Because these genes are such powerful guardians of the genome, damage may result in short latency time between exposures and clinically detectable disease and a young age at the time of diagnosis of cancer. Studies of genetic variants in metabolizing genes, including the examples shown in Table 4 , generally have reported few or no consistent increases in breast cancer risk with the gene variant alone. The majority of the susceptibility genes that have been investigated with regard to environmental exposures can be implicated in cellular oxidative damage that may contribute to the carcinogenic process.
Oxidized species, or reactive molecules, are created by Phase I enzyme activation of exogenous agents Table 2 , from endogenous hormones, and from other free radical sources, such as fatty acid oxidation. A general marker of genotoxicity is oxidative damage to DNA e. Enzymes of this kind also are involved in the uptake and delivery of pain medications, chemotherapy drugs, and hormones that may be substrates for several enzymes e. Phase II detoxification or deactivating enzymes conjugate genotoxic oxidation products from environmental exposures into readily eliminated metabolites including sulfates, glucuronides, and acetates.
If deactivation mechanisms were lower in a subgroup with excessive oxidative damage, then this subgroup might be at an increased risk for a number of diseases. A number of examples demonstrate how Phase II enzymes alter individual levels of biomarkers of exposure. In epidemiologic studies, more significant findings for the gene variant alone with breast cancer risk have been reported for the Phase II deactivating enzymes compared with Phase I pathways. However, there are multiple metabolic pathways that control oxidation processes.
The majority of genes related to metabolism Table 4 are expressed primarily in the liver, so that a carcinogenic effect on mammary epithelium would require that active metabolites be transported to the breast, unless they have an indirect effect such as to raise or lower systemic hormone levels. GST and CYP1A1 are expressed in breast tissue, although the isoforms do not necessarily reflect the known gene variants. Because the prevalence of the known gene variants is low, current epidemiologic studies are too small to detect a gene effect that yields a relative risk below 2.
There are four CYP1A1 variants that have been scrutinized in epidemiologic studies; genotoxic potential is suspected for minor variants that code for more rapid metabolism and that are inducible by various exposures. However, the NATs also conjugate, or deactivate, oxidative intermediates; slow metabolizers would be at risk if this were the exposure of interest. The GST family of enzymes conjugates electrophilic substances to their glucuronide metabolites, which are biologically inactive and are excreted readily.
Conversely, studies of GST expression in tissue have been reported to find no correlation with survival. Because the variants in these genes are so rare, research is limited with regard to their interactions with environmental factors. The resulting P53 mutational spectrum appears to vary with ethnicity and geographic distribution, which is consistent with an environmental etiology.
The action of many compounds, including the OCs as transcription factors, is believed to be mediated through the ER or other hormone receptors e. In addition, levels of hormone synthesizing and metabolizing enzymes may be induced by environmental substances and thereby alter levels of other exposures.
Breast cancer—epidemiology, risk factors, and genetics
Nevertheless, the majority of genetic variants exist in all populations, albeit in different proportions. The phenotypic potential, or the overall distribution of such genotypes, appears to hold great promise for identifying an environment gene or profile associated with breast cancer risk.
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Dietary intake also is important to consider with metabolizing enzymes, particularly antioxidants, which, with detoxifying enzymes, may reduce oxidative damage and thereby alter both the transcriptional and mutagenic effects of environmental agents. Environmental epidemiologic research generally has disregarded the fact that environmental exposures are entwined intimately with social, behavioral, and psychosocial factors. It has been theorized that the type of tumor may represent socioenvironmental exposure.
Breast Cancer and the Environment Research Centers
The biologic sequence of events leading to cancer no doubt coincides with certain times of vulnerability during life and latency for cancer Table 1. Much epidemiologic and experimental evidence suggests the need to investigate mutagenic exposures that occur early in a woman's life, even in utero. Russo et al. In animals, a large number of chemical exposures may alter the onset of puberty vaginal opening. White girls exposed to higher versus lower levels of PBBs in utero reportedly experienced an earlier age at menarche.
Chemical exposures also have been reported to be associated with menstrual function during the reproductive years. We believe more research is needed to identify environmental exposures experienced in early life that may affect breast cancer risk. Because breast cancer risk may vary depending on the timing of exposure, the future examination of environmental risk factors should take into consideration the age or time period in a woman's life during which these exposures occur.
Efforts must be made to identify resources for undertaking research concerning the role of environment in the development of breast cancer, both with regard to populations available for study and methodologies used to assess multiple risk factors. Opportunities should be developed that will enable research to be undertaken within the contexts of the environmental etiologies discussed earlier. A number of general as well as specific opportunities were suggested by the Environmental Working Group.
