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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Feline leukemia virus (FeLV) infection is common among cats where contact is high. The virus can be transmitted readily between cats. It causes a variety of haemopoietic and lymphoid neoplasms; the most common types are alimentary, multicentric and thymic lymphosarcoma and lymphatic leukaemia. The virus is involved in the aetiology of certain other diseases including anaemia, glomerulonephritis and an immunosuppressive syndrome which predisposes cats to intercurrent infections. Many infected cats mount an immune response and do not suffer from any of these. The immune status is shown by serum antibody levels to feline leukaemia virus associated cell membrane antigens. Cats with a titre of 32 or more are most unlikely to suffer any ill effects and may eliminate the virus infection. The outcome of infection in an individual cat depends on the immunological competence of the cat, the dose of virus received and its ability to induce immunosuppression. FeLV infection can be detected by examination of tissues by electron microscopy, and by culture of virus from plasma and other tissues. In the United States, a method is now in use for the detection of leukaemia virus antigen in peripheral blood leukocytes; this is carried out on ordinary blood films. Successful prototype vaccines have been developed against FeLV. This paper describes the natural history of the virus, the diseases in which it is implicated and discusses recently developed diagnostic methods.
Vet Rec 1975 Jan 04
PMID:Feline leukaemia virus and its clinical effects in cats. 16 15

Mouse chromosome segregating somatic cell hybrids were established between a mouse thymic leukemai cell line (GRSL) and Chinese hamster E36 cells. The GRSL cells specifically bound purified Rauscher leukemia virus gp70 while the E36 cells exhibited no binding. The hybrids selectively bound Ruascher gp70 depending on the presence of a mouse cellular gene for the ecotropic murine luekemia gp70 receptor. A syntenic relationship was observed between the DIP-3 chromosome marker (on chromosome 5) and the gp70 receptor in primary clones and subclones of these hybrids; this was confirmed by chromosome analysis. The involvement of H-2 in the binding of Rauscher MuLV gp70 could be ruled out, because discordancies of the receptor presence and H-2 absence as well as of the receptor absence and H-2 presence type could be observed. Our results indicate that the Rec-1 (replication ecotropic MuLV) gene of Gazdar et al. (4) may well be the receptor gene for the ecotropic murine leukemia virus.
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PMID:Identification of a mouse gene required for binding of Rauscher MuLV envelope gp70. 43 56

Three cases of monocytic leukaemia in dogs are reported. Clinically, they all showed dullness, lymph node enlargement and hepato-spenomegaly and the overt illness was of short duration. Haematologically, the white blood cell count was raised to different degrees in each case. The great majority of white cells were monocytes and monoblasts; their cytological, cytochemical and electron microscopic features are described. Only a mild degree of anaemia was present in all cases. Pathological examinations, carried out in two of the dogs, showed widespread leukaemic infiltration of bone marrow, spleen, lymph nodes, liver and other organs. Differentiation of this syndrome from other forms of haemopoietic neoplasia is discussed.
Vet Rec 1975 Jan 11
PMID:Monocytic leukaemia in the dog. 105 99

A cat experimentally infected with feline immunodeficiency virus (FIV) but known to be free of feline leukaemia virus (FeLV) developed lymphosarcoma. The lesions in the liver and kidneys were present nine months after infection, when the cat was 21 months old. The cat had no overt signs of immunodeficiency and it is suggested that the B cell activation induced shortly after FIV infection produced a large pool of proliferating lymphocytes from which the malignant cells emerged.
Vet Rec 1992 Apr 04
PMID:Lymphosarcoma in experimentally induced feline immunodeficiency virus infection [corrected]. 131 15

We analysed the organization of V delta genes and delta recombining element (delta Rec) in 27 children with B-cell precursor acute lymphoblastic leukaemia. Twenty-two of 54 alleles showed rearrangements of the T-cell receptor (TCR) delta locus. These rearrangements resulted either from D2D delta 3 (2 alleles) or V delta 2(Dn)D delta 3 (20 alleles) recombinations, and the other V delta and delta Rec were not rearranged. Of 23 alleles with deletion of C delta and rearrangements of J alpha, V delta 2, V delta 4 and V delta 5 appeared to rearrange to J alpha on five alleles. With regard to the relationship between the rearranged V alpha/delta and J alpha genes, gene segments 5' to V delta 2 frequently rearranged to J alpha more proximal to C alpha, whereas V delta 2 and gene segments 3' to V delta 2 showed a tendency to rearrange to J alpha distal to C alpha. Based on these findings, we suggest that the initial recombination event of the TCR-alpha/delta gene may be D2D delta 3 joining, followed by V delta 2 recombination with the D2D delta 3 complex. It was also suggested that use of V alpha/delta and J alpha/delta may depend on the distance between the involved V alpha/delta and J alpha/delta at least in B-lineage cells. These rearrangements in B-precursor cells appear to be aberrant. However, this recombinational process may be one of the normal differentiation pathways in T-lineage cells, because cells with a V delta 2(Dn)D delta 3 rearrangement were detected in 0.1-0.01% of normal peripheral mononuclear cells by the polymerase chain reaction.
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PMID:Developmental process of the T-cell receptor alpha and delta gene assembly in B-cell precursor acute lymphoblastic leukaemia. 164 73

