Accession Number : ADA474861


Title :   The Human L1 Element Causes DNA Double-Strand Breaks in Breast Cancer


Descriptive Note : Final rept. 1 Aug 2005-31 Jul 2006


Corporate Author : TULANE UNIV HEALTH SCIENCE CENTER NEW ORLEANS LA


Personal Author(s) : Deininger, Prescott L


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/a474861.pdf


Report Date : 01 Aug 2006


Pagination or Media Count : 44


Abstract : The source of mutagenesis for the establishment and maintenance of cancer is complex. However, defects in DNA repair genes in the double-strand break repair pathway are cancer predisposing. My lab has characterized a new potentially important source of double-strand breaks (DSBs) in human cells and are interested in characterizing which DNA repair genes act on this particular source of DNA damage. Selfish DNA accounts for 45% of the human genome. We have recently demonstrated that one particular selfish DNA, the L1 retrotransposon, creates DSBs via its endonuclease domain. The important conclusions from the published work are that 1) the human retrotransposon L1 creates DSBs and 2) the DSB repair gene ATM is required for L1 retrotransposition. To additionally characterize the roles of ATM and the ATM-related genes, BRCA1 and BRCA2, in L1-induced DSBs, we developed a new vector system to suppress their expression which is compatible with L1 assays. These constructs should also be of general utility.


Descriptors :   *DEOXYRIBONUCLEIC ACIDS , *VECTOR ANALYSIS , *STRANDS , *BREAST CANCER , MAINTENANCE , DAMAGE , GENOME , GENES , CELLS(BIOLOGY) , REPAIR , MUTATIONS , HUMANS


Subject Categories : Biochemistry
      Medicine and Medical Research


Distribution Statement : APPROVED FOR PUBLIC RELEASE