukemic cells in the irradiated primary recipients clearly showed that they originated in the PRM donors. Two leukemic lines were established from leukemias developing in the secondary recipients and both expressed surface markers of hematopoietic progenitor cells as well as markers of T cells. We suggest that PRM could serve as an animal model to investigate development of chemotherapy-related leukemia in humans.

Animals↗

PubMed1976

Chromosome studies in "preleukemia". III. Myelofibrosis.

Cytogenetic studies were done on 18 patients with myelofibrosis or the closely related syndrome, undifferentiated myeloproliferative disorder (MPD). Clones of cells with chromosome abnormalities were demonstrated in the blood of eight individuals, including two with a history of radiation therapy and two with "acute myelofibrosis". Trisomy 8 was present in the latter two patients, but otherwise, there was no consistent cytogenetic pattern or correlation with specific hematologic findings. Sixteen of these patients have been followed for more than 1 year or until death; none has progressed to leukemia. The results indicate that chromosome abnormalities are relatively common in this disorder, but as with polycythemia vera, and unlike some other "preleukemic" states, the aberrant clones in myelofibrosis do not appear to indicate that clinical leukemia is imminent.

Adolescent↗

PubMed1979

Acute leukemia and preleukemia in eight males in a family: an X-linked disorder?

Eight males in a family died of acute leukemia or a potentially preleukemic blood disease. Three patients were descendants of a man through his first wife, and the other five through his second wife. The pattern of disease in the family suggests X-linked inheritance through the two wives, although other mechanisms cannot be excluded. No detectable action of environmental leukemogens was observed in this family disorder.

Acute Disease↗

PubMed1984

An analysis of prognostic factors in preleukemia: interest of bone marrow scintigraphy.

Simultaneous bone marrow scintigraphy with 99m Technetium colloids and 111 Indium transferrin was performed on 34 cases of preleukemic anemias and was shown to be of good prognostic value. Groups of different outcome were defined: for a normal and parallel uptake of the two markers, 90% of the patients died of acute leukemia; for a low Indium and high Technetium uptake, only 1 patient out of 15 died of leukemia (P less than 0.001). Standard clinical and hematological data were of no predictive value. Iron kinetic data and CFU/GM colony growth were correlated to the scintigraphic results. Taken together, these three kinetic parameters have a good sensitivity and specificity for the prognosis of preleukemic states.

Aged↗