The biological revolution – towards a mechanistic understanding of the impact of diet on cancer risk

Mathers, John C.

doi:10.1016/j.mrfmmm.2004.01.011

Cited by 27 publications

(12 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There is some evidence that a higher intake of antioxidants was associated with a decrease in the frequency of chromosomal damage in human lymphocytes [17,18]. Therefore, we investigated the association of diet with risk of subgroups of NHL according to the presence or absence of the t (14;18).…”

Section: Introductionmentioning

confidence: 99%

Dietary factors and risk of t(14;18)-defined subgroups of non-Hodgkin lymphoma

Chiu

Davé

Ward

et al. 2008

Cancer Causes Control

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Dietary factors and risk of t(14;18)-defined subgroups of non-Hodgkin lymphoma

Chiu

Davé

Ward

et al. 2008

Cancer Causes Control

View full text Add to dashboard Cite

show abstract

“…Dietary polyphenols is thought to have a direct inhibition by interaction with the catalytic site of the DMNT1 or it could have an influence on the methylation status indirectly. A number of cultured cells, animal models and human clinical trials have shown the protective role of dietary polyphenols against a number of cancers, including pancreatic cancer (111). However, understanding the timing of intervention is critical in cancer prevention, particularly for an aggressive cancer such as pancreatic cancer which lacks early biomarkers of detection.…”

Section: Dna Methylation and Nutrigenomicsmentioning

confidence: 99%

Epigenetics and Pancreatic Cancer: The Role of Nutrigenomics

Lyn‐Cook¹

2012

Pancreatic Cancer - Molecular Mechanism and Targets

View full text Add to dashboard Cite

“…Such damage includes mutations, aberrant epigenetic marking, chromosomal damage and telomere shortening [9]. During cancer development, a number of tumour suppressor genes are silenced (by both mutations and by epigenetic mechanisms) and oncogenes are inappropriately expressed.…”

Section: Overview Of Cancer Biologymentioning

confidence: 99%

Overview of genes, diet and cancer

Mathers

2007

Genes Nutr

View full text Add to dashboard Cite

Quantitative epidemiological analysis suggests that about one third of the variation in cancer risk can be attributed to variation in dietary exposure but it has proved difficult, using conventional epidemiological approaches, to identify which dietary components, in what amounts and over what time-scales are protective or potentially hazardous. Work in this area has been hampered by the lack of robust surrogate endpoints. However, the rapidly accumulating knowledge of the biological basis of cancer and the application of post-genomic technologies are helping the development of novel biomarkers of cancer risk. Genomic damage resulting in aberrant gene expression is the fundamental cause of all cancers. Such damage includes mutations, aberrant epigenetic marking, chromosomal damage and telomere shortening. Since both external agents and normal cell functions, such as mitosis, subject the genome to frequent and diverse insults, the human cell has evolved a battery of defence mechanisms which (a) attempt to minimize such damage (including inhibition of oxidative reactions by free radical scavenging and the detoxification of potential mutagens), (b) repair the damage or (c) remove severely damaged cells by shunting them into apoptosis. When such defences fail and a tumour becomes established, further genomic damage and further alterations in gene expression enable the tumour to grow, to cope with anoxia, to develop a novel blood supply (angiogenesis), to escape from the confines of its initiation site and to establish colonies elsewhere in the body (metastasis). All of these processes are potentially modifiable by food components and by nutritional status. In addition, interactions between dietary (and other environmental and lifestyle) factors and genetic make-up [seen principally in the assembly of single nucleotide polymorphisms (SNPs) which is unique to each individual] contributes to interindividual differences in cancer risk.Keywords Cancer Á Gene expression Á Diet Á Biomarkers Á Epigenetics Diet and cancer epidemiologySince the extensive quantitative analyses of Doll and Peto [1] more than two decades ago, it has been clear that dietary factors explain about one third of the variation in cancer risk with smoking being responsible for a further third. More recent comprehensive reviews of the evidence base undertaken by the American Institute of Cancer Research/World Cancer Research Fund [2] and by the Department of Health in the UK [3] confirm the importance of diet as a modifier of cancer risk. The revelation that lifestyle factors are major determinants of cancer risk forms the basis for the assertion that 75-80% of cancer cases under age 65 years are potentially preventable [1]. Some of the best evidence for relationships between dietary exposure and cancer risk comes from large prospective cohort studies. The European Prospective Investigation into Cancer and Nutrition (EPIC) which has recruited over half a million people in ten European countries to investigate the relationships between diet, me...

show abstract

The biological revolution – towards a mechanistic understanding of the impact of diet on cancer risk

Cited by 27 publications

References 46 publications

Dietary factors and risk of t(14;18)-defined subgroups of non-Hodgkin lymphoma

Dietary factors and risk of t(14;18)-defined subgroups of non-Hodgkin lymphoma

Epigenetics and Pancreatic Cancer: The Role of Nutrigenomics

Overview of genes, diet and cancer

Contact Info

Product

Resources

About