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)

The developing eyes of CFW/D mice inoculated at birth with a neurovirulent mutant (ts1) of Moloney murine leukemia virus (MoMuLV), nonneurovirulent wild type (wt) MoMuLV, and conditioned virus-free medium were studied comparatively by immunohistochemistry, lectin histochemistry and light microscopy. Cellular targets for viral antigen expression in the eye were identical in both ts1 and wt MoMuLV-infected mice. Viral antigen first was observed in endothelial cells of the retina and subsequently spread in a spatial and temporal pattern consistent with normal vascularization of the developing retina. The virus also was observed in (1) epithelial cells of the bulbar and palpebral conjunctiva, ora ciliaris retinae, and lacrimal gland; (2) endothelial cells of the ciliary body, iris, choroid, and sclera; (3) amacrine cells of the retina; and (4) smooth muscle cells and endothelia of the periocular muscle. Although ts1 MoMuLV induced a spongiform encephalopathy in the brain and spinal cord, structural lesions were not observed in the retina or other ts1 MoMuLV-infected ocular structures; differentiation of the retina was normal. The lectin Ricinus communis agglutinin-I (RCA-I) labeled (1) endothelial cells of the hyaloid vessels, tunica vasculosa lentis, retina, ciliary body, iris, choroid, and sclera; (2) epithelial cells of the cornea, bulbar and palpebral conjunctiva, ora ciliaris retinae, and lacrimal gland; (3) smooth muscle cells and endothelia of the periocular muscle; (4) inner segments of the photoreceptor layer; and (5) amacrine cells of the retina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ocular infection with a murine neurovirulent retrovirus does not cause retinal degeneration. 174 Mar 69

Interferons (IFNs) have established antitumor action; the mechanism underlying this effect is, however, not yet clear. To probe the possible contribution of inhibition of angiogenesis, we have assessed angiogenesis in the mouse initiated by either human or murine tumor cell lines. Whether test cells were inoculated in the dermis or tumor fragments were grafted onto the cornea, tumor-induced angiogenesis (TIA) was inhibited by IFNs. TIA was also inhibited by the potent IFN inducer polyriboinosinic-polyribocytidylic acid. The effect of IFN was species specific; human IFNs inhibited human tumors and mouse IFNs inhibited murine tumors. This effect suggested that in contrast to other angiogenesis inhibitors, IFNs modulated the signal for angiogenesis produced by the tumor cells. Tumor cells treated in vitro with homologous IFN were significantly (P less than 0.005) less competent to initiate angiogenesis than were untreated cells. Inhibition of angiogenesis was achieved whether vascular response was assessed 1 or 3 days after tumor cell inoculation, suggesting that antiangiogenesis activity was independent of the antiproliferative effects of IFNs. To further substantiate this, L1210 leukemia cells, resistant to the antiproliferative effects of IFNs, were treated with 500 units/ml IFN-beta. IFN had no effect on their proliferation, but in four separate experiments, L1210R cells were impaired in their ability to induce angiogenesis. Thus, inhibition of TIA by IFNs was species specific, occurred at least partly by modulation of the signal inducing angiogenesis, and was expressed in the absence of antiproliferative effects. IFNs also inhibited immunologically induced angiogenesis, whether initiated by allogeneic lymphocytes (LIA) or by the mouse's own T-cells in response to an exogenous antigen (sheep RBC). LIA was markedly suppressed by treatment of host mice with homologous IFN-beta. For example, mean vessel counts induced by allogeneic mouse lymphocytes were decreased from 22.8 +/- 1.4 (SE) to 12.5 +/- 0.8 (P less than 0.0001); mouse IFN-beta had no corresponding effect on xenogeneic human lymphocytes (mean vessel counts decreased to 21.7 +/- 2.6 from 22.7 +/- 2.0). Treatment with human IFN-alpha, -beta, or -gamma in vitro or host mice in vivo reduced the ability of inoculated human peripheral blood lymphocytes to initiate xenogeneic LIA. Inhibition of LIA required a lower dose and/or a shorter incubation period than that needed to modulate TIA. Treatment of the donor of the allogeneic spleen cells in vivo with murine IFN or inducers also resulted in lesser LIA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Inhibition of angiogenesis by interferons: effects on tumor- and lymphocyte-induced vascular responses. 244 62

