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At least 649 records · Page 36Linked to original sources
PubMed1978

A combined assay for the rapid preliminary detection of structural retroviruses.

This report describes the use of equilibrium gradients, RNA dependent DNA polymerase assays and electron microscopy (EM) in a combined assay for the rapid preliminary detection of intact retroviruses in crude preparations. Positive combined assays of platelets from preleukemic patients corresponded with karyotypic abnormalities found in these patients. Reconstruction experiments with Rauscher Leukemia Virus added to buffer or disrupted mouse spleen demonstrated the ease of detecting 10(9) or greater particles/g crude tissue, and the effects of buffer or added protein.

Animals↗
PubMed1978

[Modifications of genetic markers during malignant blood disease].

Genetic marker changes in malignancy are related to an acquired disfunction of the genetic material in stem cells. This disfunction always leads to the lack of antigen; whenever we evidenced a new specificity it was an unconverted substrate. In malignant states modifications are multiple, polyclonal and independent. This least feature explains the extent of the process giving that disfunction. The evidence of a genetic defect is supported by the simultaneous decrease of the primary gene product: the glycosyl-transferase (ABO locus). In some other malignant carcinoma, blood group specificities were observed, their meaning is not well explained. Blood group specificities associated to carcino embryogenic antigen (CEA) or to some mucins could be related to the structure of macromolecular carriers.

ABO Blood-Group System↗
PubMed2002

Transient modifications of respiratory capacity in thymic cells during murine radioleukemogenesis.

The evolution of mitochondrial oxidative phosphorylation was studied during cancer induction in a model of thymic radiolymphomagenesis in C57BL/Ka mice. During the preneoplastic period, thymuses displayed an increase of the cytochrome c oxidase activity and oxygen consumption together with oxidative DNA damage assessed by the presence of the 8-hydroxydeoxyguanine DNA base modification. These transient changes in mitochondrial functional activity were not observed in thymuses of mice rescued from lymphoma development by a bone marrow graft, suggesting an important role of mitochondria for neoplastic transformation in this model, which might therefore be of interest to test the utilization of antioxidants for the prevention of radiation-induced malignancies.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1998

A rare atypical myeloproliferative-disorder-like hemopathy with marked dysplasia, peripheral dominant myeloblast proliferation and extramedullary hematopoiesis was converted into typical acute myeloid leukemia with an interval of complete hematological remission.

We describe a patient with leukocytosis with all the stages of neutrophilic series, peripheral dominant myeloblast proliferation, marked dysplasia of myeloid and erythroid series, and extramedullary hematopoiesis of the lymph nodes. A cytogenetic study of the bone marrow cells showed normal karyotype, and molecular analysis of the leukemic cells showed negative for BCR-ABL by RT-PCR. After chemotherapy, the patient went into complete remission with a normal blood and bone marrow profile with no dysplasia. On relapse, the hematological findings showed a typical bone marrow dominant acute myeloid leukemia, with the leukemic cells having a chromosomal abnormality. The patient exhibited the combined features of myeloproliferative disorder, myelodysplastic syndrome, peripheral dominant myeloblast proliferation (so-called peripheral leukemia) and typical acute myeloid leukemia throughout the clinical course. This is thought to be a rare overlapping disease involving these distinct hematological conditions that do not usually occur in the same patient.

Acute Disease↗
PubMed1997

Leukemogenesis by Moloney murine leukemia virus: a multistep process.

Moloney murine leukemia virus is a prototypical simple retrovirus that has been an extremely useful model for leukemogenesis. Important steps in leukemogenesis include proviral activation of cellular proto-oncogenes, generation of mink cell focus-inducing recombinants, and early (preleukemic) virus-induced changes in hematopoiesis.

Animals↗
PubMed1985

Established leukemia cell lines: their role in the understanding and control of leukemia proliferation.

For investigation of mechanisms of leukemogenesis and control of proliferation of leukemia cells, various preleukemic hematopoietic progenitor cell lines and leukemia cell lines have been established. The role of these established cell lines in understanding leukemogenesis and control of leukemia cell proliferation is described. The results of studies on biological characteristics of numerous human leukemia-lymphoma cell lines suggest that the heterogeneity in various markers of the cell lines reflects different patterns of normal hematopoietic cell differentiation. Then, recent studies on the control of proliferation of leukemia cells by induction of terminal differentiation with the use of established leukemia cell lines both in vitro and in vivo are described. Therapeutic significance of the results obtained with these leukemia cell lines is also discussed.

Animals↗
PubMed2001

Role of Bcl-2 family proteins and caspase-3 in sanguinarine-induced bimodal cell death.

Sanguinarine, a benzophenanthridine alkaloid, has anticancer potential through induction of cell death. We previously demonstrated that sanguinarine treatment at a low level induced apoptosis or programmed cell death (PCD) in the Bcl-2 low-expressing K562 human erythroleukemia cells, and that a high level induced blister cell death (BCD); whereas Bcl-2 overexpressing, sanguinarine-treated JM1 pre-B lymphoblastic cells displayed neither apoptosis nor BCD morphologies. Here, we report that sanguinarine-treated K562 cells, when analyzed by western blot, showed significant increase in expression of the pro-apoptotic Bax protein in apoptosis, but not in BCD. cDNA expression array of PCD in K562 cells failed to reveal the presence of Bax at the gene transcript level, which suggests that this cell death process does not require de novo protein synthesis. Treated JM1 cells, on the other hand, showed an increase in the expression of Bcl-2 protein in both forms of cell death, but failed to show Bax expression. The role of other members of the Bcl-2 family remained negligible. Caspase-3 activation was observed in apoptosis of K562 cells but not in BCD or in sanguinarine-treated JM1 cells. These results suggest that sanguinarine in K562 cells induces apoptosis through increasing Bax and activating caspase-3, whereas sanguinarine-induced BCD involves neither. These results also suggest that in JM1 cells, Bcl-2 may play a role in susceptibility of cells to induction of apoptosis and BCD.

