Results 191 to 200 of about 40,097 (234)
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Human Retinoblastoma Susceptibility Gene
1990It is clear that the RB-deficient tumor cells lost their tumorigenicity in nude mice after regaining the RB gene expression. However, the mechanism of tumor suppression by the RB gene is still unknown. More studies on the biological activities of RB protein, pp110RB, are necessary to answer this question.
C C, Lai, W H, Lee
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Molecular characterization of the retinoblastoma susceptibility gene
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 1993Retinoblastoma is recognized as a hereditary cancer. Genetic and epidemiological analysis of the disease has been incorporated into a two-hit mutational inactivation hypothesis of the origin of retinoblastoma. The molecular cloning and characterization of the retinoblastoma gene and gene product has allowed a critical testing of this two-hit hypothesis.
D W, Goodrich, W H, Lee
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Studies on the human retinoblastoma susceptibility gene
Journal of Cellular Biochemistry, 1988AbstractThe retinoblastoma susceptibility (RB) gene is unique among other cloned cancer genes because its causal role in a human cancer, retinoblastoma, was established by classical genetic methods before its isolation. Earlier hypotheses and experimental data suggested that inactivation of a gene in chromosome band 13q14 resulted in retinoblastoma ...
W H, Lee, R, Bookstein, E Y, Lee
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Structure and expression of the Xenopus retinoblastoma gene
Developmental Biology, 1992We have cloned a Xenopus homology (XRb1) of the human retinoblastoma susceptibility gene. DNA sequence analysis shows that the XRb1 gene product is highly conserved in many regions. The leucine repeat motif and many of the potential cdc2 phosphorylation sites, as well as potential sites for other kinases, are retained.
O H, Destrée +8 more
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Identification of Mutations in the Retinoblastoma Gene
2003Mutations in the retinoblastoma gene (RBl) predispose to the formation of ocular tumors. Following the cloning of RBI in 1986 (1), polymorphic restriction enzyme sites within RBl were used to "track" the mutant gene within affected families using linkage analysis (2, 3).
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The gene responsible for the development of retinoblastoma and osteosarcoma
Cancer, 1988The gene responsible for the formation of both retinoblastoma and osteosarcoma recently has been isolated. This represents the first human recessive cancer gene ever cloned. Structural deletions within one or both retinoblastoma gene alleles were commonly noted in the retinoblastomas and an osteosarcoma.
W F, Benedict, Y K, Fung, A L, Murphree
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Regulation of the Urokinase Gene by the Retinoblastoma Protein
DNA and Cell Biology, 1994The promoter of the human urokinase plasminogen activator (uPA) gene contains a sequence identical with the retinoblastoma control element (RCE) of the murine c-fos gene, as well as several Sp1 binding sites. In a number of cell lines, the uPA promoter is activated during enforced expression of the retinoblastoma protein, pRB.
U, Novak, L, Paradiso, J A, Hamilton
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Parental origin of mutations of the retinoblastoma gene
Nature, 1989Retinoblastoma and osteosarcoma arise from cells that have lost both functional copies of the retinoblastoma gene. Using the cloned retinoblastoma gene and other linked polymorphic loci, it is possible to reconstruct the sequential loss of the two homologous gene copies that precedes the development of these tumours. In non-hereditary tumours, the loss
T P, Dryja +5 more
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Retinoblastoma gene in mouse neural development
Developmental Genetics, 1996The retinoblastoma gene (Rb) was the first tumor suppressor gene to be cloned [Dryja et al., 1986; Friend et al., 1986; Lee et al., 1987], and, as a consequence, has been studied intensively within the context of cell cycle regulation and oncogenesis. However, a number of recent findings indicate that the retinoblastoma gene product (pRb) likely plays ...
R S, Slack, F D, Miller
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The role of the retinoblastoma gene in tumour pathogenesis
Clinical Oncology, 1992Retinoblastoma is a rare tumour. The gene involved in the formation of retinoblastoma has been identified, and it has since been shown to be implicated in many other tumour types. In addition, patients with the familial form of retinoblastoma are known to be at an increased risk of developing second primary, non-ocular, malignancies.
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