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PubMed1992

Bone marrow dysfunctions preceding acute leukemia in children: a clinical study.

This is a review of preleukaemic states in children. In a prospective series of 109 children with AML the overt disease was preceded by MDS in 22 cases. Ten of these patients had Down's syndrome. Advanced FAB groups were represented in the series. An important subgroup is the bone marrow monosomy 7 syndrome. Cytogenetic anomalies are common in MDS, and multiple and complicated abnormalities develop in nearly all patients with progressing disease. Some children die before transformation to overt ANLL. Transformation usually occurs, few children survive. With cytostatic treatment the risk of irreversible aplasia is great. The choice of schedule should therefore be carefully considered. Bone marrow transplantation has proved beneficial in a number of cases, but these are still quite few. The dysfunction of the bone marrow preceding ALL is due to transient aplastic anaemia--spontaneous remission--overt ALL, often FAB type L1, immunophenotype CALLA. The ALL reacts to the same treatment as de novo ALL of the same type and the prognosis is the same.

Bone Marrow Transplantation↗
PubMed1992

The treatment of acute myeloid leukaemia preceded by the myelodysplastic syndrome.

Most cases of acute myeloid leukaemia in the elderly and about 15% of the cases in younger patients follow a myelodysplastic disease. This disease may differ biologically from de novo AML making cure more difficult. Understanding post-MDS AML is difficult because of its preponderance in the elderly and the many complicating factors of treating old people. However, it is likely that post-MDS AML is more resistant to chemotherapy than de novo AML, that periods of pancytopenia last longer following chemotherapy and remissions are shorter. In younger patients high complete remission rates are achievable with aggressive chemotherapy and good supportive care. Such patients are best served by subsequent allogeneic bone marrow transplantation if possible, and if not then bone marrow autograft or a maintained remission should be considered. For older patients cure is unlikely and the choice between low-dose cytarabine and aggressive chemotherapy must be made if treatment is to be contemplated at all. The former leads to less hospitalisation and fewer side effects, but the latter gives a greater chance of a complete remission. This will not be long lasting.

Acute Disease↗
PubMed1992

Complications and treatment of the myelodysplastic syndromes.

The major complications of the myelodysplastic syndromes (MDS) are related to cytopenia and evolution to acute myeloid leukemia (AML). Hematopoietic growth factors are only of limited benefit to alleviate the cytopenia. Therapy in MDS patients over the age of 50 should aim at prolonging survival while limiting the risk of toxicity. Those with stable disease should only receive supportive care; those with progressive cytopenia should have a trial with low-dose chemotherapy. Aggressive chemotherapy should only be reserved for those failing low-dose therapy. Therapy in MDS patients under the age of 50 should aim at cure of the disease. Although aggressive chemotherapy can induce complete remission in the majority of these patients, remission is usually short. Allogeneic bone marrow transplantation is probably the only curative option in these patients and should be the treatment of choice.

Antineoplastic Agents↗
PubMed1993

Preleukemic proliferative changes in murine bone marrow after single and multiple 7,12-dimethylbenz(a)anthracene (DMBA)-applications.

The effect of a leukemia-inducing treatment on early changes in kinetic parameters of murine bone marrow cells were investigated. Mice were treated i.p. one, four and eight times at biweekly intervals with 1 mg DMBA. Up to nine weeks after the last injection, CFU-S number, proliferation ability of bone marrow cells (PF), cell doubling time (td) and the compartment ratio (CR) were measured. Following multiple DMBA injections, CFU-S number and PF were decreased whereas CR and td increased, thus indicating persisting stem cell injury and proliferative compensation in the hemopoietic amplification compartment. A single DMBA injection had no effect. It is concluded that a first DMBA injection induces cytotoxic (and genotoxic) damage in the bone marrow leading simultaneously to a strong proliferation stimulus and a hindered proliferation ability of HSC, some of which will be predisposed for further mutagenic treatment. The following DMBA injections meet strongly proliferating HSCs, thus enhancing the probability for the loss of proliferation control/terminal differentiation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

The protein kinase C inhibitor H7 blocks phosphorylation of stathmin during TPA-induced growth inhibition of human pre-B leukemia REH6 cells.