Alkaloids↗
PubMed2001

Role of mononuclear phagocyte system in hemopoiesis regulation in AKR/JY mice during preleukemic period.

Feeder activity of bone marrow adherent cells and peritoneal macrophages is decreased and colony-stimulating and erythropoietic activity of unfractionated bone marrow increased in highly leukemic AKR/JY mice in comparison with CBA/CaLac mice. At the same time maturation of hemopoietic precursor cells in AKR/JY mice is delayed compared to controls. This indicates compensatory activation of nonadherent elements of the hemopoiesis-inducing microenvironment against the background of suppressed activity of adherent elements. Hence, leukemogenic virus produced a systemic damage to target cells (e.g. mononuclear phagocyte system), which probably represent a mechanism of leukemic transformation in AKR/JY mice.

Animals↗
PubMed1983

Immunoglobulin heavy-chain switching in pre-B leukaemias.

Immunoglobulin gene expression is initiated in pre-B cells by rearrangements of heavy-chain variable genes V, D and J, for transcription together with the constant region gene C mu (refs 1-7). The subsequent joining of light-chain V-J genes in the kappa or lambda families leads to formation of complete IgM molecules, which are then expressed on the surface of B cells. Heavy-chain isotype switching has been thought to occur later and to involve CH gene rearrangement via deletion of DNA between a switch site 5' to C mu and a switch site 5' to the downstream C gamma, C epsilon or C alpha gene expressed by a mature plasma cell. On the other hand, isotype switching has been seen in human pre-B-cell leukaemias and in a murine pre-B-cell line before light-chain gene rearrangements and without C mu gene deletion. To explore further the isotype switching in pre-B cells, we used monoclonal antibodies in immunofluorescence assays to allow unambiguous assignment of the heavy-chain isotypes expressed by individual leukaemic cells in 11 pre-B-cell leukaemias. Switching in these leukaemic clones invariably led to expression of gamma 1 heavy-chain and kappa light-chain determinants, occasionally together with gamma 4 and alpha. These results indicate a nonrandom order for heavy-chain isotype switching and for light-chain isotype expression, and also suggest that a mechanism exists for coordinating the two events.

Antibodies, Monoclonal↗
PubMedDate not supplied

Mutations of the Kirsten-ras proto-oncogene in human preleukaemia.

The myelodysplastic syndrome (MDS) or preleukaemia is a haematological disorder characterized by low blood counts, bone marrow cells of abnormal appearance and progression to acute leukaemia in as many as 30% of patients. The distinctive preleukaemic and leukaemic phases of this disease make it an attractive model for neoplastic progression in human tumours. We reasoned that, because dominantly transforming genes (such as mutant alleles of ras proto-oncogenes) are found so frequently in acute leukaemia, the search for these genetic lesions during the clinical course of patients with MDS might give us insight into the function of oncogenes in leukaemogenesis. We report here that bone marrow cells from two of four patients with preleukaemia, and from one patient who progressed to acute leukaemia from MDS, contained a transforming allele of the Ki-ras proto-oncogene. In one preleukaemic patient, a novel mutation in codon 13 of this ras gene was detected in bone marrow cells harvested 1.5 years before the acute leukaemia developed. Our findings provide evidence that ras mutations may be involved in the early stages of human leukaemia.

Adult↗
PubMed1980

Levamisole: evidence for activity on human haemopoietic progenitor cells.

Levamisole, which has immunostimulant activity, is now being used to treat some forms of cancer. We report that the drug enhances granulocyte colony formation. The mechanism of action appears to be partly through modulation of molecules on cell membranes. The molecular content of colony-stimulating activity (CSA) released into leucocyte-conditioned medium by cells of leukaemic and some preleukaemic patients can be quantitatively altered by levamisole, both in vitro and in vivo, but the CSA produced is qualitatively similar to that released by normal cells. The demonstrated levamisole enhancement of colony formation, and altered CSA types detected in leucocyte-conditioned medium, makes this drug a promising candidate for treatment of selected leukaemic states and in preleukaemia.

Adult↗
PubMed1987

Second malignancies in children treated for non-Hodgkin's lymphoma and T-cell leukaemia with the UKCCSG regimens.

Eight children treated between 1977 and 1983 with the UK Children's Cancer Study Group's non-Hodgkin lymphoma (NHL) and T-cell protocols have developed second malignancies within 7 years of commencing treatment. Five developed acute non-lymphoblastic leukaemia and a sixth died from infection while pancytopenic with a pre-leukaemic marrow. The other malignancies were cerebral astrocytoma and an undifferentiated low grade sarcoma. These eight children were included among 261 children studied in the first UKCCSG NHL and T-cell trials giving an actuarial incidence of 7.8% second malignancy at 7 years. Six had received adjuvant radiotherapy which may have contributed to the high incidence of second malignancy.

Adolescent↗