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)

Using a radioimmunoassay the serum concentration of the N-terminal propeptide of type III procollagen (P-III-P) was measured in 35 patients with chronic myeloproliferative disorders, including idiopathic myelofibrosis (n = 10), osteomyelosclerosis (n = 4), transitional myeloproliferative disorder (n = 5), polycythaemia vera (n = 10) and chronic myelogenous leukaemia (n = 6). The normal range in 35 healthy controls was 4.9-11.7 ng/ml. The serum concentration of P-III-P increased with increasing degrees of bone marrow reticulin fibrosis. By contrast, almost normal levels were detected in osteomyelosclerosis with an indolent clinical course, in which an excessive deposition of mature collagen fibres was found, representing mainly type I collagen. These observations indicate that the serum P-III-P level is positively correlated to the degree of bone marrow reticulin fibrosis, whereas levels are near normal in patients with osteomyelosclerosis and stable disease. Measurement of serum P-III-P may be a useful indicator of disease activity in myelofibrosing conditions.
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PMID:Serum procollagen III peptide in chronic myeloproliferative disorders. 408 33

Specific viral transformation rather than cell selection can explain the previously observed increase in the proportion of type III procollagen compared to type I procollagen in BALB 3T3 cells transformed by Kirsten murine sarcoma virus (Ki-MSV). Two subclones of BALB 3T3 A31 were productively infected with with a temperature-sensitive Ki-MSV in the presence of helper murine leukemia virus (MLV), resulting in virtually complete transformation of cultures and eliminating selection of transformed foci. Analysis of radioactive collagen, derived from procollagen by pepsin treatment, showed that both of the tsKi-MSV/MLV-transformed subclones contained a 4-fold greater proportion of type III procollagen than did control MLV-infected cultures. A nonproducer derivative exhibited an even greater change (10-fold), indicating that viral replication was irrelevant. After 48 hr at a nonpermissive temperature, tsKi-MSV-transformed cells retained a high proportion of type III procollagen, suggesting that either this change is not induced by src protein or else there is a slowly reversible or irreversible step involved. Alternatively, type III procollagen mRNA may be long lived. In contrast, the relative rate of procollagen synthesis in transformed cells was clearly regulated by src protein. Translation of mRNA from cells preincubated at permissive or nonpermissive temperatures revealed that the decreased relative rate can be explained by a simultaneous small decrease in the level of procollagen mRNA and a large increase in mRNA for noncollagen proteins.
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PMID:Mechanisms of Kirsten murine sarcoma virus transformation-induced changes in the collagen phenotype and synthetic rate of BALB 3T3 cells. 627 40

Mouse embryo Mus musculus castaneous epithelial cells, transformed with Moloney murine sarcoma virus (MSV) or with ecotropic murine leukemia virus (MuLV), were analyzed for production of pericellular matrix glycoproteins. The nontransformed, MSV-transformed, and MuLV-transformed cells produced fibronectin, laminin, type I collagen, and small amounts of type III collagen when studied by immunofluorescence using specific antibodies. The virus-transformed epithelial cells produced enhanced amounts of fibronectin into their growth media. Nontransformed M. musculus castaneous epithelial cells mainly produced type I collagen, as shown by metabolic labeling and polypeptide analysis. A significant increase in the glycoprotein production was seen by the MuLV-transformed cells, whereas small changes in the collagen production were apparent after MSV transformation. MuLV-transformed cells produced increased amounts of type I collagen and also some collagenous polypeptides that comigrated with procollagen type IV chains. The ratio of the procollagen type I chains deposited in the matrix was altered in transformed cells. Radioactive surface labeling of the cells revealed changes of the high-molecular-weight glycoproteins in both the MSV- and the MuLV-transformed cells. Unlike virus-transformed fibroblastic cells, these transformed epithelial cells deposited and retained connective tissue glycoproteins in their pericellular matrices. The results indicate that viral transformation modulates the pericellular matrix and surface glycoproteins of cultured mouse epithelial cels. The ability of virus-transformed epithelial cells to deposit pericellular matrices is a major difference between them and virus-transformed fibroblastic cells.
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PMID:Pericellular matrix and cell surface glycoproteins of virus-transformed mouse epithelial cells. 627 76