The human pre-B acute lymphoblastic leukemia cell line REH6 was used to analyze the regulation of a ubiquitous intracellular phosphoprotein stathmin (Mr 19,000, pl = 5.6-6.2). We demonstrated by 32P-labeling that the short (1 h) treatment of the REH6 cells with the tumor promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), resulted in a rapid phosphorylation of at least three (P1, P2 and P3) stathmin isoforms without an alteration of stathmin isoform expression. Furthermore, Western blot analysis with specific antiserum showed that the prolonged period (48 h) of TPA treatment partially reduced protein levels particularly of two (N2 and P2) stathmin isoforms. The potent and relatively specific protein kinase C (PKC) inhibitor, 1,(5-isoquinolinesulphonyl)2methylpiperasine dihydrochloride (H7), partially inhibited these TPA effects, whereas the specific calmodulin inhibitor R24571 (calmidazolium) had no effect upon these events. Our findings suggest that stathmin phosphorylation in REH6 cells could be in part mediated by PKC activation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

Clonal dominance of RadLV-induced lymphomas.

RadLV-induced leukemogenesis begins with the emergence of a pleioclonal population of preleukemic (PL) cells, which subsequently gives rise to a monoclonal lymphoma. We have recently found that the pleioclonal-->monoclonal transition may occur early during the PL latency and long before the eruption of a full blown lymphoma. We sought to find out what causes one PL clone to become dominant. Our working hypothesis was that a dominant clone(s) at the PL stage has the ability to inhibit the development of other, recessive clones. Since some premalignant characteristics of a progenitor clone are probably maintained in the descending lymphoma, we studied whether tumors that developed after injection of a high dose (HD) of PL cells were dominant over tumors that developed after injection of a limiting dose (LD) of PL cells. To identify dominant clones, HD and LD lymphomas were mixed in a co-culture and the outgrowth of one clone over the other was determined by T beta-TCR rearrangement analysis. A checker-board combination of seven lymphomas revealed a dominance hierarchy scale. Lymphomas induced directly by the virus (without transfer) were dominant over both HD and LD lymphomas. High dose lymphomas were dominant over LD lymphomas and LD lymphomas were always recessive. The speed at which a dominant lymphoma outgrew the co-culture suggested that dominance is acquired through the ability of the prevailing cells to actively suppress the growth of recessive cells.

Animals↗
PubMed1996

Arylsulfatase B in Kurloff cells: increased activity of anionic isoforms in guinea pig acute lymphoblastic leukemia.

We examined the in vivo role of Kurloff cells (KC), guinea pig natural killer cells, during the development of L2C leukemia, by analysing changes in the arylsulfatases (Asases) in the lysosomal Kurloff body. The Kurloff body is rich in acid phosphatase, esterase and proteoglycans, as are large granular lymphocyte granules. Moreover, the Kurloff body contains lysosomal Asase B, with unusual anionic isoforms. Injection of L2C cells elicited a three-fold increase in KC Asase activity on day 6. The increase in KC Asase activity was correlated with the number of circulating L2C cells. The basic Asase form (pl 8) was lost, and a concomitant increase in anionic isoforms (pl 5-6) was observed on day 6. The role of the latter in cytolysis was investigated by examining their capacity to lyse L2C target cells. We conclude that Asase participates in cytolysis when lysis is mediated by the complete assembly of cytolytic proteins. Changing and increasing KC Asase activity during leukemia development may be a marker for activated KC in vivo. These findings suggest that the cytolytic activation of KC occurs during the preleukemic period.

Animals↗
PubMed1996

Severe congenital neutropenia terminating in acute myeloid leukemia: disease progression associated with mutations in the granulocyte-colony stimulating factor receptor gene.

Severe congenital neutropenia (SCN) is a heterogeneous disease condition with a variable family history and a propensity to progress towards myelodysplastic syndrome (MDS) and acute myeloblastic leukemia (AML). In a subgroup of patients, point mutations in the G-CSF-R gene have been found. These nonsense mutations result in the truncation of the C-terminal cytoplasmic region, a subdomain that is crucial for G-CSF induced maturation. SCN patients with mutations in the G-CSF-R gene appear to be predisposed to develop AML. Here, we recapitulate our view of how defective G-CSF-R may contribute to neutropenia and leukemogenesis.

Acute Disease↗
PubMed1991

"Never been done before"--consultative issues in innovative therapies.

The transition of a medical or surgical procedure from impossible to standard therapy requires a stage of experimentation, during which research priorities must be balanced with the interests of the patient. This paper examines such a "first case," and the interpersonal and group dynamics that play a part in the choice of a specific patient to be the first to receive that procedure.

Adult↗
PubMed1984

Detection of circulating immune complexes by a Clq/protein A-ELISA during the preneoplastic stages of feline leukemia virus infection.

