Scholars@Duke
Chang Lung Lee

Chang Lung Lee

Associate Professor in Radiation Oncology
Radiation Oncology
Box 91006, Durham, NC 27708
B220 LSRC Bldg, 308 Research Dr, Box 91006, Durham, NC 27708

Featured Works

Acute DNA damage activates the tumour suppressor p53 to promote radiation-induced lymphoma.

Journal article Nat Commun · September 24, 2015 Featured Publication Genotoxic cancer therapies, such as chemoradiation, cause haematological toxicity primarily by activating the tumour suppressor p53. While inhibiting p53-mediated cell death during cancer therapy ameliorates haematologic toxicity, whether it also impacts c ... Full text Link to item Cite

Atm deletion with dual recombinase technology preferentially radiosensitizes tumor endothelium.

Journal article J Clin Invest · August 2014 Featured Publication Cells isolated from patients with ataxia telangiectasia are exquisitely sensitive to ionizing radiation. Kinase inhibitors of ATM, the gene mutated in ataxia telangiectasia, can sensitize tumor cells to radiation therapy, but concern that inhibiting ATM in ... Full text Link to item Cite

p53 functions in endothelial cells to prevent radiation-induced myocardial injury in mice.

Journal article Sci Signal · July 24, 2012 Featured Publication Radiation therapy, which is used for the treatment of some cancers, can cause delayed heart damage. In the heart, p53 influences myocardial injury that occurs after multiple types of stress. Here, we demonstrated that p53 functioned in endothelial cells to ... Full text Link to item Cite

Generation of primary tumors with Flp recombinase in FRT-flanked p53 mice.

Journal article Dis Model Mech · May 2012 Featured Publication The site-specific recombinases Cre and Flp can mutate genes in a spatially and temporally restricted manner in mice. Conditional recombination of the tumor suppressor gene p53 using the Cre-loxP system has led to the development of multiple genetically eng ... Full text Link to item Cite