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 DNA polymerase of Rauscher murine leukemia virus is strongly and specifically inhibited by nontemplate, single-stranded polyribonucleotides with either the resident viral RNA, native calf-thymus DNA, or poly[d(A-T)] as templates. These inhibitory homopolymers are apparently bound to the template site of the polymerase, since they interact competitively with the template. The strength of the inhibition depends on the particular homopolymer used: poly(U) > poly(G) >> poly(A) > poly(C). The K(i) for poly(U) was 0.08 mug/ml, which represents an apparent affinity six times greater than that observed for viral RNA. No such inhibition was observed with a highly purified DNA polymerase from mouse embryos or the Escherichia coli enzyme.
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PMID:Inhibition of the DNA polymerase of Rauscher leukemia virus by single-stranded polyribonucleotides. 528 79

The nucleotide sequence of the long terminal repeat (LTR) of bovine leukemia virus, a unique oncogenic retrovirus of cattle, was determined. The LTR consisted of 530 base pairs (bp) with an inverted repeat of 6 bp at its 5' and 3' ends, flanked by a direct repeat of 6 bp of host cell origin. A tRNAPro binding site for minus-strand DNA synthesis followed the 5' LTR. The U3 region contained putative transcriptional promoters, "CAT" box and "TATA" box, but they had peculiar sequences (C-C-A-A-C-T and G-A-T-A-A-A-T). The U3 region also contained a potential enhancer element, whose sequence partially resembled those of other viral and cellular, especially of immunoglobulin, enhancers. The most striking structural feature of the LTR was an exceptionally long R region (228 bp), which separated a poly(A) addition signal (A-A-T-A-A-A) from a poly(A) site as far apart as 260 bp. The long R region was suggested to form a large stable hairpin structure on a nascent RNA chain, making the two transcription termination signals close together and thus ensuring normal termination of the chain. This structural feature of the bovine leukemia virus LTR was analogous to that of human T-cell leukemia virus LTR and, in fact, slight sequence homology (at most 50%) was observed between the R regions of these two retroviruses, indicating their evolutionary relationship. The unique structural feature of bovine leukemia virus and human T-cell leukemia virus LTRs may thus bear some relation to the biological features commonly shared by these retroviruses.
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PMID:Bovine leukemia virus: unique structural features of its long terminal repeats and its evolutionary relationship to human T-cell leukemia virus. 608 46

This paper reports the occurrence of renal cell carcinoma, hepatoma and malignant hepatic mixed tumor in a 22-year-old male with ataxia-telangiectasia (AT). Incidence of various malignant neoplasms is high in the patients with AT. The majority of these are lymphoreticular tumors and leukemia, and epithelial tumors are rare. This report is the first case with renal cell carcinoma and the second with hepatoma. The reason for a low incidence of epithelial tumors in AT is still obscure. It is possible that as the result of abnormal aging the tumors expected in the aged will occur in longer survivors with AT.
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PMID:Ataxia-telangiectasia with renal cell carcinoma and hepatoma. 625 35

Adult T-cell leukemia virus (ATLV) is a human retrovirus closely associated with adult T-cell leukemia. The integrated provirus DNA and cDNA from virion RNA were molecularly cloned and their structures were analyzed. Clone lambda ATM-1 of an integrated provirus DNA in the MT-1 cell line, established from adult T-cell leukemia cells by cocultivation with cord lymphocytes, contained DNA about 13,000 base pairs (bp) long and long terminal repeats (LTR) at both ends of the viral sequence that were about 8,000 bp long. These two LTR sequences were linked to cellular sequences with direct repeats of 7 bp. Each LTR consisted of 754 bp including inverted repeats of 2 bp at the ends and the T-A-T-A-A box, characteristics in common with those of LTRs of other known retroviruses. Adjacent to the 5' LTR there was a sequence identical to the tRNAPro binding site in murine leukemia virus, suggesting that tRNAPro is a primer for reverse transcription of the viral genome. From these structural features, the mechanism of ATLV replication was suggested to be the same as that of other known animal retroviruses. However, the length of the small terminal repeats at the ends of the RNA genome, 228 +/- 1 bases, is much longer than the lengths, up to 80 bases, of those in avian, mouse, or primate retroviruses so far analyzed. These findings suggest that ATLV should be classified in a distinct group of retroviruses with bovine leukemia virus which also makes unusually long strong-stop cDNA.
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PMID:Human adult T-cell leukemia virus: molecular cloning of the provirus DNA and the unique terminal structure. 629 64

We have determined the nucleotide sequence in the U3-R regions of the long terminal repeat (LTR) associated with NFS-Th-1 xenotropic murine leukemia virus (MuLV) DNA and the LTR components of five endogenous proviruses cloned from BALB/c mouse chromosomal DNA. The five endogenous MuLV LTRs contained the regulatory signals thought to be important in viral transcription, such as "TATAA" and CCAAT-like boxes. A unique feature in four of the endogenous LTRs was the presence of a highly conserved 190-base-pair (bp) insert bounded by 6-bp direct repeats located 48 bp upstream from the C-C-A-A-T sequence. This segment was absent from LTRs associated with ecotropic, xenotropic, or mink cell focus-forming (MCF) MuLV proviruses. All five endogenous LTR segments also contained a 14-bp duplication of a sequence located near the 5' end of the first component of the long (greater than 72-bp) direct repeat of ecotropic and MCF MuLV LTRs. An evolutionary scheme relating LTRs associated with endogenous MuLV proviral DNAs to those found in ecotropic or xenotropic proviruses is presented. Nucleotide sequence analysis also suggested that the U3 region of the MCF247 MuLV LTR is derived from an NFS xenotropic related MuLV.
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PMID:Endogenous murine leukemia proviral long terminal repeats contain a unique 190-base-pair insert. 630 1

