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Hereditary Cancer, Oncogenes, and Antioncogenes

Alfred G. Knudson
- 01 Apr 1985 - 
- Vol. 45, Iss: 4, pp 1437-1443
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This article is published in Cancer Research.The article was published on 1985-04-01 and is currently open access. It has received 1243 citations till now. The article focuses on the topics: Mutation (genetic algorithm) & Carcinogenesis.

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Citations
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A genetic model for colorectal tumorigenesis

TL;DR: A model for the genetic basis of colorectal neoplasia that includes the following salient features is presented, which may be applicable to other common epithelial neoplasms, in which tumors of varying stage are more difficult to study.
Journal ArticleDOI

Genetic alterations during colorectal-tumor development.

TL;DR: It is found that ras-gene mutations occurred in 58 percent of adenomas larger than 1 cm and in 47 percent of carcinomas, which are consistent with a model of colorectal tumorigenesis in which the steps required for the development of cancer often involve the mutational activation of an oncogene coupled with the loss of several genes that normally suppress tumors.
Journal ArticleDOI

A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma

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.
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Clues to the pathogenesis of familial colorectal cancer

TL;DR: Molecular features of "familial" cancers were compared with those of sporadic colon cancers, and a mechanism for familial tumorigenesis different from that mediated by classic tumor suppressor genes is suggested.
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Mutations in the p53 gene occur in diverse human tumour types

TL;DR: It is suggested that most tumours with allelic deletions of chromosome 17p contain p53 point mutations resulting in amino-acid substitutions, and p53 gene mutations are clustered in four 'hot-spots' which exactly coincide with the four most highly conserved regions of the gene.
References
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Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage

TL;DR: N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.
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Chromosomal Deletion and Retinoblastoma

TL;DR: A new case of a deletion of the long arm of chromosome 13 is reported and its relation to previously reported cases is considered and the relation between the two genetic groups is considered.
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Somatic inactivation of genes on chromosome 13 is a common event in retinoblastoma.

TL;DR: It is tentatively concluded that induction of a retinoblastoma tumour requires the somatic inactivation of genes near the ESD locus including the remaining normal gene at the retinOBlastoma (RB) locus.
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Retinoblastoma: a prototypic hereditary neoplasm.

TL;DR: From such a study it is concluded that the hereditary and nonhereditary forms of this, and probably many other, tumors arise by similar processes and that the study of hereditary forms can contribute to the understanding of cancer generally.
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The aniridia-Wilms tumor association: The critical role of chromosome band 11p13☆

TL;DR: These patients and their karyotypes substantiate the critical importance of chromosome band 11p13 (or its hemizygous representation) in the development of aniridia and an associated Wilms tumor diathesis, as had been suggested previously.
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