The availability of cloned lines of bone marrow stromal cells could facilitate the analysis of their role in hemopoietic cell development. The 266AD cell line was isolated from a colony of lipid-accumulating bone marrow cells growing in a collagen gel. 266AD cells have subsequently been maintained by passage in tissue culture plastic flasks about every 10 days for greater than 10 mo. Subconfluent cultures of cells are fibroblast-appearing, but in confluent cell sheets, prominent foci of lipid-containing cells develop in both uncloned and four separate cloned cell lines. Supernatants from confluent cultures containing lipid-laden cells contain granulocyte-macrophage colony-stimulating activity (GM-CSA) for normal bone marrow cells and can induce differentiation of Abelson virus transformed murine promonocytic leukemia cells. 266AD cells were originally isolated in the presence of hydrocortisone, but hydrocortisone is not necessary for lipogenesis to occur. Growth of bone marrow cells in a collagen gel matrix provided a way to isolate stromal cells, and the 266AD cell line provides a means to examine the relationships between stromal cell lipogenesis and regulation of granulopoiesis.
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PMID:Lipid accumulation and production of colony-stimulating activity by the 266AD cell line derived from mouse bone marrow. 629 27

Integration of the Moloney murine leukemia virus (M-MuLV) into the germ line of Mov-13 mice blocked formation of stable alpha 1(I) collagen mRNA and led to an embryonic lethal mutation. A 14-kilobase fragment representing the integration site of the virus was molecularly cloned and identified as the alpha 1(I) collagen gene. Sequence and nuclease S1 mapping analyses were performed to characterize the position of the proviral genome in relation to the transcriptional map of the mutated gene. The results indicated that the virus has inserted into the first intron 19 base pairs downstream of the intron/exon boundary. Sequence comparison showed a striking homology of exon sequences and sequences up to 215 base pairs upstream of the mRNA start between the mouse and the human alpha 1(I) collagen gene. This indicates that the sequences upstream of the mRNA start are highly conserved during evolution, suggesting that this region has an important role in the control of tissue-specific collagen expression.
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PMID:Insertion of retrovirus into the first intron of alpha 1(I) collagen gene to embryonic lethal mutation in mice. 632 98

In 9 patients with myeloproliferative diseases (MPD) (6 with myelofibrosis, MF, 1 with Ph1 positive chronic granulocytic leukaemia, CGL, 1 with primary eosinophilia, PE, 1 with pre-leukaemia syndrome, preL) collagen, epinephrine, and ADP-induced aggregation, N-ethylmaleimide-induced malondialdehyde (MDA) production, beta-thromboglobulin (beta-TG) plasma levels, and platelet turnover were studied. Collagen-induced aggregation was found to be normal in 7 patients, absent in 1, and reduced in 1. In all but 3 patients, aggregation with ADP was markedly reduced. Epinephrine-induced aggregation was decreased in 7 patients. No difference was found between mean MDA production in MPD (3.21 +/- 0.50 nmol/10(9) PLTs) and in control group of 21 normal subjects (3.04 +/- 0.26 nmol/10(9) PLTs). Mean beta-TG levels were significantly higher (P less than 0.01) in MPD patients (165.00 +/- 28.29 ng/ml) than in healthy controls (81.76 +/- 14.63 ng/ml). Mean platelet production half-time was significantly shorter in MPD (2.48 +/- 0.24 d) than in the control group (3.43 +/- 0.17 d), after adjustment for age by covariance analysis (P less than 0.005). Our data do not indicate an abnormal prostaglandin synthesis and are consistent with the hypothesis that a disseminated intravascular platelet aggregation might take place in MPD patients.
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PMID:Defective platelet aggregation and increased platelet turnover in patients with myelofibrosis and other myeloproliferative diseases. 646 Oct 58

In a child with acute megakaryoblastic leukemia--severe thrombocytopenia and myelofibrosis, EM studies on bone marrow showed a strict topographic relationship between the presence of clusters of abnormal megakaryocytes and the increased number of fibroblasts and extracellular fibers. Megakaryocytes and platelets lacked alpha-granules while the plasma thromboglobulin level was three times the normal level. This suggested that the alpha-granular proteins were synthesized but not retained in alpha-granules. If this occurs, the increased marrow levels of platelet-derived growth factor and factor 4 would favor the proliferation of fibroblasts and the synthesis of collagen, and thereby promote myelofibrosis. After therapy-induced remission, the number of marrow megakaryocytes decreased, the alpha-granules were normally produced, the plasma beta-thromboglobulin level was normal and the myelofibrosis disappeared. These observations suggest that during acute megakaryoblastic leukemia, an acquired gray-platelet syndrome occurs and that the local excretion of alpha-granule proteins triggers the myelofibrosis.
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PMID:Myelofibrosis and acute megakaryoblastic leukemia in a child: topographic relationship between fibroblasts and megakaryocytes with an alpha-granule defect. 646 1