The first case of ataxia-telangiectasia (AT) with dysgerminoma of the right ovary, papillary carcinoma of the thyroid, and adenocarcinoma of the pancreas is reported. There is the characteristic trend of the occurrence of the malignant neoplasms in AT. Lymphoreticular neoplasms and leukemia are most frequently seen in the younger patients with AT. On the other hand, epithelial malignant neoplasms are frequently seen in the longer survivors with AT. Literature also shows that nucleomegaly is due to precocious or abnormal aging.
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PMID:Ataxia-telangiectasia with dysgerminoma of right ovary, papillary carcinoma of thyroid, and adenocarcinoma of pancreas. 646 38

Five patients with primary immunodeficiency and cancer are presented. Two children with ataxia-telangiectasia developed acute lymphoblastic leukemia and malignant lymphoma of B-like origin with chromosome damage and unusual prevalence of antibodies to E.B.V. early antigen. A bone sarcoma occurred in a patient with common variable hypogammaglobulinemia. At least two infants who died with severe combined immunodeficiency had at autopsy congenital myelomonocytic leukemia and malignant lymphoma. These cases indicate the high risk for development of cancer in patients with primary abnormalities of the immune system and suggest the heterogeneity and complexity of pathogenic mechanisms.
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PMID:[Primary immunologic deficiencies and cancer. 5 anatomo-clinical case reports]. 657 32

Lymphoreticular malignancies occur frequently in association with ataxia-telangiectasia (A-T). This paper presents one new case and reviews all 19 known cases of A-T and acute lymphoblastic leukemia (ALL). The leukemia is associated with poor prognostic factors: male sex, older age, high white blood cell count, and T or B-cells. There have been no long-term survivors; recently, prolonged remissions have been attained. These patients appear to be at special risk for infections secondary to the immunodeficient state associated with A-T and ALL therapy. A heightened sensitivity to the neurotoxic effects of vinca alkaloids and central nervous system irradiation seems to be present.
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PMID:Ataxia-telangiectasia and acute lymphoblastic leukemia. 692 16

We report a new case of ataxia-telangiectasia (AT) and acute lymphoblastic leukemia (ALL) and review all 21 known cases of AT and ALL. Leukemia in these patients is associated with a male predominance, age older than 10 years at diagnosis, a white blood cell count higher than 50,000 mm3, and a fatal course. Four patients have been reported who developed T-cell leukemia, 3 null-cell leukemia and 1 B-cell leukemia. The AT-ALL patients appear to be at risk for infections related to their immunodeficient status and ALL chemotherapy. In addition, neurologic deterioration has been noted during the early phase of therapy.
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PMID:Ataxia telangiectasia and acute lymphoblastic leukemia: report of a case. 695 May 88

Cultured cells from patients inheriting the rare cancer-prone and radiotherapy-sensitive disorder ataxia-telangiectasia (A-T) exhibit anomalies in cell cycle control and protein kinase C (PKC)-mediated upregulation of p53 protein following exposure to ionizing radiation. It remains unclear, however, as to whether this irregularity in a p53-dependent signal transduction pathway controlling the G1/S checkpoint is causally linked to the most consistent molecular hallmark of A-T-namely, marked attenuation in the inhibition of replicative DNA synthesis at early times (< or = 2 h) after irradiation [radioresistant DNA synthesis (RDS)]. We report here that treatment of normal human fibroblast strains with inhibitors of calmodulin (CaM) (i.e. W7 and W13) and CaM-dependent protein kinases II and IV (i.e. KN62) prior to radiation exposure elicits an 'A-T-like' RDS phenotype, whereas treatment with PKC inhibitors (e.g. staurosporine) does not produce this response. Moreover, at 1 h post-gamma irradiation A-T fibroblasts undergo normal induction of p53 protein while exhibiting the RDS trait. At later times (e.g. 4 h) following irradiation, however, these A-T cells contain abnormally low levels of p53 protein, as do their lymphoblastoid cell line counterparts during the entire post-gamma ray incubation period. On the other hand, human cells which either lack the p53 gene completely (i.e. HL60 leukemia cells) or harbor a germline mutation in the gene (i.e. Li-Fraumeni syndrome cells) shut down their DNA replication machinery normally upon sustaining radiation damage. We thus conclude that the transitory delay in DNA synthesis routinely experienced by human cells in the face of radiation injury is mediated through a CaM-dependent regulatory cascade which involves neither PKC nor p53 protein. Accordingly, A-T cells appear to be malfunctional in at least two distinct radiation-responsive signalling pathways, one regulating the G1/S checkpoint and governed by p53 and PKC and another controlling passage through S phase and requiring CaM.
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PMID:Characterization of the signal transduction pathway mediating gamma ray-induced inhibition of DNA synthesis in human cells: indirect evidence for involvement of calmodulin but not protein kinase C nor p53. 747 84


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