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)

Seventy five patients with large spleens were investigated in order to establish the causes of splenomegaly in Northern Nigeria, to define further the diagnostic criteria of tropical splenomegaly syndrome (TSS), and to study its pathogenesis. Investigations included examination of liver biopsy, bone marrow cytology, lymphocyte response to phytohaemagglutinin (PHA), serum immunoglobulins and complement, and the presence of immunoglobulin and complement fixed in Kupffer cells. Thirty patients had TSS, five chronic lymphatic leukaemia (CLL), four a syndrome of gross lymphoid hyperplasia (GLH) distinct from TSS, CLL and the lymphomas, and twenty three miscellaneous conventional diseases. In thirteen cases no definite diagnosis could be established. TSS was found to be predominantly a disease of female Fulani cattle herders. Its essential characteristics were splenomegaly in the presence of acquired immunity to malaria, a grossly raised serum IgM, a lowered serum complement, and the presence of IgM fixed in Kupffer cells. There was lymphoid hyperplasia in bone marrow, hepatic sinusoids and often blood which may be indistinguishable from that in CLL. Lymphocytes undergo normal blastogenesis to PHA. There was clinical and haematological response to proguanil therapy. Reticuloendothelial phagocytosis of IgM, probably as a complex, seems to be the essential feature of the condition. As it was impossible to identify early cases of TSS it is unclear whether IgM overproduction or phagocytosis of IgM complexes is the first stage of the disease. The precise nature of the association with malaria remains obscure. The diagnosis of CLL demanded the demonstration of an abnormally low immunoglobulin level and impaired lymphocyte responsiveness to PHA by blast transformation or 3H-thymidine incorporation, in addition to the usual haematological findings. The syndrome GLH occurred in multiparous Hausa women. It was characterised by intense lymphocytosis with active, PHA-responsive cells, and normal immunoglobulin levels. Patients responded to proguanil therapy. It is suggested that these patients have a depressed immune response to malaria, perhaps through repeated pregnancies, and to a leukaemogenic agent, both of which stimulate lymphocytosis. Antimalarial treatment at this stage may prevent the development of frank leukaemia or lymphoma. The usefulness of the various investigative procedures and the problem of managing the large number of undiagnosed cases are discussed.
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PMID:Splenomegaly in Northern Nigeria. 1 54

Studies have been carried out to determine the sensitivity of hematopoietic CFU-S from Rauscher leukemic mice to an antiserum against the disease prepared in syngeneic mice. Test of this antiserum against Rauscher virus prior to injection showed it to be effective both in vitro and in vivo. At the same time, normal serum was shown to be without effect either against the CFU-S or against the virus. Spleen CFU-S were obtained from control and leukemic mice over a sequence of days following Rauscher virus injection and assayed by transplantation technique. Prior to transplantation these were incubated in vitro in either normal syngeneic serum or syngeneic antiserum. Incubation with antiserum had no effect on CFU-S obtained from the spleens of normal mice. However, incubation in this antiserum of spleen CFU-S from Rauscher leukemic mice resulted in a reduction of up to 50% in their colony-forming ability. Additional tests with guinea pig complement suggested that the levels of inactivation seen are not complement limited. This antiserum-induced reduction in colony formation was first evident in the second week after the injection of virus, coincident with the onset of splenomegaly in the leukemic mice. Thereafter, sensitivity of CFU-S to the antiserlm could be detected up to the terminal point of the leukemia (44 days).
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PMID:Effect of antiserum on transplantable hematopoietic colony-forming units during Rauscher leukemia development. 1 56

Revistin, a substance that strongly inhibits the reverse transcriptase activity of murine leukemia virus in our screening system, was obtained from a cultured broth of a soil streptomyces which was closely related to Streptomyces filipinensis. The assay method for the activity was based on the inhibition by a test material of the incorporation of 3H-dTMP into DNA synthesized by the reverse transcriptase of an oncogenic RNA virus. Crude revistin was isolated by serial procedures of salting out with ammonium sulfate and precipitation with cetylpyridinium chloride. The crude material showed neither antibacterial nor antifungal activity. It exhibited against splenomegaly in mice caused by Rauscher leukemia virus infection.
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PMID:Revistin found by screening for inhibitors of reverse transcriptase of an oncogenic virus. 5 48

