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      Metastatic potential of SP1 mouse mammary adenocarcinoma cells is differentially induced by activated and normal forms of c-H-ras.

      Oncogene
      Adenocarcinoma, genetics, pathology, Animals, Gene Expression Regulation, Genes, ras, Mammary Neoplasms, Experimental, Mice, Neoplasm Metastasis, Proto-Oncogene Proteins, Transfection, Tumor Cells, Cultured

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          Abstract

          The mouse mammary adenocarcinoma cell line SP1 was transfected with either the activated T24-H-ras or the normal c-H-ras gene and assessed for metastatic potential in syngeneic CBA/J or nude mice. Unlike the parental control cells, which were tumorigenic but unable to metastasize from a subcutaneous site, all SP1 transfectants expressing the T24-H-ras gene were able to metastasize (predominantly to the lung). In contrast, a much smaller fraction of the clones obtained following transfection with either normal c-H-ras or pSV2neo were metastatic and, significantly, elevated expression of the c-H-ras proto-oncogene did not correlate with acquisition of metastatic potential. We conclude that activated and normal forms of the c-H-ras gene differ in their ability to confer metastatic potential to SP1 mouse mammary adenocarcinoma cells.

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