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Готові списки джерел за темами / Tumour environment / Книги

Книги з теми "Tumour environment"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Tumour environment.

Автор: Grafiati

Опубліковано: 14 березня 2023

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1

Bar-Eli, Menashe, ed. Regulation of Gene Expression in the Tumor Environment. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-8341-9.

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2

Tumote Youqi di fang zhi bian zuan wei yuan hui. Tumote Youqi zhi, 1991-2008. 8th ed. Huhehaote Shi: Yuan fang chu ban she, 2005.

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3

1925-, Altchek Albert, and Cohen Carmel J, eds. Atlas of ovarian tumors. New York: Igaku-Shoin, 1994.

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4

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Some chemicals that cause tumours of the kidney or urinary bladder in rodents and some other substances. [Lyon]: World Health Organization, International Agency for Research on Cancer, 1999.

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5

Menashe, Bar-Eli, ed. Regulation of gene expression in the tumor environment: Regulation of melanoma progression by the microenvironment: the roles of PAR-1 and PAFR. Dordrecht: Springer, 2008.

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6

M, Ponz de Leon. Familial and hereditary tumors. Berlin: Springer-Verlag, 1994.

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7

K, Dutta S., and Millis Richard M, eds. Biological effects of electropollution: Brain tumors and experimental models. Philadelphia, Pa: Information Ventures, 1986.

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8

1939-, Wilson Samuel H., and Suk William A, eds. Biomarkers of environmentally associated disease: Technologies, concepts, and perspectives. Boca Raton, FL: Lewis Publishers (CRC Press), 2002.

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9

1938-, Huff James, Boyd Jeffrey Allen 1958-, and Barrett J. Carl, eds. Cellular and molecular mechanisms of hormonal carcinogenesis: Environmental influences. New York: Wiley-Liss, 1996.

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10

1944-, Garner R. C., and Workshop on Biomonitoring and Carcinogen Risk Assessment (1989 : Queens' College, Cambridge), eds. Human carcinogen exposure: Biomonitoring and risk assessment. Oxford: IRL Press at Oxford University Press, 1991.

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11

International Conference on Environmental Mutagens (7th 1997 Rome, Italy). Satellite meeting of the 7th International Conference on Environmental Mutagens (ICEM): Workshop : quantitative modeling approaches for understanding and predicting mutagenicity and carcinogenicity : Istituto Superiore di Sanità Rome, September 3-5, 1997 : abstract book. Roma: Istituto superiore di sanità, 1997.

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12

From pink to green: Disease prevention and the environmental breast cancer movement. New Brunswick, N.J: Rutgers University Press, 2009.

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13

V, Beral, Bobrow M, Gardner M. J, and Roman Eve, eds. Childhood cancer and nuclear installations: Papers, abstracts, letters, editorials, reports, published since 1984. London: BMJ, 1993.

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14

Gofman, John W. Radiation-induced cancer from low-dose exposure: An independent analysis. San Francisco, Calif: Committee for Nuclear Responsibility, 1990.

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15

A, Barbarin Oscar, ed. Childhood cancer and the family: Meeting the challenge of stress and support. New York: Brunner/Mazel, 1987.

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16

Cancer: The evolutionary legacy. Oxford: Oxford University Press, 2000.

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17

International Agency for Research on Cancer and World Health Organization, eds. Carbon black, titanium dioxide, and talc. Lyon, France: International Agency for Research on Cancer, 2010.

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18

International Agency for Research on Cancer and World Health Organization, eds. Household use of solid fuels and high-temperature frying. Lyon, France: International Agency for Research on Cancer, 2010.

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19

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1994 Lyon, France). Some industrial chemicals. [Lyon]: International Agency for Research on Cancer, 1994.

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20

G, Huilgol N., Gopinath D. V, and Singh B. B, eds. Low level radiation and living state. Berlin: Springer-Verlag, 1994.

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21

International Conference on Carcinogenesis and Risk Assessment (9th 1995 Austin, Tex.). Etiology of breast and gynecological cancers: Proceedings of the Ninth International Conference on Carcinogenesis and Risk Assessment, held in Austin, Texas, November 29-December 2, 1995. Edited by Aldaz C. Marcelo 1956-. New York: Wiley-Liss, 1997.

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22

International Agency for Research on Cancer., ed. Some drinking-water disinfectants and contaminants, including arsenic. Lyon, France: IARC Press, 2004.

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23

Zhao, Wei, Zhe-Sheng Chen, Liwu Fu, and Yong Song, eds. Tumor Micro-environment and Drug Resistance. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-184-7.

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24

Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.

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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.

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25

Schwab, Manfred, Klaus Munk, Hartmut M. Rabes, and Peter H. Hofschneider. Genes and Environment in Cancer. Springer London, Limited, 2012.

