Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of lactoferrin were measured in immediately separated EDTA samples from 5 subjects who had received HLA identical bone marrow transplants for leukaemia or aplastic anaemia and from 7 subjects who were leukopenic as a consequence of chemotherapy for a variety of malignant conditions. Plasma lactoferrin concentrations were found to closely parallel the leucocyte count and were not found to either predict or to antedate leucocyte regeneration. Serial measurements of plasma lactoferrin in a subject with no circulating neutrophils who received a bone marrow graft revealed that the clearance of lactoferrin followed an exponential pattern and had an initial half time of 2.2 h.
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PMID:Relationship of plasma lactoferrin content to neutrophil regeneration and bone marrow infusion. 351 97

This study describes an ELISA technique with high specificity, sensitivity, accuracy and reproducibility for measurements of plasma lactoferrin. The detection limit was 0.001 microgram/ml and the median value obtained in EDTA plasma from 47 healthy adults was 0.100 microgram/ml (0.05 fractile: 0.046 microgram/ml, 0.95 fractile: 0.257 microgram/ml). The lactoferrin concentration in serum was on the average 2 1/2 times higher than in plasma. The ambient temperature did not influence the plasma concentration during the first 6 h from blood sampling to separation of plasma from the cells. In 8 patients with untreated acute leukaemia plasma lactoferrin was positively correlated to the peripheral neutrophil count. An almost parallel course in plasma lactoferrin and peripheral neutrophil number was observed in 4 patients with AML during chemotherapy. In 2 patients achieving complete remission, plasma lactoferrin increased about 6 d before the concomitant increase in neutrophil count, suggesting plasma lactoferrin as an early predictor of bone marrow regeneration.
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PMID:Lactoferrin in plasma measured by an ELISA technique: evidence that plasma lactoferrin is an indicator of neutrophil turnover and bone marrow activity in acute leukaemia. 385 82

The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells. Under normal conditions, AIF suppresses colony and cluster formation by an Ia-antigen-positive cycling subpopulation of mouse granulocyte-macrophage progenitor cells (CFU-GM). Under the same conditions, the release of AIF-inhibitory activity and granulocyte-macrophage colony stimulatory factors (GM-CSF) from an Ia-antigen-positive subpopulation of monocytes and macrophages is suppressed by LF. Within one to two days after inoculation in vivo with Friend virus complex or helper virus, mouse CFU-GM become insensitive in vitro to suppression by purified human AIF as well as crude mouse AIF, and by four days, bone marrow, spleen, and thymus cells of these mice release much greater quantities of AIF-inhibitory activity than the cells from mice injected with control medium. The Friend virus complex itself has no influence in vitro on CFU-GM from normal mice. In addition, the release of AIF-inhibitory activity from bone marrow, spleen, and resident peritoneal cells and the release of GM-CSF from resident peritoneal cells of mice infected with Friend virus complex are not suppressed by LF. The inability of AIF to suppress colony formation by bone marrow and spleen CFU-GM from mice infected with Friend virus complex is associated with the loss of Ia (I-A subregion) antigens from CFU-GM, even though CFU-GM are in cycle. The nonresponsiveness of bone marrow, spleen, and peritoneal cells from these mice to LF suppression of AIF release and the inability of LF to influence GM-CSF release from peritoneal cells is associated with loss of Ia antigens from these cells. The above abnormalities are similar to the defects noted using cells from patients with leukemia. These results suggest that mice infected with Friend virus complex can serve as a model for investigating abnormalities in cell regulation and their relationships to disease progression.
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PMID:Abnormalities in myelopoietic regulatory interactions with acidic isoferritins and lactoferrin in mice infected with Friend virus complex: association with altered expression of Ia antigens on effector and responding cells. 387 Nov 66

Lactoferrin (LF)--in various quantities--is present in human milk, secretions and polymorphonuclear neutrophils (PMN). LF's significance lies in its bacteriostatic effect on its environment. Probably it prevents bacterial uptake of iron, leads to damage of bacteria and during phagocytosis helps the organism to combat pathogens. Most likely it regulates iron absorption, and during inflammation it takes part in the plasma iron transport. LF is believed to play an important role in the regulation of granulopoiesis in the bone-marrow. From its biological effects it appears that plasma LF determinations may be useful in the clinical diagnosis of leukaemia and other malignant diseases, as well as in the study of iron metabolism.
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PMID:The biological role of lactoferrin. 388 89

