Cancer Risk Assessment (Basic and Clinical Oncology)

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The assessment of cancer risk is a complex process that requires the examination of etiological agents, real-world environments, and individual rates of exposure. This reference offers practical approaches to determine cancer risk in individuals, groups of exposed persons, and the general public in relation to individual genetic and acquired susceptibilities.

Cancer Risk Assessment (Basic and Clinical Oncology) Review

Humans are continuously exposed to carcinogens from environmental, occupational and endogenous sources. Health professionals, regulatory agencies and cancer researchers are frequently challenged to identify the causes of cancer, predict risks and to develop methods to prevent cancer. The assessment of cancer risk in individuals or the population is a complex process that reflects both science and scientific intuition. There is an exploding amount of information about the applicability and use of biomarkers, in many cases conflicting information, and a confusing array of sources to consider. New data from the Human Genome Project, the latest technologies in molecular genetics (e.g., proteomics, microarrays, high-throughput assay methods) is rapidly being incorporated into risk assessment and epidemiological studies, and there are many challenges to the interpretation of the resulting data. Databases are being developed with huge amounts of information available for public use. While it is clear that the use of biomarkers and genetic susceptibility analysis are improving our ability to predict risk in the population and the individual, this is a rapidly evolving and complicated area of research. People outside the field of molecular epidemiology, and students of molecular epidemiology need guidance about how to use and interpret biomarker data, and a context for where it improves the risk assessment process and where it does not.

This book is intended for health professionals, public health specialists, persons within regulatory agencies and cancer researchers who need not only a summary of what is recent data, but what are the approaches to evaluate future information. The major goal of this text is to provide the reader with a practical approach to conducting risk assessment for the population and the individual in the context of biomarkers and genetic susceptibilities, especially within a broader perspective of background cancer risk and an individual's exposures within a complex environment. While the risk assessment process usually focuses on a single particular exposure, people are exposed to known and potential human carcinogens from a multitude of sources (air, diet, lifestyle, etc.). When setting public health priorities, or evaluating a person with cancer (or concerned about cancer), this broader context makes the risk assessment process much more challenging. It is anticipated that the reader of this text will be able to place cancer risk within such a context, understand relative risks from different exposures, and understand how biomarkers and genetic susceptibilities can help in the risk assessment process.

Biomarkers are tests that are conducted on any biological tissue or fluid, including air. Assays that assess an individual's risk through specific genes, thereby assessing genetic susceptibilities, also is a type of biomarker. However, the term biomarker usually refers to an assay of exposure, biologically effective dose or some effect of exposure. The use of the term genetic susceptibility refers to an individual's heritable capacity to respond to exposures, which would therefore result in modifying cancer risk. Biomarkers can be used as intermediate markers of cancer risk, and are best when they reflect a mechanistic pathway to cancer. Genetic susceptibilities would therefore affect the level of biomarkers, reflecting a gene-environment interaction. The term gene-environment interactions refers to an effect of exposure that is made less or more by genetic susceptibilities; it is used generically and there are formal statistical methods to assess interactions. Most cancers are considered to be caused by carcinogenic exposures, although in most cancers the causes have not been identified (and so in most people with cancers the cause cannot be identified). However, it is numerous gene-environment interactions that actually contribute to the carcinogenic process, whereby the body also has the capacity to repair much of the damage from gene-environment interactions. Biomarkers now are enhancing our understanding about the causes of cancer, and in some cases are helping identify what caused a cancer in a particular person. The use of biomarkers is not new, however, and has been around for more than fifty years. But, the last twenty years has seen rapidly developing technologies, which has accelerated in growth over the last five years. These newer methods are providing for analytical and bioinformatic challenges, but nonetheless are showing greater promise for enhancing our risk assessment processes further.

Frequently the public and individuals with cancer make conclusions about what causes cancer that is not founded upon data, or does not use an approach that is based upon methodologies for assessing cancer causation. Often there are unfounded assumptions about chemical exposures, for example, because there is the potential for low level exposure. The public health community is obligated to understand and communicate the latest scientific data in the context of the risk assessment process for the general population, persons at high risk, and individuals within the general population. This text provides the reader with the tools to assess cancer causation with specific methodologies, rather than relying on intuition and speculation.

Cancer is a multistage process that is triggered by multiple steps through many pathways. There are many repair and protective mechanisms in people to prevent most DNA damage that would otherwise lead to cancer. Typically, the determination of a cancer risk factor requires the examination of a potential etiological agent against a background of many real etiological agents. Many new laboratory and epidemiological findings are having an impact on the way we think about cancer risk, while many principles used in the assessment of causation remain conceptually important. This book will present recent data that impacts upon population and individual cancer risks, and review the data for some of the known and potential human carcinogens. It will review the methods for determining what causes cancer and what does not. Practical approaches to the determination of cancer risk in individuals and the population will be offered, considering approaches to counseling individuals, groups of exposed persons and society.

This text is organized to provide the most current information in two ways. The first way approaches risk assessment from a methodological perspective. The reader will be provided information about carcinogenesis in general, and then specifically for chemical, radiation, viral, occupational and familial cancers. While there is overlap in some of these mechanisms (e.g., chemical carcinogenesis and occupational carcinogenesis), there can be different mechanistic approaches to consider depending on the perspective. A particular focus includes recent data for tobacco, alcohol and hormonal mechanisms in cancer risk, as these are among the major known human carcinogens and carcinogenic mechanisms. In general, the chapters provide methods to consider how people are exposed to known and suspected carcinogens, and particularly how to measure this in the workplace using industrial hygiene methods. We also provide information about differences in cancer risk within different ethnic and racial populations in the context of different exposures and mechanistic etiologies, where they exist.

The methodological approaches contained within chapters include consideration of basic epidemiological approaches, and also as they apply to molecular epidemiology. The latter will include both the use of biomarkers and genetics within an epidemiological framework. We then provide the reader with more detailed approaches to the use of genetic testing for cancer risk, using both markers in cancers and then measures of genetic damage in persons without cancer. The actual approach to risk assessment is highlighted in detail in three separate chapters. The readers are provided with the distinct approaches to population and individual risk assessment, and also with information about how regulatory agencies determine what is a carcinogen. The chapter on individual risk assessment is particularly unique as the reader is provided with a framework for evaluating on individual who has cancer, or is thought to be at risk for cancer.

The second half of the text provides the reader with cancer risk information by organ system for major cancers. It uses the principals established in the first part of the text and applies them to single organ sites. The first half of the text provides the reader with the tools to evaluate risk assessment for any organ, in the general population and the individual. The second half provides the reader with easy access to understand the risks for a particular organ site, for example when evaluating a person with a specific type of cancer. While this text provides a summary of the latest data for biomarkers and genetic susceptibilities within the risk assessment process, it cannot provide a critique of all available data. However, the methods described in the text will allow the reader to go beyond what data is provided in the organ-specific chapters.

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