The virucidal effects of streptovaricin (Sv) A, SvC, SvD, streptoval (Sval) C, Sval Fc, and streptovarone were evaluated by incubation of the drug with Rauscher leukemia virus (RLV) at 37 degrees C for 60 minutes prior to dillution and addition to cells (in vitro assay) or before ip injection into animals (in vivo assay). The in vitro and in vivo assays were plaque formation and splenomegaly, respectively. A dose-related effect was observed with all six compounds with the in vitro assay. On an equimolar basis, the Sv degradation products, i.e., Sval C, Sval Fc, and streptovarone were most inhibitory, followed by SvD; SvA and SvC were least active. At 0.0625 mumoles, the three Sv degradation products inactivated over 90% of the RLV. Similar results were obtained through the in vivo assay. At 0.06 mumoles, streptovarone, Sval C, and SvD showed 78,62, and 29% inhibition of splenomegaly, respectively; SvA and SvC were essentially inactive. A direct relationship was observed between inhibition on RNA-directed DNA polymrase of RLV by these compounds and their virucidal effects. No drug given at the time of injection, however, showed any significant effect on virus infective processes in vitro or in vivo. The reason for the lack of therapeutic effects of these compounds is discussed.
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PMID:Effects of streptovaricins and their degradation products on infectivity of Rauscher leukemia virus. 6 16

A chronic lymphatic leukaemia (CLL) with hepato-splenomegaly was treated in a 76 years old female patient by means of extracorporeal irradiation of blood (ECIB), after which a complete involution of the tumour in the spleen had taken place. Leukocytes initially increased to 35,500/mm3, amounting to 10,700/mm3 later on. The patient died of pneumonia in general cachexia. No signs of CLL could be found macroscopically after autopsy. An involution of the lymphatic infiltration could be identified microscopically in the bone-marrow.
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PMID:[Clinical treatment of chronic lymphatic leukemia by means of extracorporeal blood irradiation]. 8 Mar 60

We have recently proposed a new staging system for chronic lymphocytic leukaemia (CLL) in which patients with isolated splenomegaly are classified into a distinct stage (stage II). Twenty-three such patients (from two institutions) have been studied without recorded death in a follow-up of 18 months to 30 years. This favourable prognosis justifies separation of these 'pure splenic forms' (SCLL) which must be distinguished from what Galton has termed prolymphocytic leukaemia (PL). This distinction can be made on the basis of three criteria: (i) Clinically, SCLL has a slow uneventful course and neither anaemia and/or thrombocytopenia: (ii) cytologically PL can be distinguished from other forms of CLL though atypical forms of CLL may be confused with the former; and (iii) the study of surface membrane immunoglobulins (SmIg) showed that while lymphocytes from most patients with both PL and SCLL bore uniform SmIg, suggesting a monoclonal B-cell proliferation, there was a major quantitative difference in that whereas PL lymphocytes had a number of antigenic sites close to that of normal lymphocytes (mean: 82 000 sites per cell), SCLL lymphocytes had a drastically reduced number of sites. It is our opinion that this is an important criterion for the differential diagnosis between PL and SCLL.
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PMID:Identification of a pure splenic form of chronic lymphocytic leukaemia. 8 56