Quantitative cytochemistry of components of blood neutrophil azurophilic granules (myeloperoxidase, chloroacetate esterase, beta-glucuronidase, and acid phosphatase) and specific granules (lactoferrin) has been performed by scanning and integrating microdensitometry in 13 patients with a myelodysplastic syndrome and 11 patients with chronic granulocytic leukaemia. Both patient groups showed a reduction of enzyme activity in azurophilic granules, and also of lactoferrin, consistent with abnormal development of neutrophil granules. These cytochemical changes in blood neutrophils are similar to those found in acute myeloid leukaemia, are consistent with a leukaemic maturation defect, and may be of diagnostic value.
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PMID:Quantitative cytochemistry of blood neutrophils in myelodysplastic syndromes and chronic granulocytic leukaemia. 609 32

Bone marrow and peripheral blood cells of patients with non-leukemic neutropenia contain and elaborate a granulocyte-progenitor cell inhibitory activity. The inhibitory activity is common to the neutropenias of the various etiologies studied, which included congenital, idiopathic, autoimmune, cyclical, common variable immuno-deficiency with hypogammaglobulinemia and drug induced states. It derives from non-adherent, low density, slowly sedimenting and non-E-rosetting cells and appears to require RNA and protein synthesis, but not cell division, for its production. The material is not species specific, inhibits autologous and allogeneic normal CFUgm and leukemic CFUgm, is not cell-cycle specific in action and is most effective against granulocyte colony forming cells (CFUg), less effective against mixed granulocyte-macrophage colony forming cells (CFUgm) and least or non-effective against macrophage colony forming cells (CFUm). This inhibitory activity has no influence on cells which generate CFUc in suspension culture or on the erythroid colony forming (CFUe) and burst forming (BFUe) units. It is different from other known inhibitory activities such as lactoferrin, leukemia inhibitory activity, E type prostaglandins, interferon and immunoglobulins. This inhibitory activity, while at present an in vitro phenomenon, may be produced as a secondary response within a compromised host.
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PMID:Specific inhibitory activity against granulocyte-progenitor cells produced by non-T lymphocytes from patients with neutropenia. 616 31

Semiquantitative analysis of lactoferrin deficiency in neutrophil polymorphonuclear leucocytes in various haematological and non-haematological disease was carried out by scoring polymorphonuclear leucocytes stained for lactoferrin by the immunoperoxidase method. The staining patterns for lactoferrin were classified into four types (0-III) based on the intensity of reaction, and the sum of the ratings of 100 polymorphonuclear leucocytes was considered as "lactoferrin score" with a possible range of 0-300. As a result, significantly low lactoferrin-scores were frequently observed in acute leukaemias and the acute phase of chronic leukaemias. Of 35 cases with leukaemias, lactoferrin-negative polymorphonuclear leucocytes (type 0) were observed in the following cases: eight cases of acute myelogenous leukaemia (8/14), a case of chronic myelogenous leukaemia (1/10) in blast crisis, one of acute promyelocytic leukaemia (1/1), one of acute monocytic leukaemia (1/2), and a case of chronic myelomonocytic leukaemia (1/2) in a transitional phase to an acute myelomonocytic leukaemia. In two cases of acute myelogenous leukaemia, in which the majority of polymorphonuclear leucocytes were negative for lactoferrin, ultrastructural cytochemical study revealed total lack of specific granules in these polymorphonuclear leucocytes. This suggests that lactoferrin is localised in the specific granules of neutrophils as has been postulated previously by others.
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PMID:Lactoferrin-deficient neutrophil polymorphonuclear leucocytes in leukaemias: a semiquantitative and ultrastructural cytochemical study. 631 19