Human retroviruses, or RNA viruses, including the 2 HIV agents associated with AIDS, and the 2 HTLV agents causing leukemia, are described from the viewpoint of history, detection, serology, transformation mechanism, disease pathophysiology, genetic function, associated disease, and related viruses. Both HTLV and HIV infect the human T-lymphocytes, also known as CD4 or helper cells. Both can now be grown in culture, and their genomes are well characterized. HTLV, an acronym for human T-lymphotropic leukemia virus, causes the fulminating adult T-cell leukemia-lymphoma (ATLL), 1st described in 1977. It is prevalent in population clusters, notably in the Caribbean and in southwestern Japan, and is spread by sexual, blood and perinatal routes, as is HIV. It is thought to promote transformation of target cells by release of growth promoting, soluble factor, perhaps a product of the viral "tat" gene. Besides leukemia, HTLV-1 causes a myelopathy sometimes called tropical spastic paraparesis. HIV, formerly known as HTLV-III, causes depletion of the T-cells, and also infects the brain and nervous system. IT has also been isolated from semen, cervical secretions, saliva, monocytes, milk, endothelial cells, tears and cornea. HIV has 5 more genes than HTLV, which regulate transcription, mRNA processing and virus maturation. Parts of the HIV genome are highly heterogeneous, and mutate rapidly, notable sections of the envelope protein. Thus, HIV has 2 main subtypes, but others are known and probably exist. Approaches toward developing AIDS therapeutic agents as of 1987 are outlined: an effective drug should cross the blood-brain barrier. Several anti-viral drugs that block the enzyme reverse transcriptase area being investigated. Possible mechanisms for growth of Kaposi's sarcoma, activation of herpes type viruses, and animal viruses related to HTLV and HIV are discussed.
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PMID:Retroviruses: new viral infections in man. 289 67

Two patients developed graft versus host disease (GvHD) following allogeneic bone marrow transplantation for leukemia. One patient developed acute GvHD 12 days after transplantation, and the second developed chronic GvHD 100 days after transplantation. Tear analysis and conjunctival impression cytology were performed. The results were compared to a normal control and to another patient who was 18 months status post bone marrow transplantation with successfully treated GvHD. Tear sampling on the patient with chronic GvHD revealed greatly elevated IgG levels with an inverse IgG to IgA ratio, as compared with normals. In addition, two of three leukemia patients demonstrated decreased mucin levels in tears. Conjunctival impression cytology from the patient with chronic GvHD revealed an abundance of plasma cells.
Cornea 1988
PMID:Elevated tear IgG and conjunctival plasma cell infiltrate in a graft versus host disease patient. 334 90

Three patients with leukemia developed corneal toxicity while receiving high doses (3 g/m2) of systemic cytarabine. Symptoms began five to seven days after initiation of treatment with high doses of systemic cytarabine and consisted of ocular pain, tearing, foreign-body sensation, photophobia, and blurred vision. All three patients developed bilateral conjunctival hyperemia and fine corneal epithelial opacities and refractile microcysts that were more numerous in the central than in the peripheral cornea. The symptoms disappeared without treatment in approximately one week. The corneal changes we observed with high doses of systemic cytarabine resembled descriptions of corneal toxicity from topical cytarabine and were probably secondary to inhibition of DNA synthesis in the corneal epithelium.
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PMID:Corneal toxicity with systemic cytarabine. 693 30

The authors describe the infiltrations of the cornea in both eyes of a patient (women) who suffered from leukaemia with "long-haired cells". The treatment was successful with 2-chlordeoxyadenosine (Leustatin). Knowledge of leucaemic infiltration in the cornea is accentuated for successful treatment in connection with basic disease.
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PMID:[Leukemic infiltration of the cornea in a patient with hairy-cell leukemia]. 765 50

