Journal ArticleDOI
Effects of an Rb mutation in the mouse
Tyler Jacks,Amin Fazeli,Earlene M. Schmitt,Roderick T. Bronson,Margaret A. Goodell,Robert A. Weinberg +5 more
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TLDR
A mouse strain has been constructed in which one allele of Rb is disrupted, and heterozygous animals are not predisposed to retinoblastoma, but some display pituitary tumours arising from cells in which the wild-type Rb allele is absent.Abstract:
The retinoblastoma gene is mutated in several types of human cancer and is the best characterized of the tumour-suppressor genes. A mouse strain has been constructed in which one allele of Rb is disrupted. These heterozygous animals are not predisposed to retinoblastoma, but some display pituitary tumours arising from cells in which the wild-type Rb allele is absent. Embryos homozygous for the mutation die between days 14 and 15 of gestation, exhibiting neuronal cell death and defective erythropoiesis.read more
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Journal ArticleDOI
Cancer Cell Cycles
TL;DR: Genetic alterations affecting p16INK4a and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development.
Journal ArticleDOI
The retinoblastoma protein and cell cycle control
TL;DR: The main role of pRB is to act as a signal transducer connecting the cell cycle clock with the transcriptional machinery, allowing the clock to control the expression of banks of genes that mediate advance of the cell through a critical phase of its growth cycle.
Journal ArticleDOI
Inhibitors of mammalian G1 cyclin-dependent kinases.
Journal ArticleDOI
The regulation of E2F by pRB-family proteins
TL;DR: The rapid growth in the size of the E2F literature hides the fact that several fundamental questions have not been fully answered, and the second section of this review details five unresolved issues that have been highlighted by recent publications.
Journal ArticleDOI
Tumor spectrum analysis in p53-mutant mice.
Tyler Jacks,Lee Remington,Bart O. Williams,Earlene M. Schmitt,Shlomit Halachmi,Roderick T. Bronson,Robert A. Weinberg +6 more
TL;DR: It is reaffirm that p53 function is not required for normal mouse development and conclude that p 53 status can strongly influence tumor latency and tissue distribution.
References
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Journal ArticleDOI
Genomic sequencing
George M. Church,Walter Gilbert +1 more
TL;DR: The genomic sequencing procedures are applicable to the analysis of genetic polymorphisms, DNA methylation at deoxycytidines, and nucleic acid-protein interactions at single nucleotide resolution.
Journal ArticleDOI
Mutation and Cancer: Statistical Study of Retinoblastoma
TL;DR: The hypothesis is developed that retinoblastoma is a cancer caused by two mutational events, in the dominantly inherited form, one mutation is inherited via the germinal cells and the second occurs in somatic cells.
Journal ArticleDOI
The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product
TL;DR: The results suggest that these three DNA viruses may utilize similar mechanisms in transformation and implicate RB binding as a possible step in human papilloma virus-associated carcinogenesis.
Journal ArticleDOI
A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma
Stephen H. Friend,Stephen H. Friend,René Bernards,Snezna Rogelj,Robert A. Weinberg,Joyce M. Rapaport,Daniel M. Albert,Thaddeus P. Dryja +7 more
TL;DR: The isolation of a complementary DNA segment that detects a chromosomal segment having the properties of the gene at this locus is described, which is expressed in many tumour types, but no RNA transcript has been found in retinoblastomas and osteosarcomas.
Journal ArticleDOI
T Antigen Is Bound to a Host Protein in Sv40-Transformed Cells
TL;DR: It is reported here that the T antigen in a line of SV40-transformed mouse cells forms an oligomeric complex with a specific cell coded protein.