Over a 4-year period 203 patients with various types of leukaemia were treated by the Haematology Unit at the Johannesburg Hospital. Ten of them were suffering from the condition known as hairy-cell leukaemia or leukaemic reticulo-endotheliosis. They were all men, and ranged in age from 29 to 67 years (mean 56 years). The majority presented with pancytopenia, and there was invariably splenomegaly, while lymphadenopathy was rare. Hairy cells were identified microscopically in the peripheral blood of 7 patients and in 5 the specific cytochemical marker, tartrate-resistant acid phosphatase, was present. In addition, in a further 2 patients this feature, which was not identified in the peripheral blood, was found in the splenic cells. The bone marrow trephine biopsy specimens characteristically showed extensive lymphoid infiltration associated with a dense disordered deposition of reticulin fibres. Electron microscopical and immunological studies proved to be of doubtful diagnostic value. Splenectomy was carried out on 9 patients, and there was tumour involvement in all the spleens removed. Two patients died from septicaemia, the one before splenectomy and the other 9 months after the operation. The 8 remaining patients have had their subjective symptoms alleviated and their peripheral blood indices have been improved by splenectomy, and none has required further treatment for periods now ranging from 7 to 41 months.
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PMID:The diagnosis and management of hairy-cell leukaemia. 8 70

Two boys with Down's syndrome, recognized at birth, developed acute myelogibrosis at the ages of 19 and 21 months. The disorder presented with anaemia and splenomegaly, and clinically resembled acute leukaemia, but bone marrow histology showed a bizarre pattern with generalized fibrosis, markedly increased reticulin, large reticulum cells, and giant cells resembling megakaryocytes. The children survived 6 and 11 months from diagnosis. A third case is quoted (Hillman and Forrester, 1968) which was also studied at this hospital; the features of all 3 cases are similar. There appears to be an increased incidence of acute myelofibrosis in children with Down's syndrome, which may be a further example of the instability of the haemopoietic system in the disease. In children with Down's syndrome and unusual leukaemia-like illness, histological examination of the bone marrow may be diagnostic.
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PMID:Acute myelofibrosis in children with Down's syndrome. 12 73

A Graffi murine leukemia was utilized as a model system to investigate the effect of chemoimmunostimulation therapy. Subcutaneous inoculation of approximately 1.0 times 10(6) tumor cells resulted in a rapidly growing tumor at the site of inoculation and subsequent development of splenomegaly and lymphoadenopathy. All animals succumbed to the leukemia within 24 to 30 days. Treatment of diseased animals with two courses of cytoxan over a 2-week period resulted in a remission period of approximately 16 to 18 days before relapse and eventual death of approximately 70% of the drug-treated animals. A significant number of long-term survivors (50 to 83%) was obtained in groups of animals that received combined drug plus BCG or C. parvum therapy. In contrast, the administration of MER (a methanol-extracted residue of BCG) to animals in a drug-induced remission period was no more effective than drug alone. The protective effect afforded by BCG and C. parvum was dependent on the time interval between drug therapy and the administration of the immunostimulators. Treatment of leukemic animals with BCG, C. parvum, or MER alone proved ineffective as all mice died at approximately the same time as untreated control animals. No leukemic cells were observed in any of the histologically examined tissues taken from long-term survivors. The implication of these results for cancer therapy is discussed.
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PMID:Histological and combined chemoimmunostimulation therapy studies against a murine leukemia. 17 Feb 12

Mouse strain G was studied for its susceptibility to various strains of murine leukemia and sarcoma viruses. Both N- and NB-tropic Friend leukemia viruses neither induced splenomegaly nor grew efficiently in strain G mice. Using the XC test, cultured embryo cells were found to be resistant, but not absolutely, to all the tested viruses, N-tropic AKR virus, N- and NB-tropic Friend leukemia viruses, NB-tropic Rauscher leukemia virus, B-tropic WN1802B virus, NB-tropic Moloney leukemia and sarcoma viruses, and N-tropic Kirsten sarcoma virus, although the resistance to Moloney leukemia and sarcoma viruses is sometimes not as strong as that for other viruses. Thus, the strain G mice are unique among mouse strains because they show resistance that is not related to the N-B tropism of murine leukemia viruses.
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PMID:Mouse strain resistant to N-, B-, and NB-tropic murine leukemia viruses. 18 26


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