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)

Nineteen cases of canine acute leukemia were diagnosed during a 4-year period. Two main categories were identified on the basis of cytologic, hematologic, and clinical features: acute lymphoid leukemia and acute myelogenous leukemia. Clinical features included history of weight loss, anorexia, shifting limb lameness, and incoordination. Physical findings were characterized by hepatomegaly, splenomegaly, mild generalized lymphadenopathy, and pallor. Ocular lesions were found in 29% of dogs with acute myelogenous leukemia. Hematologic abnormalities included anemia, thrombocytopenia, pancytopenia, leukemia, and leukoerythroblastic reactions. Results of therapy were discouraging.
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PMID:Clinicopathologic aspects of acute leukemias in the dog. 385 21

Inbred mice bearing the FV-1n marker when inoculated at birth with an ecotropic murine leukemia virus (WM 1504-E) obtained from wild mice develop a progressive central nervous system (CNS) disease manifested by hindlimb paralysis and incoordination that begins by 6 to 7 weeks of age. Studies of infected SWR/J mice at 3 days to 4 months of age indicated the following: (1) Expression of MuLV gp69/70 and p30 antigens in CNS rises beginning as early as 3 days after inoculation and increases with time. (2) Neuronal damage is evident by Day 7, and neuronal lesions develop in all mice by Day 14. (3) WM 1504-E virus can be isolated from CNS tissue by 48 hr after initiating infection. (4) Upon passage into susceptible newborn mice, the WM 1504-E isolates cause neuronal disease. (5) "Dual-tropic" mink cell focus forming (MCF) -like virus is found in splenic but not CNS tissues by 8 weeks after initiating infection. (6) MCF viruses that arise by env gene recombination between WM 1504-E and endogenous xenotropic viruses do not cause CNS disease upon inoculation into susceptible newborn mice. Similarly inoculated WM 1504-amphotropic virus (WM 1504-A) does not cause CNS disease (7). Results in SWR/J mice can be duplicated in C3H/St and C57Br/cdj mice. These observations define the wild mouse ecotropic virus as the sole infectious agent responsible and sufficient for the development of this neurologic disease. Evidently, the disease from this "slow virus infection" begins early in life shortly after introduction of the infectious agent, but becomes clinically apparent only as neuronal destruction accumulates over the lifetime of the host.
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PMID:Pathogenesis of the slow disease of the central nervous system associated with wild mouse virus. III. Role of input virus and MCF recombinants in disease. 630 90

Disease-free survival (DFS) in childhood ALL is 60%, and survival in good, average, and poor prognostic groups defined by initial WBC and age is 90, 60, and 45%, respectively. Additional immunological, morphological, biochemical, cytokinetic, and cytogenetic factors have been identified, illustrating the heterogeneity of ALL and its derivation from malignant clones at various stages of differentiation and with varying rates of proliferation. Of biologic importance, these factors may refine further the characteristic features of clinically-determined prognostic groups. Multivariate analysis of large prospective trials with homogeneous therapy will be required to determine the independent prognostic importance of these factors. Current treatment strategies in ALL include (1) tailoring therapy and its intensity to prognostic groups; (2) multiple-drug combinations in induction; (3) early use of intrathecal (IT) methotrexate (MTX); (4) CNS prophylaxis with IT MTX alone in good prognosis patients and combined cranial radiation (CXRT), 1800 rads plus IT MTX, in average and poor prognosis patients. Current studies show a CNS relapse rate of 5% in all prognostic groups. Late neuropsychological defects caused by cranial XRT and IT MTX have prompted programs designed to reduce the potential late toxicity of CNS prophylaxis. More pronounced in younger children, these abnormalities include decreased IQ, visual-motor incoordination, poor performance in mathematics, and memory dysfunction. Until 1980, more intensive induction, consolidation, and maintenance therapy had failed to prolong DFS in children with a poor prognosis. In West Germany (Berlin-Frankfurt-Muenster protocol) a 70 to 75% DFS is seen in all patients regardless of initial WBC, suggesting that effective therapy will override prognostic factors. Ultra-high-dose MTX, without cranial radiation, is also showing promise in poor prognosis patients. Other issues include the optimal duration of therapy, the role of testicular biopsies, and prophylactic testicular radiation. Recent studies suggest that prognostic factors lose their significance after 2 years of continuous complete remission and that 2 years of maintenance therapy is adequate. Bilateral open-wedge testicular biopsies have identified occult testicular disease in 8 to 10% of males. A unified approach to children with leukemia/lymphoma, a group with a particularly poor prognosis, utilizing NHL-type therapy may be more effective than conventional ALL therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute lymphoblastic leukemia in children: current status, controversies, and future perspective. 639 64

Xenotropic murine leukemia virus (MLV)-related virus (XMRV) is a new human retrovirus associated with prostate cancer and chronic fatigue syndrome. The causal relationship of XMRV infection to human disease and the mechanism of pathogenicity have not been established. During retrovirus replication, integration of the cDNA copy of the viral RNA genome into the host cell chromosome is an essential step and involves coordinated joining of the two ends of the linear viral DNA into staggered sites on target DNA. Correct integration produces proviruses that are flanked by a short direct repeat, which varies from 4 to 6 bp among the retroviruses but is invariant for each particular retrovirus. Uncoordinated joining of the two viral DNA ends into target DNA can cause insertions, deletions, or other genomic alterations at the integration site. To determine the fidelity of XMRV integration, cells infected with XMRV were clonally expanded and DNA sequences at the viral-host DNA junctions were determined and analyzed. We found that a majority of the provirus ends were correctly processed and flanked by a 4-bp direct repeat of host DNA. A weak consensus sequence was also detected at the XMRV integration sites. We conclude that integration of XMRV DNA involves a coordinated joining of two viral DNA ends that are spaced 4 bp apart on the target DNA and proceeds with high fidelity.
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PMID:Fidelity of target site duplication and sequence preference during integration of xenotropic murine leukemia virus-related virus. 2042 28