3 main aspects in understanding gene-, environmental- and social interactions :

• environmental exposures as elicitors of preventable disease,
• understanding and applying environmental exposure information to gene/environment interactions and
• understanding correlations and interactions in order to design "exposure assessment approaches".

Most cancers originate from genetic alterations be they inheritable or spontaneous somatic mutations caused by environmental stress such as radiation, UV, toxins, bacterial or viral infections. Inherited defects can lead to cancer predisposition clusters in family trees. Life story and personal fitness determine whether and when the disease appears. Other cancers, such as lung cancer are, indeed, primarily caused by external factors, but there are nonetheless genetic alterations responsible for resistance on one hand and increased sensitivity on the other hand. Hence, it makes sense to yet intensify investigation about the complex interactions between genotype and environment and possible associations with disease phenotypes and risk factors.

Some ethnic groups apparently harbour better genotypic resistance to cancers than others. For example, chronic lymphocytic leukaemia is extremely rare amongst Asians; Ewing's sarcoma, skin cancers and testicular cancer are very rare amongst coloured people.

Family clusters have been reported for virtually every form of cancer. In general, close relatives of a cancer patient face twice the common risk for developing the same type of cancer. Familial cancer clusters are often inherited, but environmental influences, mere chance, or a combination have to be considered, too. The effect of chance is considerable; within the population of the USA, the probability of sickening from cancer is about 45%, projected to a lifetime (common nonmelanoma skin cancers are included in this statistics). Thus, it is by all means probable to have at least some relatives with a history of cancer in one´s family. An inherited predisposition often manifests itself when the same organ is cumulatively affected by cancer in multiple blood relatives. In familial cancers that are triggered by environmental carcinogens, patient education regarding the avoidance of harmful exposures can help prevent or delay the onset of cancer. For example, members of melanoma-prone families who avoid intensive ultraviolet radiation exposure can substantially reduce their risk of melanoma. (Frederick P. Li, M.D., Mary C. Fraser, R.N., M.A.

Recently the familial aggregation of lung and other cancers in first-degree relatives of non-smoking lung cancer patients was analysed. The data derived from that study, included 2,465 first-degree relatives of 316 lung cancer patients who never used to smoke and 2,441 first-degree relatives of 318 healthy non-smokers, frequency matched concerning age, gender and ethnicity. Summing up, there was a 25% excess risk of any type of cancer among the first-degree relatives of lung cancer patients, and their children exhibited a cancer risk increased 2-fold compared to control offspring. There was also a 44% excess risk of young onset cancers (aged < 50) among relatives of lung cancer patients. Relatives of smoking patients had an increased risk of any cancer and a >5-fold risk of young onset lung cancer as compared to smoking control relatives. This analysis provides further evidence for the importance of genetic factors e.g. for lung cancer in persons who have never been smoking. (Gorlova O et al., 2007)