Large populations can be combined to enhance existing studies. Newly funded studies should collaborate in the early stages of the research so that data collected can be combined effectively in later analyses. Focus groups may help to identify new exposures and appropriate contexts for the assessment of risk. Research should be encouraged that will develop better tools for exposure assessment and for ecologic, occupational, cohort, and case—control studies. In keeping with the theme that etiologic and prognostic factors are useful only in so far as they are generalizable, newly identified population resources must preserve the ability to study individual populations while enabling the results to be linked with other research.
NEMA Breast Cancer Study
They also may have greater genetic susceptibility to the biologic effects of such exposures. In addition, research should consider how genetic, social, and environmental factors act within the complex hormonal milieu that leads to the development of breast cancer. Volume 97 , Issue S1. The full text of this article hosted at iucr. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account.
If the address matches an existing account you will receive an email with instructions to retrieve your username. Cancer Volume 97, Issue S1. Mary S. Wolff Ph. Julie A. Britton Ph. Valerie P. Wilson Ph.
Tools Request permission Export citation Add to favorites Track citation. Share Give access Share full text access. Share full text access. Please review our Terms and Conditions of Use and check box below to share full-text version of article. Abstract There are few unequivocably established environmental carcinogens for breast cancer in women.
No Family History : The Environmental Links to Breast Cancer
DOI Young adult Modulation of hormone metabolism Tumor progression Tumor agressivity, metastasis Dieldrin? Middle age Metastasis. Environmental Exposures That May Be Relevant for Breast Cancer Etiology and Progression Based on laboratory studies, a number of potential breast cancer carcinogens have been identified that also are known environmental contaminants Table 2.
Adapted from: Huff J. Breast cancer risks from environmental chemicals. Eur J Oncol. Chemically induced mammary gland cancer in the National Toxicology Program's carcinogenesis bioassay. Breast cancer risk and environmental exposures. Environ Health Perspect. Lipid basis is approximately Other Exposures Certain solvents and related small molecules including the chloroethylenes are reported to be carcinogens in animals and some are mammary carcinogens Table 2. Factors That Act in Concert with Exposures to Link Environment with Breast Cancer Etiology and Progression The majority of environmental exposures today either exist at concentrations too low or have carcinogenic potential too weak to be easily identified as risk factors, in contrast with very strong associations between smoking and lung cancer or between radiation and various cancers.
Context 1. Context 2. Figure 1 Open in figure viewer PowerPoint. Data from breast cancer studies were from controls for whom information was available. Susceptibility: variability in metabolizing enzymes Phase I metabolizing enzymes. Phase II metabolizing enzymes. Genes that control metabolizing enzymes The majority of genes related to metabolism Table 4 are expressed primarily in the liver, so that a carcinogenic effect on mammary epithelium would require that active metabolites be transported to the breast, unless they have an indirect effect such as to raise or lower systemic hormone levels.
DNA repair. Concept 3. Context 4. Temporal effects, or timing of environmental risk factors The biologic sequence of events leading to cancer no doubt coincides with certain times of vulnerability during life and latency for cancer Table 1. Environmental and heritable factors in the causation of cancer— analyses of cohorts of twins from Sweden, Denmark, and Finland.
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Bestselling Series. Harry Potter. Popular Features. New Releases. Description No Family History presents compelling evidence of environmental links to breast cancer, ranging from everyday cosmetics to industrial waste. Sabrina McCormick weaves the story of one survivor with no family history into a powerful exploration of the big business of breast cancer. As drugs, pink products, and corporate sponsorships generate enormous revenue to find a cure, a growing number of experts argue that we should instead increase focus on prevention-reducing environmental exposures that have contributed to the sharp increase of breast cancer rates.
Other books in this series. Social Theory and Aging Jason L. Add to basket. Public Sociology Ben Agger. Shades of Loneliness Richard Stivers. Navigating Technomedia Sam Han. Community on Land Janel M. Review quote No Family History shows us ordinary people discovering the extraordinary truth of how to prevent most cancer. It forces us to ask the crucial questions: Who profits from causing, detecting, and treating cancer?
Why do we hear so much about the search for a cure, and so little about preventing cancer in the first place? The society of breast cancer is chock full of beliefs-about genes, chemicals, cures, female beauty, and the value of early detection. It's about time that a thoughtful sociologist shined a light on this dark and terrifying landscape and turned over a few rocks. No Family History is an important corrective to pink ribbons and positive thinking. McCormick's text is full of disturbing details, in the form of statistics and individual obstacles.
Plenty of studies are cited to support her claims
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