Abstract IA04: Pancreatic cancer etiology: digging into the unknown
Authors: Malats Núria 
Published: December 2016

Abstract
It goes without saying that pancreatic cancer has been, and is, out of control. Not only this, its mortality both in Europe and USA is increasing and will likely increase further. Genetics and biology have done really well, but we have cured more mice than patients. Therefore, urgent actions are needed, including primary, secondary (screening) and tertiary prevention interventions
PDAC is a paradigm of the failure of current cancer research strategies. While incremental progress is being done in the treatment of advanced disease, there has been less focus on primary and secondary prevention leading to a lack of early diagnosis markers and a lack of a definition of high-risk population. Therefore, to dissect the intricate etiological scenario leading to pancreas cancer development is a must.
Family history of cancer defines a tiny proportion of the population at risk. A large proportion of familial aggregation of pancreatic cancer lacks a “clear” cause (probably because there are many different “causal genes”. Nevertheless, the largest burden of the disease, the sporadic form of pancreas cancer, is a complex and heterogeneous phenotype caused by inherited genetic, lifestyle, and environmental highly correlated factors closely related with chronic inflammation. Epidemiological studies have classically approached the analysis of risk factors on a “one-by-one basis”. However, this strategy is too simplistic when considering the reality, where multiple genetic and non-genetic factors concur within a given individual. This fact, together with evidence of interactions and correlations between these factors, supports the use of multifactorial strategies as a must to mimic biology. In this regard, we have explored the time-dependent association between multimorbidity patterns and pancreatic cancer and have found that diabetes and gastric conditions presented the highest risk. I will discuss the significance of these findings. Their translation into the clinics may help in diagnosing pancreatic cancer patients at earlier stages.
Trans-disciplinary efforts to generate, merge, and integrate epidemiological with genomics, epigenomics, and metagenomics data provide a unique opportunity to exploit the power of omics technology, health research, and integration knowledge to make progress in dissecting the intricate etiological scenario leading to pancreatic cancer.
To build an integrative risk prediction model for pancreas cancer by integrating omics biomarkers with epidemiological and clinical data requires large international standardized longitudinal studies that gather exhaustive data and samples. Once validated, these tools will allow to define high-risk populations and to implement primary and secondary prevention interventions to eventually reduce incidence and mortality and, ultimately, impacting on society, innovation, and economy. However, it may be that the window of opportunity provided by the natural history of pancreas cancer is narrower than we would wish.
Citation Format: Núria Malats.{Authors}. Pancreatic cancer etiology: digging into the unknown. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr IA04.