A 17-year-old woman was admitted for bone marrow transplantation with the diagnosis of atypical Philadelphia-negative chronic myelogenous leukemia (aCML), cytogenetically characterized by trisomy 8 as the sole chromosome aberration. A striking feature was a congenital opacity of the right cornea. Chromosomal analysis of skin fibroblasts were performed and revealed a mosaic for trisomy 8. Commonly, a distinct clinical picture leads to the diagnosis of trisomy 8 mosaicism syndrome (T8ms), but an extreme phenotypic variability has been observed. To our knowledge the development of an aCML in a patient with T8ms has not been reported. A review of the literature revealed that an association to other hematological disorders had been described in two cases. The question of whether our patient's aCML was a random event or not is discussed. The patient is now 24 months post transplant and shows no evidence of disease. Her Karnofsky score is 100%. We conclude that it might be worthwhile to look for an associated constitutional trisomy 8 mosaicism in all patients with trisomy 8 leukemia.
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PMID:Atypical chronic myelogenous leukemia in a patient with trisomy 8 mosaicism syndrome. 843 24

The authors describe a female patient suffering from hairy-cell leukaemia. Already at the onset of the disease, apart from marked splenomegaly, sonography revealed marked retroperitoneal lymphadenopathy. During the subsequent course skin changes developed such as vasculitis and leukaemic infiltrates of the cornea on both eyes. The patient was successfully treated with 2-chlorodeoxyadenosine (2-CdA, Leustatin).
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PMID:[An unusual course in hairy-cell leukemia with marked abdominal lymphadenopathy, leukemic infiltration of the cornea and skin changes]. 892 22

PCR analysis and Western blotting revealed the expression of the mineralocorticoid receptor (MCR) and the epithelial sodium channel (ENaC) genes at the level of RNA, DNA, and protein in several leukemic cell lines, fibroblasts from human cornea, and epithelial cells from ocular tissues. Following immunofluorescence, the MCR appeared to be primarily nuclear whereas the ENaC was almost exclusively membrane-bound. Paradoxically, the MCR-specific antagonist ZK 91587 actually stimulated the multiplication of human erythroblastic leukemia cells, contrary to the inhibitory effect of the antagonist RU 26752 on the multiplication of corneal fibroblasts; both effects were opposed by aldosterone. In quantitative PCR, both basal and aldosterone-induced levels of ENaC were diminished by ZK 91587 in the corneal fibroblast, in contrast to the stimulation observed in the retinal pigmentary epithelium. Thus, contrary to the existing notions, (a) antimineralocorticoids can act both as agonists and antagonists, and (b) the receptor-mediated action of mineralocorticoids on the sodium channel is not restricted to the epithelial cell.
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PMID:Paradoxical effects of mineralocorticoids on the ion gated sodium channel in embryologically diverse cells. 1077 7

With evolving diagnostic and therapeutic advances, the survival of patients with acute leukaemia has considerably improved. This has led to an increase in the variability of ocular presentations in the form of side effects of the treatment and the ways leukaemic relapses are being first identified as an ocular presentation. Leukaemia may involve many ocular tissues either by direct infiltration, haemorrhage, ischaemia, or toxicity due to various chemotherapeutic agents. Ocular involvement may also be seen in graft-versus-host reaction in patients undergoing allogeneic bone marrow transplantation, or simply as increased susceptibility to infections as a result of immunosuppression that these patients undergo. This can range from simple bacterial conjunctivitis to an endophthalmitis. Leukaemia can present as pathology in the adnexae, conjunctiva, sclera, cornea, anterior chamber, iris, lens, vitreous, retina, choroid, and optic nerve. Recognition of the varied ocular presentations is also important in assessing the course and prognosis of leukaemia. We have presented a systematic approach taking each part of the eye in turn and outlining how leukaemia has been shown to affect it.
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PMID:Ophthalmic manifestations of acute leukaemias: the ophthalmologist's role. 1537 62


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