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Livros sobre o tema "Genetic risk factor"

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Autor: Grafiati

Publicado: 7 de julho de 2024

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1

Petrakis, Peter L. Alcoholism, and inherited disease. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute on Alcohol Abuse and Alcoholism, 1985.

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2

Young, Ian D. Introduction to risk calculation in genetic counselling. Oxford: Oxford University Press, 1991.

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3

J, Alberts Mark, ed. Genetics of cerebrovascular disease. Armonk, NY: Futura Pub. Co., 1999.

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4

Uri, Goldbourt, De Faire Ulf e Berg Kåre, eds. Genetic factors in coronary heart disease. Dordrecht: Kluwer Academic, 1994.

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5

Offit, Kenneth. Clinical cancer genetics: Risk counseling and management. New York: Wiley-Liss, 1998.

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6

Kåre, Berg, ed. Genetic approaches of coronary heart disease and hypertension. Berlin: Springer-Verlag, 1991.

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7

Garte, Seymour J. Genetic susceptibility to cancer. Boston: Kluwer Academic, 1998.

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8

Symposium on Phenotypic Variation in Populations: Relevance to Risk Assessment (1986 Brookhaven National Laboratory). Phenotypic variation in populations: Relevance to risk assessment. New York: Plenum Press, 1988.

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9

A, Levin Morris, e Strauss Harlee S, eds. Risk assessment in genetic engineering. New York: McGraw-Hill, 1991.

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10

Young, Ian D. Introduction to risk calculation in genetic counseling. 2^a ed. Oxford [England]: Oxford University Press, 1999.

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11

Young, Ian D. Introduction to risk calculation in genetic counseling. 3^a ed. Oxford: Oxford University Press, 2007.

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12

Marin, Noelle. Ovarian cancer: The signs, symptoms, treatments, and genetic risk factors. [United States]: Fort Press, 2010.

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13

Seshadri, Sudha, e Stéphanie Debette. Risk factors for cerebrovascular disease and stroke. Oxford: Oxford University Press, 2016.

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14

Gould, Randi L. Cancer and genetics: Answering your patients' questions. Huntington, NY: PRR, 1997.

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15

1960-, Foulkes William D., e Hodgson S. V, eds. Inherited susceptibility to cancer: Clinical, predictive, and ethical perspectives. Cambridge: Cambridge University Press, 1998.

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16

Batsheva, Bonné-Tamir, e Adam Avinoam, eds. Genetic diversity among Jews: Diseases and markers at the DNA level. New York: Oxford University Press, 1992.

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17

Bland, Jeffrey. Genetic nutritioneering. Los Angeles: Keats Pub., 1998.

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18

Brener, Milton E. Evolution and empathy: The genetic factor in the rise of humanism. Jefferson, N.C: McFarland & Co., 2008.

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19

Hiroshi, Hiai, e Hino Okio, eds. Animal models of cancer predisposition syndromes. Basel: Karger, 1999.

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20

Epigenetics in Cancer Prevention: Early Detection and Risk Assessment Workshop (2001 Bethesda, Md.). Epigenetics in cancer prevention: Early detection and risk assessment. New York: New York Academy of Sciences, 2003.

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21

Obe, G. Cancer risk evaluation: Methods and trends. Weinheim: Wiley-Blackwell, 2011.

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22

Morris, Joi L. Positive results: Making the best decisions when you're at high risk for breast or ovarian cancer. Amherst, N.Y: Prometheus Books, 2010.

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23

Teichler-Zallen, Doris. To test or not to test: A guide to genetic screening and risk. New Brunswick, N.J: Rutgers University Press, 2008.

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24

Teichler-Zallen, Doris. To test or not to test: A guide to genetic screening and risk. New Brunswick, N.J: Thorndike Press, 2009.

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25

V, Hodgson S., ed. A practical guide to human cancer genetics. 3^a ed. Cambridge: Cambridge University Press, 2007.

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26

Hodgson, S. V. A practical guide to human cancer genetics. Cambridge [England]: Cambridge University Press, 1993.

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27

Ueland, Per Magne, e Rima Rozen. MTHFR polymorphisms and disease. Georgetown, Tex: Landes Bioscience, 2005.

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28

Robert, Cloninger C., e Begleiter Henri, eds. Genetics and biology of alcoholism. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1990.

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29

Seshadri, Sudha, e Stéphanie Debette, eds. Risk Factors for Cerebrovascular Disease and Stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199895847.001.0001.

