Cancer is one of the leading causes of mortality. It is a heterogeneous disease that is caused by changes to genes regulating cell signalling and proliferative behaviour.
In 2012, approximately 1.1 million men were diagnosed with prostate cancer, making it the second most common male cancer worldwide. There is wide global variation in prostate cancer incidence, with almost 70% of cases occurring in more developed regions of the world. While some of this variation has been attributed to differences in prostate-specific antigen (PSA) based screening practices, studies also have suggested exposure to environmental risk factors including radiation, hormones and cigarette smoking as some of the risk factors for developing prostate cancer. In addition, nutritional factors and physical activity may play a direct role or may indirectly affect prostate cancer risk via an impact on adiposity. Recently, studies have generated epigenetics, metabolomics and proteomics data in large populations. This mult-iomics data could be used to understand the molecular changes that occur in prostate cancer and informed biological pathways between exposures and prostate cancer. To understand prostate cancer at a molecular level, identifying the relevant mutations and discovering their role in the oncogenetic process is critical.
The overall aim of this research theme is to understand the molecular mechanisms of this complex disease which could lead to better understanding of prostate cancer aetiology, early prostate cancer detection, improved drug delivery and higher survival rates in patients. We would like to welcome submission of original research, short reports, systematic reviews, and mini-review articles based on the following topics:
- Molecular mechanisms of prostate cancer with emphasis on systemic approaches
- Prostate cancer genomics
- Systematic analyses regarding metabolomics, proteomics and epigenetic changes in prostate cancer
- Causal relationships between modifiable risk factors and molecular alterations in prostate cancer
Cancer is one of the leading causes of mortality. It is a heterogeneous disease that is caused by changes to genes regulating cell signalling and proliferative behaviour.
In 2012, approximately 1.1 million men were diagnosed with prostate cancer, making it the second most common male cancer worldwide. There is wide global variation in prostate cancer incidence, with almost 70% of cases occurring in more developed regions of the world. While some of this variation has been attributed to differences in prostate-specific antigen (PSA) based screening practices, studies also have suggested exposure to environmental risk factors including radiation, hormones and cigarette smoking as some of the risk factors for developing prostate cancer. In addition, nutritional factors and physical activity may play a direct role or may indirectly affect prostate cancer risk via an impact on adiposity. Recently, studies have generated epigenetics, metabolomics and proteomics data in large populations. This mult-iomics data could be used to understand the molecular changes that occur in prostate cancer and informed biological pathways between exposures and prostate cancer. To understand prostate cancer at a molecular level, identifying the relevant mutations and discovering their role in the oncogenetic process is critical.
The overall aim of this research theme is to understand the molecular mechanisms of this complex disease which could lead to better understanding of prostate cancer aetiology, early prostate cancer detection, improved drug delivery and higher survival rates in patients. We would like to welcome submission of original research, short reports, systematic reviews, and mini-review articles based on the following topics:
- Molecular mechanisms of prostate cancer with emphasis on systemic approaches
- Prostate cancer genomics
- Systematic analyses regarding metabolomics, proteomics and epigenetic changes in prostate cancer
- Causal relationships between modifiable risk factors and molecular alterations in prostate cancer
