Cancer and the Environment Gene-Environment Interaction (2002) / Chapter Skim
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3. The Links between Environmental Factors, Genetics, and the Development of Cancer
3. The Links between Environmental Factors, Genetics, and the Development of Cancer
Pages 25-35
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From page 25... ...
For example, discoveries that both essential and nonessential dietary nutrients can markedly influence several key biological events including cell cycle regulation, processes involved in replication or transcription, immunocompetence, and factors involved with apoptosis, or programmed cell death have strengthened convictions that specific foods or components may markedly influence cancer risk. Analyses of the incidence of cancer in twin pairs and in families are traditional methods for answering questions about the relationships between cancer etiology, genes, and the environment.
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From page 26... ...
Some of the strongest evidence linking diet and cancer comes from the epidemiological observation that increased vegetable and fruit consumption is associated with a reduction in the risk for cancers of the mouth and pharynx, esophagus, lung, stomach, colon, and rectum. Likewise considerable evidence points to a host of essential and nonessential nutrients as modifiers of cancer risk at a variety of sites.
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From page 27... ...
Since several of the identified genes are involved in the pathways leading to apoptosis, it is possible that agents such as limonene could play a role in the cell signaling involved in programmed cell death. Similarly, studies with a variety of other nutrients, including selenium, isothiocyanates, and allyl sulfide, have been reported to modify at least 20 different gene products associated with cancer prevention.
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From page 28... ...
Considerably more information is needed about how genetic polymorphisms influence the response to dietary components and ultimately cancer risk, added Milner. Unquestionably, cancer is intertwined with environmental factors including diet.
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From page 29... ...
Studies with various animal and in vitro models, initiation and promotion models, adenoma carcinoma models, and immortalized human cells provide evidence that polygenic mechanisms are important in cancer, at least in experimental systems. Almost all of the known cancer syndromes are monogenic and conform to a two-stage model of development; that is, they require inactivation of two copies of a tumor suppressor gene in order to initiate.
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From page 30... ...
This phenomenon is typical of polygenic disease. Hemminki reported that the twin and family data quantified nonshared environmental effects as ranging from 40 to 90 percent for different cancers.
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From page 31... ...
These genes are so named because they prevent cancer by recognizing defective cell programming. The p53 gene recognizes the signal created by a precancerous condition and responds by killing the cell by a process called programmed cell death, or apoptosis.
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From page 32... ...
Cancer formation is a multistage process involving the activation of protooncogenes and the inactivation of tumor suppressor genes. Harris explained how carcinogens could affect any of these stages through genetic and epigenetic mechanisms.
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From page 33... ...
For example, mutations in the evolutionanly conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer, and the p53 mutational spectra differ among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the mutagenic mechanisms and the function of specific regions of p53.
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From page 34... ...
Molecular epidemiology also explores host cancer susceptibilities, such as carcinogen metabolic activation, DNA repair, endogenous mutation rates, and inheritance of mutated tumor suppressor genes. Substantial interindividual variation for each of these biologic end points has been shown, highlighting the need to assess cancer risk on an individual basis.
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From page 35... ...
The interactions of multiple modifier genes with various environmental factors that is, gene-environment interactions explain why cancer rates vary across populations, among exposed groups, and even within families. The research community is now studying cancer with an expanded and enhanced view of environmental health and exposures that include factors such as diet, lifestyle, metabolic alterations, socioeconomic status, and various environmental exposures.
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