Activation of the T24 bladder carcinoma transforming gene is linked to a single amino acid change

  title={Activation of the T24 bladder carcinoma transforming gene is linked to a single amino acid change},
  author={Elizabeth J Taparowsky and Yolande Suard and Ottavio Fasano and Kenji Shimizu and Mitchell Goldfarb and Michael Wigler},
Several different transforming genes have been observed in the DNA of a variety of tumours and tumour cell lines of human and rodent origin by the ability of these genes to induce morphological transformation in NIH 3T3 cells1–5. The transforming gene found in a human bladder carcinoma cell line, T24, is H-ras-1, the human homologue of the Harvey sarcoma virus oncogene (v-H-ras)6–9. In the present study we have compared the H-ras-1 genes cloned from T24 and normal human DNA. The H-ras-1 gene… 
Mechanism of activation of human ras genes cloned from a gastric adenocarcinoma and a pancreatic carcinoma cell line.
A rasN gene from a human gastric adenocarcinoma which efficiently induced both morphological transformation and tumorigenicity of NIH3T3 cells in a transfection assay is identified and sequence analysis reveals a G to A change within codon 12, which is presumably responsible for its biological activity.
Conversion of ras genes to cancer genes.
The cellular precursor of Harvey and Balb sarcoma virus, termed proto-ras, from certain tumors registers most frequently as an apparent cancer gene in the gene transfer assay with NIH 3T3 cells, but the role of the cellular ras gene as a human cancer gene is debatable.
Human colon carcinoma Ki-ras2 oncogene and its corresponding proto-oncogene
We isolated cDNA clones corresponding to the normal human Ki-ras2 gene and to the transforming allele of the Ki-ras2 gene present in the human colon carcinoma cell line SW480. These two cDNAs encode
Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient.
The mutational event responsible for the malignant activation of a K-ras oncogene in a squamous cell lung carcinoma of a 66-year-old man was identified and appears to be specifically associated with the development of a human neoplasm.
Activation of the c-K-ras oncogene in a human pancreas carcinoma.
Structure of the Ki-ras gene of the human lung carcinoma cell line Calu-1
A common modular structure for ras gene products in which the variable region forms a physiologically important combining site is proposed.
Biological properties of human c-Ha-ras1 genes mutated at codon 12
To provide insight into structural requirements involved in p21 activation, 20 mutant c-Ha-ras1 genes are constructed by in vitro mutagenesis, each encoding a different amino acid at codon 12, suggesting a requirement for an α-helical structure in this region of the polypeptide.
Dispersion of the ras family of transforming genes to four different chromosomes in man
An understanding of the genetic relationship of the c-ras genes and additional genetic loci possibly involved in neoplastic transformation would be greatly facilitated by placement of the ras genes on the human chromosome map.
Identification of transforming gene in two human sarcoma cell lines as a new member of the ras gene family located on chromosome 1
A molecular clone containing part of the transforming gene from two human sarcoma cell lines, HT1080 and RD, has been obtained and shown to represent a new member of the human ras gene family. The
Characterization of human transforming genes from chemically transformed, teratocarcinoma, and pancreatic carcinoma cell lines.
The results show that the transforming gene activated in the teratocarcinoma cell line is identical to the neuroblastoma transforming gene and that the Transformation gene of the pancreatic carcinoma cellline is a human homologue of rasK.


T24 human bladder carcinoma oncogene is an activated form of the normal human homologue of BALB- and Harvey-MSV transforming genes
A transforming gene isolated from T24 human bladder carcinoma cells is closely related to the BALB murine sarcoma virus (MSV) onc gene (v-bas), which implies that rather subtle genetic alterations have led to the activation of the normal human homologue of v-bas as a human transforming gene.
Transforming genes of human bladder and lung carcinoma cell lines are homologous to the ras genes of Harvey and Kirsten sarcoma viruses.
Results indicate that the transforming genes of these human tumor cell lines are the cellular homologs of two retroviral transforming genes.
A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogene
A single amino acid substitution appears to be sufficient to confer transforming properties on the gene product of the T24 human bladder carcinoma oncogene.
Isolation and preliminary characterization of a human transforming gene from T24 bladder carcinoma cells
It is found that T24, a cell line derived from a human bladder carcinoma, can induce the morphological transformation of NIH 3T3 cells, and the gene responsible for this transformation is human in origin, <5 kilobase pairs in size and homologous to a 1,100-base polyadenylated RNA species found in T24 and HeLa cells.
Transforming activity of human tumor DNAs.
  • T. Krontiris, G. Cooper
  • Biology, Chemistry
    Proceedings of the National Academy of Sciences of the United States of America
  • 1981
It is suggested that dominant mutations or gene rearrangements can result in the activation of cellular transforming genes in some human tumors.
Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene
Examination of homologies between retroviral oncogenes and transforming sequences defined by transfection reveals that the human bladder carcinoma (EJ) oncogene is homologous to the Harvey sarcoma
Passage of phenotypes of chemically transformed cells via transfection of DNA and chromatin.
These experiments prove that in five mouse and rat cell lines the chemically induced phenotype is encoded in DNA, and the sequences specifying the transformed phenotype behave as a dominant allele in the NIH3T3 recipient cells.