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Berkeley, CA, United States

The Regents Of The University Of California and Exogen Biotechnology Inc. | Date: 2015-02-27

Kits, methods and systems for providing a service to provide a subject with information regarding the state of a subjects DNA damage. Collection, processing and analysis of samples are also described.

Chiolo I.,University of Southern California | Tang J.,Lawrence Berkeley National Laboratory | Tang J.,Exogen Biotechnology Inc. | Georgescu W.,Lawrence Berkeley National Laboratory | And 2 more authors.
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis | Year: 2013

Repair of double strand breaks (DSBs) is essential for cell survival and genome integrity. While much is known about the molecular mechanisms involved in DSB repair and checkpoint activation, the roles of nuclear dynamics of radiation-induced foci (RIF) in DNA repair are just beginning to emerge. Here, we summarize results from recent studies that point to distinct features of these dynamics in two different chromatin environments: heterochromatin and euchromatin. We also discuss how nuclear architecture and chromatin components might control these dynamics, and the need of novel quantification methods for a better description and interpretation of these phenomena. These studies are expected to provide new biomarkers for radiation risk and new strategies for cancer detection and treatment. © 2013 Elsevier B.V.

Tang J.,Exogen Biotechnology Inc. | Georgescu W.,Lawrence Berkeley National Laboratory | Deschamps T.,Exogen Biotechnology Inc. | Yannone S.M.,Exogen Biotechnology Inc. | And 3 more authors.
Cancer Metastasis - Biology and Treatment | Year: 2015

The constant damage of DNA in human cells is considered the main cause of aging and cancer. In this review, we discuss the most lethal form of DNA damage, the DNA double strand break (DSB), and how it relates to cancer. DSB sensor proteins in the nucleus detect DNA breaks within minutes following damage. These proteins are now routinely labeled by immunocytochemistry, and access to high throughput fluorescence microscopy and robotics open the door to rapid measurement of DSB levels in individuals. This method, often referred as the DSB foci assay, leads to images showing small bright spots at the site of each damage in the nucleus. We first discuss how energy consumption in the cell leads to detectable baseline levels of foci per cell measured in peripheral blood lymphocytes. Mathematical kinetics are then described to infer both genetic defects in DNA repair and environmental factors influencing these levels. We emphasize ionizing radiation, which is the principal environmental factor that increases DSB levels. Mathematical models associating a mutation probability for each DSB have been used to explain the dose dependence of cancer incidence observed after exposure to high doses of radiation. The main assumption in these models is that high mutation frequency can eventually lead to tumor suppressor gene deletion or oncogene amplification. We conclude by suggesting that the growing stream of genetic and phenotypic measurements related to DNA repair and DNA damage will lead to more accurate predictive tools for cancer risk and individualized cancer prevention. © Springer International Publishing Switzerland 2015

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