A microscale ELISA immune complex assay which utilized a solid phase C1q and a Protein A-peroxidase enzyme conjugate is described. This ELISA was used to detect and quantitate circulating immune complexes (CIC) during the initial feline leukemia virus infection. Significant increases in CIC were seen in the cats which were transiently infected at weeks three through eight after viral exposure. A persistent elevation in CIC was observed in the one cat which developed a persistent viremia. The addition of EDTA to the serum strongly interfered with this assay.

Animals↗
PubMed1989

Chemotherapy and immunotherapy of bovine leukosis.

To prevent the progression of the disease, we treated leukemic or preleukemic cows with (1) adriamycin (ADM) entrapped in liposomes conjugated with monoclonal antibody, c143, against tumor-associated antigens (TAA) of bovine leukemic cells and (2) an immunotherapy using an immunopotentiator consisting of the cell wall skeleton of Nocardia rubra (N-CWS). Five leukemic or preleukemic cows with TAA-positive peripheral blood lymphocytes (PBL) received four injections of ADM alone (0.4 mg/kg body weight) or c143-conjugated liposomes containing the same dose of ADM (L-ADM-c143) through the jugular vein at about 4-day intervals. In three animals treated with L-ADM-c143, the TAA-positive cells gradually decreased with treatment and finally two animals became TAA-negative during a 6-week period and a 14-week period after treatment, respectively. About 6 weeks later, however, TAA-positive cells gradually increased. In the control, two animals treated with ADM alone showed no decrease of TAA-positive cells. Five TAA-positive animals with enlarged subcutaneous lymphatic nodules, each nodule estimated to be from 1 to 4 cm3 in size, were treated by injection of N-CWS into the tumors. Complete regression of tumor was observed in seven out of ten tumors treated in five animals. Decrease of TAA-positive cells was also observed in PBL for all five treated animals. In one animal, the TAA-positive cells remained low for at least 280 days after treatment. This study documents that ADM treatment and intralesionally administered N-CWS are effective in the treatment of bovine leukosis.

Adjuvants, Immunologic↗
PubMed1986

T-cell markers in the thymus during methylnitrosourea-induced leukemogenesis.

T-cell leukemias were induced in adult BDF1 mice by a single i.v. injection of 50 mg/kg of methylnitrosourea (MNU). During the latency period and in leukemic mice the expression of peanut agglutinin (PNA) receptors, terminal deoxynucleotidyl transferase (TdT) and thymus leukemia antigen (TLm4) in the thymus was studied. First, TLm4-positive thymocytes were found 6 wk after MNU. Further, there was a continuous reduction of the percentage of PNA-positive thymocytes. The expression of TdT remained unaltered late in the latency period and in leukemic mice. Four phenotype patterns could be defined for the expression of TdT and PNA in thymocytes: PNA+ TdT+, PNA+ TdT-, PNA- TdT+ and PNA- TdT-. Thymuses negative for TdT were rare, the majority was PNA+ TdT+. However, thymuses late after MNU treatment and leukemic thymus were PNA- TdT+. The discrepancy in the expression of PNA and TdT as cellular markers in leukemic mice as compared to normal cell populations is discussed.

Animals↗
PubMed1995

In vitro modulation of preleukemic AKR mouse macrophage function by bacterial immunomodulators.

Spleen macrophages from 1- and 4-month-old preleukemic AKR mice were stimulated in vitro with the bacterial immunomodulators lipopolysaccharide (LPS), peptidoglycan monomer (PGM) and muramyl dipeptide (MDP), in order to study their migration ability and mitochondrial enzyme activity. Macrophages from 1-month-old AKR mice, characterized by higher functional activity, failed to demonstrate any changes in the parameters studied after in vitro stimulation with the employed compounds. Conversely, the depressed macrophage function, spontaneously developed in 4-month-old AKR mice, most probably related to the preleukemic state, improved significantly and to about the same extent with all three immunomodulators.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1982

Diagnostic and prognostic significance of chromosome abnormalities in marrow and mitogen response of lymphocytes of acute nonlymphocytic leukemia.