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26

Schwab, Manfred, Klaus Munk, Hartmut M. Rabes, and Peter H. Hofschneider. Genes and Environment in Cancer. Springer, 2012.

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27

Zedeck, Morris S., and Martin Lipkin. Inhibition of Tumor Induction and Development. Springer, 2013.

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28

Zedeck, Morris S., and Martin Lipkin. Inhibition of Tumor Induction and Development. Springer London, Limited, 2013.

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29

Bar-Eli, Menashe. Regulation of Gene Expression in the Tumor Environment : Regulation of Melanoma Progression by the Microenvironment: The Roles of PAR-1 and PAFR. Springer London, Limited, 2008.

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30

Bar-Eli, Menashe. Regulation of Gene Expression in the Tumor Environment: Regulation of Melanoma Progression by the Microenvironment - The Roles of Par-1 and Pafr. Springer Netherlands, 2010.

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31

Visualizing Early-Stage Breast Cancer Tumors in a Mammographic Environment Through a 3-Dimensional Mathematical Model. Storming Media, 1999.

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32

Millis, Richard M., and S. K. Dutta. Biological Effects of Electropollution: Brain Tumors and Experimental Models. Info Ventures, 1986.

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33

Cellular and Molecular Mechanisms of Hormonal Carcinogenesis: Environmental Influences. Wiley-Liss, 1996.

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34

Wilson, Samuel H., and William A. Suk. Biomarkers of Environmentally Associated Disease: Technologies, Concepts, and Perspectives. Taylor & Francis Group, 2010.

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35

Golan, Amos. Advanced Inference in the Real World. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199349524.003.0006.

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In this chapter I continue the voyage into info-metrics in action, with an emphasis on more advanced info-metric inference in real-world environments. I develop a sequence of increasingly complex applications. In the first example, the maximum entropy method is extended for inferring interval information, with an application to weather data. The next example introduces additional conditional information into the constraints. It is a laboratory example, complemented with simulated data matched to observed population frequencies. The last example is the most complex, using surprisal analysis and Bayes’s rule to infer conditional probabilities from brain tumor data. In each problem the quantities whose entropy is maximized are identified and motivated. These examples demonstrate the power and generality of the info-metrics framework by showing that it allows inference in a variety of realistic settings.

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36

Todd, Stacy, and Nick Beeching. Fungal infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0315.

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Fungi, comprising yeasts, moulds, and higher fungi, have a worldwide distribution and are uncommon causes of disease in healthy individuals. However, over the last 20 years, invasive fungal disease (IFD) has become an increasing cause of morbidity and mortality. This is probably due to the increasing numbers of patients with underlying host conditions, which predispose to opportunistic IFD (e.g. transplant and anti-tumour necrosis factor immunosuppression, HIV, or chronic lung disease), and to increased recognition of endemic IFD (e.g. histoplasmosis), which cause disease in both immunocompetent and immunocompromised hosts in selected geographic locations. Diagnosis of IFD remains a challenge. Symptoms are often non-specific, and a definite diagnosis requires invasive sampling with appropriate laboratory testing of these samples. Non-invasive tests are being developed, but their positive and negative predictive values still need validation. Diagnostic criteria (‘proven, probable, and possible’) established primarily for use in research and clinical trials can also prove useful in clinical environments. However, the most important step in identifying patients with IFD is to consider the diagnosis in those at risk. This chapter will focus on the commonest causes of IFD (Candida spp., Aspergillus spp., Cryptococcus spp., and histoplasmosis).

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37

Zhang, Xuehong, Eunyoung Cho, and Hans-Olov Adami. Kidney Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0023.

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The etiology of kidney cancer remains largely unknown. Cigarette smoking, obesity, and hypertension are well-established risk factors for kidney cancer. Although the current evidence is relatively mixed, other emerging risk factors include use of nonsteroidal anti-inflammatory drugs (NSAIDs), occupational exposure to trichloroethylene, and high parity in women. In contrast, physical activity and alcohol consumption have been consistently inversely associated with risk of kidney cancer. There is no convincing evidence of a causal link with any other specific food items or nutrients. Most kidney cancers are sporadic, and current studies of common genetic variants report mixed results, but genetic variations may also contribute to the etiology of kidney cancer. Further research is warranted to identify new environmental causes, to better understand the genetic and molecular processes, and to account for different molecular subtypes with specific genetic or tumor characteristics.

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38

Tomatis, Lorenzo. Indoor and Outdoor Air Pollution and Human Cancer. Springer, 2012.

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39

Tomatis, Lorenzo. Indoor and Outdoor Air Pollution and Human Cancer. Springer London, Limited, 2012.

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40

Wilson, Samuel H., and William A. Suk. Biomarkers of Environmentally Associated Disease: Technologies, Concepts, and Perspectives. Taylor & Francis Group, 2002.

