Accession Number : ADA336577
Title : DNA Cleavage/Repair and Signal Transduction Pathways in Irradiated Breast Tumor Cells.
Descriptive Note : Annual rept. 1 Sep 96-31 Aug 97
Corporate Author : VIRGINIA COMMONWEALTH UNIV RICHMOND
Personal Author(s) : Gewtrtz, David
PDF Url : ADA336577
Report Date : SEP 1997
Pagination or Media Count : 27
Abstract : These studies were designed to understand the role of c-myc and the p53 protein in the pathway leading to growth arrest in the breast tumor cell and in the relative refractoriness of breast tumor cells to the induction of apoptotic cell death. An additional component of this work was to investigate the repair of double-strand breaks induced by ionizing radiation (and by the radiomimetic, bleomycin) in breast tumor cells having wild-type versus mutant p53 genes and the relationship of double-strand break repair to apoptotic cell death. We have determined that radiosensitivity does not appear to be a function of p53 in breast tumor cells which fail to undergo apoptotic cell death and that suppression of c-myc may be a component of the signal transduction pathway leading to growth arrest in response to radiation only in p53 positive breast tumor cells. We have also determined that ionizing radiation fails to suppress the activity of the transcription factor E2F in breast tumor cells, suggesting the existence of a previously unidentified mechanisms for loss of restriction point control in the breast tumor cell. Finally, preliminary studies indicate that acquisition of a pleiotropic phenotype incorporating genomic instability and delayed reproductive death may be linked to mutagenesis induced by radiomimetic agents in 184B5 breast epithelial cells.
Descriptors : *NEOPLASMS, *DEOXYRIBONUCLEIC ACIDS, *CELLS(BIOLOGY), *IONIZING RADIATION, *GROWTH(PHYSIOLOGY), *BREAST CANCER, ACQUISITION, ARRESTING(PROCESS), MUTATIONS, REPAIR, SIGNALS, TRANSDUCERS, IRRADIATION, RESPONSE(BIOLOGY), DEATH, CLEAVAGE, MAMMARY GLANDS, RADIATION TOLERANCE.
Subject Categories : Anatomy and Physiology
Distribution Statement : APPROVED FOR PUBLIC RELEASE