The leukemia-associated cell surface antigen p 24 is found on normal platelets as well as on Bernard Soulier syndrome and thrombasthenia type I platelets. ALB6 IgG (a monoclonal antibody against p 24) induces the aggregation of platelets from normal donors but not from thrombasthenia. In contrast, ALB6 Fab inhibits platelet aggregation induced by collagen, ADP, thrombin, ionophore A 23187 and ALB6 IgG. The results suggest that ALB6 interferes with a mechanism common to all aggregation pathways; the possible mechanisms are discussed.
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PMID:Characteristics of platelet aggregation induced by the monoclonal antibody ALB6 (acute lymphoblastic leukemia antigen p 24). Inhibition of aggregation by ALB6Fab. 657 11

A clinical phase (spent phase) in the course of polycythaemia vera (PV) cases is described as enlargement of the spleen in spite of treatment, frequent cytopenia of one or several lines, persistent red cell hypervolaemia with considerable increase of plasma volume, persistence of myeloid hyperplasia with no collagen myelofibrosis or osteomyelosclerosis, absence of hepatosplenic erythroblastic metaplasia, as shown by radio-iron kinetics and/or 111In-transferrin scintigraphy. The frequency of this phase was 5% in a study where it was not systematically sought, but it could in fact be greater. Its occurrence is not related to the clinical and biological parameters of PV. On the other hand, it is significantly more frequent and earlier in patients treated by phlebotomies than in those treated by myelosuppression (32P). In four of the 12 cases, this phase was rapidly followed by an acute leukaemia. In eight cases there was a 1-5 year interval before a myelofibrosis with splenic myeloid metaplasia. This evolution could at this stage be delayed by chemotherapy. The efficacy of splenectomy should be studied.
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PMID:The 'spent' phase of polycythaemia vera: hypersplenism in the absence of myelofibrosis. 658 68

Two patients, a 43-year-old woman and a 62-year-old man, developed benign peripheral nerve sheath tumors (neurofibromas) of the lacrimal gland, in the former case of the deep orbital lobe, and in the latter of the palpebral lobe. A neurogenic tumor was not seriously considered clinically in either case, because of the paucity of previous reports on the occurrence of neural tumors in the lacrimal fossa region. Instead, in the first case a benign mixed tumor was considered the most likely clinical diagnosis, whereas in the second the coexistence of a swelling in the parotid gland raised the possibilities of a lymphoid tumor or a leukemia. Due to unusual light microscopic features, transmission electron microscopy was required to secure unequivocal diagnoses. In the orbital lobe tumor, an encapsulated spindle cell proliferation without nuclear palisading but with focal areas of myxoid change suggested either a cellular benign mixed tumor or a schwannoma. The palpebral lobe lesion displayed a myxoid spindle cell proliferation that had splayed apart the ducts and acinae of the lacrimal gland, to impart the overall appearance of a benign mixed tumor. The ducts, however, were multilaminar rather than possessing the usual double cellular layer seen in classical benign mixed tumors, and the glandular units contained zymogen granules, which are typically not seen in benign mixed tumors. Electron microscopy disclosed in both lesions the presence of interrupted basement membrane material partially surrounding the tumor cells, long spacing collagen (banded basement membrane material), and poorly developed desmosomes, features compatible with a neural tumor. Neither myofilaments, tonofilaments, nor ductal-type granules sometimes observed in benign mixed tumors were discovered. The tumor cells in these cases therefore failed to demonstrate clear-cut Schwann cell characteristics (eg, continuous basement membranes, pseudo-mesaxons, tangles of cell processes), and more closely resembled perineural cells that have been described in ultrastructural studies of peripheral nerve tumors including neurofibromas of other sites.
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PMID:Benign peripheral nerve sheath tumors (neurofibromas) of the lacrimal gland. 667 40


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