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Risk Factors for Cerebrovascular Disease and Stroke describes environmental and genetic determinants for cerebrovascular disease and stroke from the perspective of an international group of neurologists, epidemiologists, and geneticists who are at the forefront of research and education on these issues. Unlike other books in the field, which solely deal with physiology, diagnosis, and management of stroke, this essential book discusses prevention factors as well as the causes. This unique book takes a comprehensive approach to risk prediction while integrating epidemiological, genetic, and statistical principles explained in a way that is easy for the clinical trainee to understand. The section on genetic risk factors for various types of stroke is unique in its depth and up-to-date information. Clinicians, residents, fellows and academics in neurology, geriatrics, internal medicine, epidemiology, genetics, public health professionals, and preventative cardiologists, as well as nurses, practitioners and physician assistants will find this a handy source for years to come.

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30

Hinks, Anne, e Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0043.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now an additional 12 JIA susceptibility loci with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.

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31

Gaff, Clara, Louise Keogh e Elizabeth Lobb. Communicating genetic risk. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198736134.003.0034.

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The discovery of cancer predisposing genetic mutations has heightened community awareness of the link between family history, genetic constitution, and personal risk. The component of an individual’s cancer risk that is due to their genetic make-up can be described as their ‘genetic risk’. Knowledge of genetic risk can assist both individuals with cancer and unaffected individuals to make decisions about healthcare and inform relatives who may share that genetic risk. Accordingly, patients seek advice about their risk and its implications and management from general practitioners (primary healthcare physician) or cancer specialists. In this chapter, we discuss the interlinked processes of risk assessment, risk perception, and risk communication in the context of genetic risk of cancer. While this is only one component of an individual’s risk of cancer—other factors including lifestyle, medical history, and environmental exposures—the principles of risk communication are applicable to each of these individual risk factors.

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32

Hinks, Anne, e Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_002.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.

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33

Hinks, Anne, e Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_003.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.

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34

Putaala, Jukka, e Nicolas Martinez-Majander. Risk factors. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0002.

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Risk factors in young-onset stroke include both traditional and unconventional as well as both chronic and temporal ones. In young patients, unconventional risk factors such as oral contraceptive use, antiphospholipid antibodies, genetic thrombophilia, acute infections, illicit drug use, and migraine may play a greater role than in elderly patients. However, recent large studies have challenged this traditional view suggesting that young adult stroke would occur mostly due to such unconventional risk factors. These studies have shown a high prevalence of in particular modifiable behavioural risk factors, including physical inactivity, high-risk alcohol consumption, and smoking. Since consequences of a young-onset stroke are greater regarding quality-adjusted life and economic impact, detection and treatment of especially modifiable risk factors are of paramount importance. This chapter reviews the burden of both traditional and less well-documented risk factors in young ischaemic stroke patients and discusses their strength of evidence and mechanisms of association.

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35

Holdt, Lesca M., e Daniel Teupser. Genetic background of atherosclerosis and its risk factors. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0002.

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This chapter is concerned with how atherosclerosis risk is modulated by a complex interplay between genetic and environmental risk factors. The contribution of genetics to the variability of atherosclerosis risk is estimated as 50%. Recent genome-wide association studies have led to the identification of over 50 gene variants which modulate atherogenesis. Risk factors for atherosclerosis are also partly genetically determined and some of the variants which play a role in atherogenesis overlap with those modulating its risk factors. However, the current relevance of these findings for clinical practice is limited, mainly due to the small effect sizes of identified risk variants with insufficient discriminatory power, and a large portion of the genetic contribution to atherosclerosis is still unknown. The major promise therefore lies in understanding the pathophysiology of newly identified genes with the perspective of novel therapeutic approaches.

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36

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Informa Healthcare, 2001.

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37

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Taylor & Francis Group, 2001.

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38

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Taylor & Francis Group, 2001.

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39

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Taylor & Francis Group, 2001.

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40

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Taylor & Francis Group, 2001.

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41

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Taylor & Francis Group, 2001.

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42

Offit, Kenneth. Clinical Cancer Genetics: Risk Counseling and Management. Not Avail, 2008.

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43

Garte, Seymour. Genetic Susceptibility to Cancer. Springer, 2011.

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44

Garte, Seymour. Genetic Susceptibility to Cancer. Springer London, Limited, 2012.

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45

Garte, Seymour. Genetic Susceptibility to Cancer. Springer London, Limited, 2013.

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46

Choy, Wai Nang. Genetic Toxicology and Cancer Risk Assessment. Taylor & Francis Group, 2001.

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47

Genetic toxicology and cancer risk assessment. New York: Marcel Dekker, 2001.

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48

Bianchi, Filippo, e Salvatore De Rossi. Aneuploidy: Etiology, Disorders, and Risk Factors. Nova Science Publishers, Incorporated, 2012.

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49

CLARK, ROSS D. Medical, Genetic & Behavioral Risk Factors of the Sporting Breeds. Xlibris, 2017.

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50

Woodhead, Avril. Phenotypic Variation in Populations:Relevance to Risk Assessment (Basic Life Sciences). Springer, 1988.

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