Molecular Mechanisms and Biomarkers Group
Exposures to environmental or endogenous risk factors can cause alterations in the structure and function of the human genome, which, in turn, can drive the development and progression of cancer. Such detrimental changes affect the essential gene and protein functions within the cells, and consequently the complex cellular circuitry and interactions that control cell growth, replicative potential, survival, and responses to stress. Identifying both the causes and the consequences of these changes is essential for understanding the mechanisms of cancer development, for cancer hazard prediction, and for designing efficient cancer prevention strategies.
Epidemiological studies characterize the potential roles of the environment in a wide range of human cancers, whereas the precise mechanisms by which environmental exposures promote cancer development and progression can be elucidated by mechanistic studies that rely on modern molecular profiling methodologies. These approaches include genomics, epigenetics, bioinformatics, and computational analysis of complex data sets. Among the cancer-associated molecular changes, genome-scale patterns of somatic genetic alterations in tumours and normal tissues serve as fingerprints of individual sources of mutagenesis and provide clues about possible cancer-causing factors as well as key cancer driver events. Such patterns and their impact can be further validated and functionally tested in innovative experimental models and molecular epidemiology studies applied to a wide range of environmental exposure settings. Overall, this approach has the power to strengthen multidisciplinary research on cancer etiology and the identification of modifiable cancer risk factors.