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Control of Expression of Insulin-Like Growth Factor II in Stromal Cells of Breast Cancer

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Annual summary rept. 1 Jul 2000-30 Nov 2002

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Our hypothesis is that unique genes on human chromosomes are involved in the progression of breast cancer from an insulin-dependent to insulin-independent state, During breast cancer development, tumors progress from an insulin-dependent to an insulin-independent state. In order to simulate the progression of breast cancer from an insulin-dependent to insulin-independent state, our lab developed the following three cell line model system. The parental cell line that was used was CAL51, an ER-, wild type p53 carrying, metastatic breast cancer cell line that has the unique feature of being diploid in chromosome number. Additionally, CAL51 displays the tumorigenic phenotype including rapid population doubling time in the absence of insulin, anchorage-independent growth in soft agar culture, and rapid tumor formation in athymic nude mice. Through microcell-mediated chromosome transfer, chromosome 17 was introduced to create the suppressed cell line CAL 17. As stated, this cell line exhibits a suppressed phenotype contrasting CAL51 in that has an increased population doubling time, loss of anchorage-independent growth and nontumorigenicity. Our laboratory has applied the technique of retroviral insertional mutagenesis to induce insulin-independent revertant cell lines from chromosome 17-mediated suppressed breast cancer. After culturing for two months in the absence of insulin, we isolated and established 48 revertant cell sublines termed RICs Retrovirus-induced Insulin-independent Cell that displayed insulin-independent growth. It should be noted that while the suppressed cell line CAL 17 is insulin-independent, the tumorigenic cell line, CAL51 and revertant cell lines, RICs, are insulin-independent.

Subject Categories:

  • Genetic Engineering and Molecular Biology
  • Anatomy and Physiology
  • Medicine and Medical Research

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