Serum levels of lactoferrin, lysozyme and myeloperoxidase have been established in 31 healthy children. On average, serum lactoferrin was 330 micrograms/1, serum lysozyme 1638 micrograms/1 and serum myeloperoxidase 174 micrograms/1. Serum myeloperoxidase was, on average, significantly higher in children than in adults (p = 0.01), whereas serum lactoferrin and serum lysozyme were equal to those of adults. In a group of infection-prone children (n = 31), both serum lactoferrin and serum myeloperoxidase, but not the serum lysozyme levels, were significantly lower (p less than 0.001 and p = 0.002, respectively) than those of the reference children in spite of normal intracellular contents and even somewhat higher peripheral blood polymorphonuclear counts. Based on the assumption that serum lactoferrin and serum myeloperoxidase reflect turnover and activity of neutrophil granulocytes, the findings could suggest reduction in these respects and could be one contributing factor to the high infection propensity of these children. Serum levels of the three proteins have also been measured in 10 children with suspected or various forms of manifest leukemia. It is suggested that the levels reflect turnover and stage of maturation of the myeloid and monocytic cells and could, therefore, aid in the understanding and diagnosis of these diseases.
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PMID:Serum-levels of lactoferrin, lysozyme and myeloperoxidase in normal, infection-prone and leukemic children. 631 52

New technology allows highly sensitive flow cytometric detection and quantitative analysis of intracellular antigens in normal and malignant hemopoietic cells. With this technology, the earliest stages of myeloid and lymphoid differentiation can easily and reliably be identified using antibodies directed against (pro-)myeloperoxidase/MPO, CD22 and CD3 antigens, respectively. Particularly for the analysis of undifferentiated acute myeloblastic leukemia (AML) cells, the immunological demonstration of intracellular MPO or its enzymatically inactive proforms is highly relevant, since other myeloid marker molecules such as CD33, CD13, or CDw65 are either not restricted to the granulomonocytic lineage or appear later in differentiation. By combining MPO staining with staining for lactoferrin (LF), undifferentiated cells can be distinguished from the granulomonocytic maturation compartment in bone marrow, since LF is selectively expressed from the myelocyte stage of differentiation onward. The list of informative intracellular antigens to be used in leukemia cell analysis will certainly expand in the near future. One candidate, intracellular CD68, has already been tested by us, and results are presented. Also dealt within this article are surface marker molecules not (as yet) widely used in leukemia cell analysis but with the potential to provide important additional information. Among them are the surface structures CD15, CD15s, CDw65, CD79a (MB-1), CD79b (B29), CD87 (uPA-R), and CD117 (c-kit).
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PMID:Flow cytometric analysis of cell-surface and intracellular antigens in leukemia diagnosis. 753 75

In murine leukemia virus-induced myeloid leukemias, insertional mutagenesis of the c-myb locus has been shown to occur frequently. Proto-oncogene activation is achieved in most leukemias by integration of murine leukemia virus upstream of exons 3 or 4 or by integration into exon 9 with consequent truncation of the protein. The present study investigates the effect of ectopic expression of full-length c-myb or c-myb containing amino- or carboxyl-terminal truncations (minus 47 and 248 amino acids, respectively) on granulocyte differentiation in vitro. Recombinant myb retroviruses were used to infect an interleukin 3-dependent progenitor cell line, 32Dcl3, which undergoes terminal differentiation to mature neutrophilic granulocytes in the presence of granulocyte colony-stimulating factor. Overexpression of c-myb did not abrogate the interleukin 3 dependency of the parental cell line. However, cells expressing all forms of c-myb were blocked at an intermediate stage of granulocyte differentiation and continued to proliferate in the presence of granulocyte colony-stimulating factor. After 14 days in medium with granulocyte colony-stimulating factor, myb-expressing cultures predominantly consisted of promyelocytes with some myelocytes and almost undetectable numbers of neutrophilic granulocytes. This suggested that early stages of granulocyte differentiation were not inhibited, a finding that was further supported by the induction of myeloperoxidase, a biochemical marker of promyelocytes. Interestingly, the expression of lactoferrin, known to be a marker of late stages of granulocyte differentiation, was completely inhibited in the cells infected with myb viruses. It was concluded that c-myb expression blocked granulocyte differentiation to the terminal mitotic stages and that deletion of the NH2-terminal 47 amino acids and/or the COOH-terminal 248 amino acids of c-myb neither enhanced nor diminished this effect.
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PMID:Only late, nonmitotic stages of granulocyte differentiation in 32Dcl3 cells are blocked by ectopic expression of murine c-myb and its truncated forms. 753 40


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