It has been the overarching focus of Dr. Weterings' career to study the relevance of DNA repair mechanisms during carcinogenesis and to utilize the gained knowledge to design novel cancer therapies. Deficiencies in DNA double strand break (DSB) repair mechanisms are often driving forces behind carcinogenic events, but can also be exploited for therapies based on a synthetic lethality approach. In addition, DSB repair is also involved in the development of radiation- and chemo-refractive cancers. Therefore, his research focuses on 1) the elucidation of key factors of DSB repair and their interactions, and 2) the development of specific inhibitors of these factors for use as cancer therapeutics or radiation- or chemo-sensitizing agents.
Dr. Weterings has approximately 15 years of experience in this field and his exploits have encompassed both basic and translational research. Several of his publications have altered the current textbook model of non-homologous end-joining mediated DSB repair.
Since 2012 Dr. Weterings has been in charge of his own laboratory and research group at the University of Arizona (UA) Cancer Center and he successfully competed for extramural as well as internal grants. He has set up several fruitful collaborations within and outside of the cancer center. These collaborations include, for instance, a partnership with Dr. Anne Cress (Cellular and Molecular Medicine, UA) regarding the role of DSB repair factors on oncogenic translocation events in prostate cancer, as well as a joint study with Drs. Daruka Mahadevan and Josef Vagner (UA) which focusses on the development of novel DSB repair inhibitors.