Chromosomes of bone marrow from 28 patients with acute nonlymphocytic leukemia (ANLL) (26 with AML, 2 with AMMoL), 19 of whom had chromosome abnormalities, were studied; 11 cases exhibited previously unreported karyotypic abnormalities. The marrows of two cases had 8-21 translocations associated with an iso-X chromosome in the female patient and with 9q13- and a missing Y in the male patient. Usually, AML patients with a 8-21 translocation have been considered to have a good prognosis; however, our cases had rather short survival times. Therefore, the prognosis of AML with an 8-21 translocation but associated with other abnormalities is still not clear. Centromere spreading (CS), which was originally reported in marrow cells of megaloblastic anemia (B12 and folic acid deficiency), was detected in leukemic cells, disappeared during remission, and reappeared on relapse. These findings suggest that CS may be a new type of abnormality in AML. In two patients with atypical hypoplastic anemia and hemolytic anemia, chromosome abnormalities were detected at the anemic stage. One case with CS was associated with atypical hypoplastic anemia and developed AML after 1 year; the other with 48,XY,+i(1q),+3,/12 and -14 had hemolytic anemia and developed AMMoL 3 weeks later. Interestingly, identical clones were detected both before and after the clinical diagnosis of leukemia. These cases strongly support the concept that some chromosome abnormalities precede the clinical manifestations of leukemia. The present study also revealed that lymphocytes in ANLL respond poorly to PHA in the presence of high numbers of blasts but do respond well to mitogens during remission. Therefore, the response of lymphocytes to PHA may serve as one criterion for determining remission.

Adult↗
PubMed1983

Hematologic and cytogenetic study of two cases of acute leukemia associated with breast cancer.

The authors present two cases of patients with breast cancer with lymph node extension and who both had surgery. As a pancytopenia with hypercellular bone marrow was discovered at the same time in the first patient, she received no complementary treatment; 4 months later, she presented with an acute lymphocytic leukemia (ALL) for which a remission was easily induced, but she died of a pulmonary infection. The second patient received local radiotherapy (50 grays) and adjuvant chemotherapy (Alkeran for 26 months). Forty-seven months after the diagnosis of breast cancer and 16 months after the end of the treatment, an acute nonlymphoblastic leukemia (ANLL; M6) was diagnosed after 8 months of a preleukemic state. Treatment did not produce any results and death occurred on the 17th day. Cytogenetic studies on the bone marrow cells of both patients were performed. In the first patient in the ALL phase normal cells coexisted with a 47 chromosome clone, the extra chromosome being a D (+ 13?). In the second patient, several karyotype abnormalities were already present in the preleukemic state and also during the acute leukemic phase. No normal mitoses were found; hypodiploidy was present as well as major abnormalities such as markers, rings, and, among others, the systematic loss of a #5 and a #7. The first patient seems to have presented with a de novo ALL, associated with the malignant tumor; whereas, the second patient showed all the characteristics of an induced ANLL. The clinical, hematologic, and cytogenetic characteristics of these two patients are analyzed and compared to those of other cases in the literature.

Adenocarcinoma↗
PubMed1984

Translocation 1;7 in dyshematopoiesis: possibly induced with a nonrandom geographic distribution.

Eight patients with various hematologic disorders had an identical chromosomal aberration in their bone marrow or unstimulated peripheral blood, a translocation t(1;7) interpreted as t(1;7)(p11;p11). The translocation chromosome replaced one normal chromosome #7; therefore, the karyotype of the abnormal cells was trisomic for 1q and monosomic for 7q. Including four cases from the literature, a total of 12 patients (4 women, 8 men) with this translocation are known at the moment. The translocation does not seem to be associated with a specific disorder, but almost all patients had a preleukemic syndrome during some stage of their disease. It is very remarkable that 11 of the 12 patients lived in the Netherlands, and 7 patients had a history of iatrogenic exposure to alkylating agents or irradiation; one patient was a radiation worker and another one had a history of toxic exposure to chloramphenicol. It is suggested, therefore, that the t(1;7) is a possibly induced chromosomal aberration with a clearly nonrandom geographic distribution.

Adult↗
PubMed1985

Karyotypic evolution in patients with myelodysplastic syndromes.

Serial cytogenetic studies were performed in 33 patients with myelodysplastic syndrome in order to establish the frequency of karyotypic evolution and to correlate the chromosome and clinical findings during the course of the disease. Fifteen of the 33 patients (45%) showed abnormalities in the first cytogenetic study and this percentage increased to 57% during the course of the disease. A stable karyotype (normal or abnormal) was found in 19 patients (58%), whereas the rest (42%) showed an unstable karyotype. Trisomy 8, monosomy 7, and del5q were the most frequent abnormalities, not only at presentation, but also during karyotypic evolution. Seven patients (23%) with a known evolution proceeded to leukemia; four of them had stable (22%) and three unstable (25%) karyotypes; however, 33% of patients with unstable karyotypes and only 5% with stable karyotypes died from complications of the disease. Our results suggest that karyotypic evolution is relatively frequent in these patients; this evolution could be related to a poor clinical prognosis, either evolving to leukemia or death.

Acute Disease↗