The mouse homolog of the Gibbon ape leukemia virus (GALV) receptor (Glvr-1) was mapped to mouse Chromosome 2 (Chr 2) by Southern blot analysis of somatic cell hybrids and positioned on this chromosome using an interspecies genetic cross. Mouse Chr 2 also encodes a receptor (Rec-2) for the wild mouse virus M813. To investigate whether Glvr-1 and Rec-2 could be the same gene, we sought evidence for sequence homology between the env- genes of their respective viruses. Southern blot hybridization with GALV-derived env and pol-env probes failed to detect any homology between GALV and M813, but did show that all mouse species tested carry numerous copies of GALV-related sequences. We speculate that a functional receptor for GALV-related viruses was expressed during Mus evolution.
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PMID:The mouse homolog of the Gibbon ape leukemia virus receptor: genetic mapping and a possible receptor function in rodents. 164 8

Retrovirus receptors remain a largely unexplored group of proteins. Of the receptors which allow infection of human and murine cells by various retroviruses, only three have been identified at the molecular level. These receptors include CD4 for human immunodeficiency virus, Rec-1 for murine ecotropic virus, and GLVR1 for gibbon ape leukemia virus. These three proteins show no homology to one another at the DNA or protein level. Therefore, work to date has not shown any general relationship or structural theme shared by retroviral receptors. Genes for two of these receptors (CD4 and Rec-1) and several others which have not yet been cloned have been localized to specific chromosomes. In order to assess the relationship between GLVR1 and other retroviral receptors, we mapped the chromosome location of GLVR1 in human and mouse. GLVR1 was found to map to human chromosome 2q11-q14 by in situ hybridization and somatic-cell hybrid analysis. This location is distinct from those known for receptors for retroviruses infecting human cells. Glvr-1 was then mapped in the mouse by interspecies backcrosses and found to map to chromosome 2 in a region of linkage conservation with human chromosome 2. This mouse chromosome carries Rec-2, the likely receptor for M813, a retrovirus derived from a feral Asian mouse. These data raise the interesting possibility that Rec-2 and Glvr-1 are structurally related.
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PMID:Localization of the human gene allowing infection by gibbon ape leukemia virus to human chromosome region 2q11-q14 and to the homologous region on mouse chromosome 2. 167 62

To gain a better understanding of the organization of the complex T-cell antigen receptor alpha/delta (TCR alpha/delta) locus, a deletional analysis using the known six variable (V) regions of the TCR delta was performed in informative leukemic cell lines and fresh leukemias. We and others have previously reported a high incidence of V delta 2-(D)-D delta 3 rearrangements in non-T, non-B-lymphoid precursor acute lymphocytic leukemia (LP-ALL). In contrast V delta 4, V delta 5, V delta 6 rearrangements were rare or absent. V delta-J alpha rearrangements were found in LP-ALL and in T-ALL. Our deletion and rearrangement data combined with that of others suggest the following 5' to 3' organization of the TCR alpha/delta locus: V delta 6-(V delta 4-V alpha 1.2)-V alpha 12.1-V alpha 13.1-V delta 1-V delta 17.1-V delta 5-delta Rec-V delta 2-D/J/C delta-V delta 3-TEA-psi J alpha-J alpha G. The frequency of rearrangements of the various V delta genes suggests preferential use of the V delta most proximal to D/J delta.
Leukemia 1991 Aug
PMID:Organization of the T-cell receptor delta locus by deletional analysis of acute lymphoblastic leukemias and leukemic cell lines. 183 1

A mouse cDNA that confers susceptibility to ecotropic murine leukemia viruses following transfection into human EJ cells has been cloned and sequenced. We show that this sequence is likely to be Rec-1, the chromosome 5 locus originally defined by studies with somatic cell hybrids as responsible for virus susceptibility, and provide a specific chromosomal map position for this locus by analysis of an interspecies backcross. This locus maps in the distal region of chromosome 5 and is thus not within the cluster of retrovirus-related genes near the centromere.
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PMID:Genetic mapping of a cloned sequence responsible for susceptibility to ecotropic murine leukemia viruses. 215 67

The prevalence of feline calicivirus (FCV), feline leukaemia virus (FeLV) and feline immunodeficiency virus (FIV) antibodies were assessed in 78 British and 18 North American household cats with chronic stomatitis and in appropriate controls. In British cats, FCV was significantly (P less than 0.005) more prevalent in both hospital (92 per cent) and general practice (79 per cent) cases compared to their controls (19 per cent in both cases). A similar difference in prevalence of FCV was noted in North American cats where 50 per cent of cases were positive compared to 0 per cent of controls (P less than 0.01). FeLV prevalence was low in all chronic stomatitis populations. A significantly higher prevalence of antibody to FIV was found in British hospital cases (81 per cent) compared with time-matched controls (16 per cent) (P less than 0.001): a similar rate was found in the general practice cases (75 per cent) for which no controls were available. In the North American sample, FIV antibody status was similar in cases (54 per cent positive) and their age, sex and breed matched controls (50 per cent). The possible role of FCV and FIV in the pathogenesis of feline chronic stomatitis is discussed.
Vet Rec 1989 Apr 01
PMID:Prevalence of feline calicivirus, feline leukaemia virus and antibodies to FIV in cats with chronic stomatitis. 254 29


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