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41

Wilson, Samuel H., and William A. Suk. Biomarkers of Environmentally Associated Disease: Technologies, Concepts, and Perspectives. Taylor & Francis Group, 2002.

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42

Tangen, Catherine M., Marian L. Neuhouser, and Janet L. Stanford. Prostate Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0053.

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Prostate cancer is the most common solid tumor and the second leading cause of cancer-related mortality in American men. Worldwide, prostate cancer ranks second and fifth as a cause of cancer and cancer deaths, respectively. Despite the international burden of disease due to prostate cancer, its etiology is unclear in most cases. Established risk factors include age, race/ancestry, and family history of the disease. Prostate cancer has a strong heritable component, and genome-wide association studies have identified over 110 common risk-associated genetic variants. Family-based sequencing studies have also found rare mutations (e.g., HOXB13) that contribute to prostate cancer susceptibility. Numerous environmental and lifestyle factors (e.g., obesity, diet) have been examined in relation to prostate cancer incidence, but few modifiable exposures have been consistently associated with risk. Some of the variability in results may be related to etiological heterogeneity, with different causes underlying the development of distinct disease subgroups.

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43

IARC Working Group on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Chemicals Present in Industrial and Consumer Products, Food and Drinking-Water. International Agency for Research on Cancer (I A R C) (UN), 2013.

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44

Chang, Ellen T., and Hans-Olov Adami. Nasopharyngeal Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0008.

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The distinctive global incidence patterns and risk factors for nasopharyngeal carcinoma (NPC) make this a unique malignancy that represents an epidemiologic challenge. NPC is rare throughout most of the world but relatively common in southern China, Southeast Asia, the Arctic, North Africa, and the Middle East. This pattern is determined in part by the geographic and ethnic distribution of established risk factors for NPC, which include early/aberrant Epstein Barr virus infection, Chinese-style salted fish consumption, family history, certain human leukocyte antigen alleles, and tobacco smoking. Other possible NPC risk factors include certain dietary, occupational, and infectious exposures and genetic variants. Risk factors for NPC in low-incidence regions, where tumors are more often of squamous cell histology than in high-incidence regions, are poorly understood, as are etiologic interactions among genetic, environmental, and infectious risk factors for NPC.

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45

Thompson, Jonathan P. Anaesthesia for vascular surgery. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0058.

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Vascular surgical patients are at higher risk of cardiovascular morbidity and mortality than other surgical patients, and perioperative care remains challenging. However, vascular surgical practice is changing, with the expanding use of endovascular techniques to treat patients with vascular disease, improvements in medical therapy, and the evolution of evidence-based approaches to preoperative assessment. Preoperative assessment should concentrate on identifying and optimizing potentially correctable medical conditions, in particular cardiovascular disease. Successful outcomes depend on good anaesthetic techniques with emphasis on meticulous attention to detail and maintaining cardiovascular function and stability. Good communication with surgical and radiological colleagues is also vital. Anaesthesia for major vascular surgery also requires expertise in managing major haemorrhage, the use of invasive monitoring and cardioactive drugs, and regional anaesthesia. Knowledge and skills in the use of specific techniques for monitoring and protection against organ dysfunction are required. Endovascular surgery may be performed in dedicated operating suites or within the radiology department so the anaesthetist needs to be aware of considerations for anaesthesia in an isolated environment. This chapter details the management of patients presenting for the commonest major vascular procedures. All aspects of perioperative care for patients with abdominal and thoracic aortic aneurysms, occlusive aortic and peripheral vascular disease, and carotid stenosis are discussed. Anaesthesia for open surgery, endovascular and hybrid procedures, and elective and emergency procedures are included. The benefits of regional and general anaesthetic techniques are considered, where appropriate. The chapter also incorporates the anaesthetic management for less common procedures to treat carotid body tumours, thoracic outlet syndrome, and for thoracoscopic sympathectomy.

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46

Ovarian Toxicology, Second Edition. Taylor & Francis Group, 2013.

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47

(Editor), Eve Roman, Valerig Beral (Editor), and Martin Bobrow (Editor), eds. Childhood Cancer & Nuclear Installations. Bmj Publishing Group, 1993.

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48

(Producer), World Health Organization, ed. Occupational Exposures in Petroleum Refining; Crude Oil and Major Petroleum Fuels. IARC Vol 45 (Iarc). World Health Organisation, 1989.

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49

(WHO), World Health Organization, and IARC. Some Industrial Chemicals (Iarc Monographs on the Evaluation of Carcinogenic Risks to Humans). World Health Organisation, 1994.

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50

(Editor), N. G. Huilgol, D. V. Gopinath (Editor), and B. B. Singh (Editor), eds. Low Level Radiation and the Living State. Narosa Publishing House,India, 1994.

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