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dc.contributor.authorLee, Yong Eunen_US
dc.date.accessioned2016-07-11T17:55:09Z
dc.date.available2016-07-11T17:55:09Z
dc.date.issued2016
dc.identifier.urihttps://hdl.handle.net/2144/16992
dc.description.abstractCancer is a genetic disease caused by an unregulated expansion of a clone of cells (Sompayrac, 2004). The genetic abnormalities in cancer are the consequences of defective DNA replication, repair, maintenance, and modification, genetic background, and exposure to mutagens (Alexandrov et al., 2013). Ionizing radiation (IR), a mutagen exposed to cancer patients during clinical radiotherapy (RT), can cause DNA damage, genomic instability, and mutagenesis (Sherborne et al., 2015). While RT has been effective in treating cancer, it increases the risk of second malignant neoplasm (SMN), a severe delayed complication associated with mainly pediatric cancer survivors many decades after the treatment of their first cancer (Robison & Hudson, 2014). As the mortality of patients with childhood cancer has been decreasing, cases of radiation-induced cancers has been increasing (Robison & Hudson, 2014). The considerable contribution by RT to SMN risk illustrate the need to characterize the genetic mechanism directly responsible for radiation-induced malignancies. To better our understanding of the mutational landscape of SMNs, our specific aims are to identify potential driver mutations implicated in radiation-induced malignancies through genome and transcriptome analysis and to assess whether genetic background, specifically germline polymorphisms and mutations in tumor suppressor gene TP53, has an impact on the formation of secondary malignancies.en_US
dc.language.isoen_US
dc.subjectMedicineen_US
dc.titleIntegrated genomic and transcriptomic analyses of radiation-induced malignanciesen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2016-06-18T22:28:35Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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