Books on the topic 'Carcinoma Endometrio'

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1

Li, Shen-yi, and En-yu Wang. Endometrial Carcinoma. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74821-9.

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2

1942-, Wang En-yu, and Seta Michihiro, eds. Endometrial carcinoma. Beijing: People's Medical Pub. House, 1990.

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3

Beatriz, Jiménez-Ayala Portillo, ed. Endometrial adenocarcinoma: Prevention and early diagnosis. Basel: Karger, 2008.

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4

Hedrick Ellenson, Lora, ed. Molecular Genetics of Endometrial Carcinoma. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43139-0.

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5

Kuramoto, Hiroyuki, and Masato Nishida, eds. Cell and Molecular Biology of Endometrial Carcinoma. Tokyo: Springer Japan, 2003. http://dx.doi.org/10.1007/978-4-431-53981-0.

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6

Seiichiro, Fujimoto, ed. Paraaortic lymph node metastasis in gynecologic malignancies. Sapporo, Japan: Hokkaido University School of Medicine, 2000.

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7

Cook, Linda S., Angela L. W. Meisner, and Noel S. Weiss. Endometrial Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0047.

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Endometrial cancer is rare among women of reproductive age, but in older women can occur at an annual rate of up to 50 –100 per 100,000. The incidence varies more than five-fold across regions of the world, with the rates generally being highest in North America and Europe. Endometrial cancer can be classified into two broad histologic groups: the more common type I tumors (e.g., endometrioid adenocarcinoma), which have a relatively good prognosis (case-fatality in the neighborhood of 20%); and the less common type II tumors (e.g., serous carcinoma), which have a poorer prognosis. The endometrium is a hormone-responsive tissue, and there is a large body of evidence to support a hormonal basis for carciogenesis. Specifically, exposure to high levels of circulating estrogens increases endometrial cancer risk, especially for type I cancer, whereas exposure to progestogens reduces risk.
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8

Seta, Michihiro, Shen-yi Li, and En-yu Wang. Endometrial Carcinoma. Springer London, Limited, 2012.

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9

C, Malkin J., and Tindall V. R. 1928-, eds. Endometrial carcinoma. Duphar Medical Relations, 1988.

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10

Carton, James. Gynaecological pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0012.

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This chapter covers gynaecological pathology and includes vulval skin diseases, benign vulval tumours, vulval carcinoma, vaginal infections, vaginal tumours, cervical carcinoma, cervical screening, endometriosis, endometrial carcinoma, uterine leiomyomas (fibroids), uterine leiomyosarcoma, functional ovarian cysts, benign non-epithelial ovarian tumours, benign epithelial ovarian tumours, borderline epithelial ovarian tumours, ovarian carcinomas, pelvic inflammatory disease, ectopic pregnancy, polycystic ovarian syndrome, hydatidiform mole, and pre-eclampsia.
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11

Mencaglia, Luca, III John R. Lurain, and Rafael F. Valle. Endometrial Carcinoma and Precursors. Informa Healthcare, 1999.

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12

Ellenson, Lora Hedrick. Molecular Genetics of Endometrial Carcinoma. Springer London, Limited, 2016.

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13

Ellenson, Lora Hedrick. Molecular Genetics of Endometrial Carcinoma. Springer, 2016.

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14

Ellenson, Lora Hedrick. Molecular Genetics of Endometrial Carcinoma. Springer, 2018.

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15

Kuramoto, H., and M. Nishida. Cell and Molecular Biology of Endometrial Carcinoma. Springer, 2012.

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16

Kuramoto, H., and M. Nishida. Cell and Molecular Biology of Endometrial Carcinoma. Springer London, Limited, 2012.

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17

Endometrial carcinoma and precursors: Diagnosis and treatment. Oxford: Isis Medical Media, 1999.

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18

(Editor), H. Kuramoto, and M. Nishida (Editor), eds. Cell and Molecular Biology of Endometrial Carcinoma. Springer, 2003.

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19

Grant, Warren, and Martin Scott-Brown. Prevention of cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0350.

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In the UK, the four commonest cancers—lung cancer, breast cancer, colon cancer, and prostate cancer—result in around 62 000 deaths every year. Although deaths from cancer have fallen in the UK over the last 20 years, the UK still suffers from higher cancer death rates than many other countries in Western Europe. In 1999, the UK government produced a White Paper called Saving Lives: Our Healthier Nation that outlined a national target to reduce the death rate from cancer by at least 20% in people under 75 by 2010. The subsequent NHS Cancer Plan of 2000 designed a framework by which to achieve this target through effective prevention, screening, and treatment programmes as well as restructuring and developing new diagnostic and treatment facilities. But do we know enough about the biology of the development of cancer for government health policies alone to force dramatic changes in survival? The science behind the causes of cancer tells us that its origin lies in acquired or inherited genetic abnormalities. Inherited gene mutation syndromes and exposure to environmental mutagens cause cancer, largely through abnormalities in DNA repair mechanisms, leading to uncontrolled cell proliferation. Although screening those thought to be at highest risk, and regulating exposure to environmental carcinogens such as tobacco or ionizing radiation, have reduced, and will continue to reduce, cancer deaths, there are many other environmental factors that have been shown to increase the population risk of cancer. These will be outlined in this chapter. However, the available evidence is largely from retrospective and cross-sectional population-based studies and therefore limits the ability to apply this knowledge to the risk of the individual patient who may been seen in clinic. Although we may be able to put him or her into a high-, intermediate-, or low-risk category, the question ‘will I get cancer, doc?’ is one that we cannot answer with certainty. The NHS Cancer Plan of 2000, designed to reduce cancer deaths in this country and to bring UK treatment results in line with those other countries in Europe, focuses on preventing malignancy as part of its comprehensive cancer management strategy. It highlights that the rich are less likely to develop cancer, and will survive longer if they are diagnosed than those who live in poverty. This may reflect available treatment options, but is more likely to be related to the lifestyle of those with regular work, as they may be more health aware. The Cancer Plan, however, suggests that relieving poverty may be more labour intensive and less rewarding than encouraging positive risk-reducing behaviour in all members of the population. Eating well can reduce the risk of developing many cancers, particularly of the stomach and bowel. The Cancer Plan outlines the ‘Five-a-Day’ programme which was rolled out in 2002 and encouraged people to eat at least five portions of fruit and vegetables per day. Obese people are also at higher risk of cancers, in particular endometrial cancer. A good diet and regular exercise not only reduce obesity but are also independent risk-reducing factors. Alcohol misuse is thought to be a major risk factor in around 3% of all cancers, with the highest risk for cancers of the mouth and throat. As part of the Cancer Plan, the Department of Health promotes physical activity and general health programmes, as well as alcohol and smoking programmes, particularly in deprived areas. Focusing on these healthy lifestyle points can potentially reduce an individual lifetime risk of all cancers. However, our knowledge of the biology of four cancers in particular has led to the development of specific life-saving interventions. Outlined in this chapter are details regarding ongoing prevention strategies for carcinomas of the lung, the breast, the bowel, and the cervix.
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