A Sarcoma of the Fowl Transmissible by an Agent Separable From the Tumor Cells

Rous, Peyton

doi:10.1084/jem.13.4.397

Cited by 853 publications

(190 citation statements)

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“…The v-src gene, encoded by Rous sarcoma virus, was the ®rst transmissible gene found to induce tumors. It was originally discovered by Peyton Rous in 1911 (Rous, 1911) as a transmissible agent that would produce tumors in chickens. The protein product of this gene, v-Src, is a tyrosine kinase with a cellular homolog, c-Src, which is found in normal cells and presumed to be a protooncogene (Czernilofsky et al, 1980) (Stehelin et al, 1976).…”

Section: Src As a Potential Oncogenementioning

confidence: 99%

Role of Src expression and activation in human cancer

2000

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Section: Src As a Potential Oncogenementioning

confidence: 99%

Role of Src expression and activation in human cancer

2000

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“…recognized for its ability to cause sarcomas in chickens (1). The transforming protein of RSV, v-src, is a cytoplasmic tyrosine kinase with constitutive activity (2,3).…”

Section: R Ous Sarcoma Virus (Rsv) Is the First Known Tumor Virusmentioning

confidence: 99%

Role of the cytoplasmic tyrosines of β1A integrins in transformation by v-src

Sakai

Jove

Fässler

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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GD25 cells lacking ␤1 integrins or expressing ␤1A with mutations of conserved cytoplasmic tyrosines (Y783, Y795) to phenylalanine have poor directed migration to platelet-derived growth factor or lysophosphatidic acid when compared with GD25 cells expressing wild-type ␤1A. We studied the effects of v-src on these cells. Transformation with v-src caused tyrosine and serine phosphorylation of wild-type ␤1A but not of Y783͞795F doubly mutated ␤1A. v-src-transformed cells had rounded and͞or fusiform morphology and poor assembly of fibronectin matrix. Adhesion to fibronectin or laminin and coupling of focal contacts to actin-containing cytoskeleton were preserved in transformed Y783͞795F cells but lost on transformation when ␤1A was wild type. Transformed Y783͞795F cells also retained ability, albeit limited, to migrate across filters, whereas transformed cells with wild-type ␤1A were unable to transverse filters. Studies of single tyrosine mutants showed that the more important tyrosine for retaining ability to adhere, assemble focal contacts, and migrate is Y783. These results suggest that overactive phosphorylation of cytoplasmic residues of ␤1A, particularly Y783, accounts in part for the phenotype of v-src-transformed cells.

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“…1'. Surprisingly, cell-free filtrates could also transmit the disease, indicating that the tumor was due to a 'filterable agent', as viruses were then called (Rous, 1911). Other chicken tumors with distinct pathologies, such as an osteochondrosarcoma that produced cartilage and bone, also proved to contain filterable agents.…”

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confidence: 99%

The road to Src

2004

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More than a quarter of a century has elapsed since the identification of the c-src proto-oncogene. During that period, we have learned that cancer arises as the result of mutations in proto-oncogenes and tumor suppressor genes, and we are now seeing the first fruits of these discoveries, in the form of targeted therapies directed against activated tyrosine kinases such as Bcr-Abl, c-Kit and the EGF receptor. But the discovery of the c-src proto-oncogene was in turn based on decades of study on an avian RNA tumor virus, Rous sarcoma virus (RSV). Here I review the work that led up to the identification of the RSV transforming gene and its protein product, and how this information in turn led to the discovery of cellular Src.

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A Sarcoma of the Fowl Transmissible by an Agent Separable From the Tumor Cells

Cited by 853 publications

References 0 publications

Role of Src expression and activation in human cancer

Role of Src expression and activation in human cancer

Role of the cytoplasmic tyrosines of β1A integrins in transformation by v-src

The road to Src

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