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Data publikacji: 25 maja 2024

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1

J, Gottlieb Geoffrey, i Ackerman A. Bernard 1936-, red. Kaposi's sarcoma: A text and atlas. Philadelphia: Lea & Febiger, 1988.

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2

G, Giraldo, red. Recent advances in AIDS and Kaposi's sarcoma. Basel: Karger, 1987.

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3

Lehnherr, Melinda. Kaposi's sarcoma in Illinois: A comparison of AIDS cases to classic cases. Springfield, Ill: Illinois Dept. of Public Health, Division of Epidemiologic Studies, 1989.

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4

G, Castello, red. Sindrome di immunodeficienza acquisita e sarcoma di Kaposi (AIDS/KS). Firenze: USES, Edizioni scientifiche, 1986.

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5

Shepherd, Frances A. Management of Kaposi's sarcoma associated with human immunodeficiency virus infection: Report. [Ottawa]: Health and Welfare Canada, 1991.

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6

Canada. Health and Welfare Canada. Management of Kaposi's Sarcoma associated with human immunodeficiency virus infection/ Francis A. Shepard. Ottawa: Health and Welfare Canada, 1991.

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7

G, Giraldo, World Health Organization i International Symposium on AIDS and Associated Cancers in Africa (2nd : 1987 : Naples, Italy), red. AIDS and associated cancers in Africa: 2nd international symposium, Naples, October 7-9, 1987. Basel: Karger, 1988.

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8

1925-, Vaeth Jerome M., red. Cancer and AIDS: 19th annual San Francisco Cancer Symposium, San Francisco Calif., March 2-4, 1984. Basel: Karger, 1985.

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9

AIDS, the acquired immune deficiency syndrome. Wyd. 2. Lancaster [Lancashire]: MTP Press, 1987.

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10

Daniels, Victor G. SIDA, sindrome de immunodeficiencia adquirida. Wyd. 2. México: Manual Moderno, 1988.

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11

L, Schmid, i Senn Hansjörg, red. AIDS-related neoplasias. Berlin: Springer-Verlag, 1988.

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12

AIDS, the acquired immune deficiency syndrome. Lancaster: MIP Press, 1985.

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13

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: The human genome project and disease prediction. Bethesda, Md: National Institutes of Health, National Cancer Institute, 1995.

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14

R, Pittelkow Mark, Iwatsuki Keiji, Green Adèle, Elwan Nagwa M i SpringerLink (Online service), red. Skin Cancer - A World-Wide Perspective. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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15

W, Jaffe Harold, Beral V, Weiss Robin i Imperial Cancer Research Fund (Great Britain), red. Cancer, HIV, and AIDS. New York: Cold Spring Harbor Laboratory Press, 1991.

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16

Meeting, United States President's Cancer Panel. President's Cancer Panel meeting: Evaluating the national cancer program, an ongoing process. Bethesda, Md: National Institutes of Health, National Cancer Institute, 1993.

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17

Meeting, United States President's Cancer Panel. President's Cancer Panel Meeting: AIDS neoplasms. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1995.

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18

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, September 10, 2007 : Evergreen Marriott Conference Resort, Atlanta, GA. [Bethesda, MD]: National Cancer Institute, 2006.

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19

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, February 1-2, 2001 : Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, California. [Bethesda, Md: National Cancer Institute, 2001.

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20

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: The information superhighway : what does it mean for cancer? [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1995.

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21

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Progress in leukemia : Inter-Continental Hotel, 505 North Michigan Avenue, Chicago, Illinois, July 20, 1995. [Washington, D.C.]: The Institute, 1995.

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22

United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting. [Bethesda, MD]: The Institute, 1992.

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23

United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting. Bethesda, Md: The Institute, 1992.

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24

United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting: Cancer and the cultures of America. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1994.

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25

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, July 29-30, 2002 : hosted by the Yakama Nation, Eagle Seelatsee Auditorium, Yakama Nation Agency Building, Toppenish, WA. [Bethesda, Md: National Cancer Institute, 2002.

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26

National Cancer Institute (U.S.), red. President's Cancer Panel Meeting: Transcript of proceedings, December 7, 2002, Marriott Wardman Park Hotel, Washington, D.C. [Bethesda, Md: National Cancer Institute, 2002.

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27

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, May 27-28, 2003 : Lisbon Marriott Hotel, Lisbon, Portugal. [Bethesda, Md.] (31 Center Dr., Room 3A-18 MSC 2440, Bethesda 20892-2440): [National Cancer Institute, 2003.

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28

United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting: Lung cancer: clinical, societal, and governmental challenges. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1994.

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29

United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting: Transcript of proceedings, November 15, 1993. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1993.

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30

United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting: Transcript of proceedings, April 7 & 8, 1994. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1994.

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31

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Evaluating the National Cancer Program : Huntsman Cancer Institute, Salt Lake City, Utah : November 19, 1999. [Bethesda, MD (31 Center Drive, Room 4A48, Bethesda, MD 20892-2473): National Cancer Institute, 1999.

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32

United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, October 12-13, 2000, Billings, Montana. Billings, MT: [National Cancer Institute, 2003.

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33

Dittmer, Dirk Peter, i Susan E. Krown. Molecular basis for therapy of AIDS-defining cancers. New York: Springer, 2010.

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34

Schmid, Luzius, i Hans-Jörg Senn. AIDS-Related Neoplasias. Springer, 2013.

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35

AIDS: 1,000 full-text statistical abstracts from the A Matter of fact database, 1984-1992. Ann Arbor, Mich: Pierian Press, 1993.

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36

AIDS Related Neoplasias. Springer Verlag, 1988.

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37

Oliver, Nora, i Elizabeth Chiao. Malignant Diseases in HIV. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0033.

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Malignancies were one of the earliest recognized manifestations that led to the eventual description of the AIDS epidemic. Kaposi’s sarcoma was one of the first entities described in association with AIDS. Subsequently, intermediate-grade and high-grade non-Hodgkin’s lymphoma, invasive cervical cancer, and primary central nervous system lymphoma were defined by the Centers for Disease Control and Prevention as “AIDS-defining conditions.” Since the advent of combination antiretroviral therapy, several other cancers that are not AIDS-defining have been found to have an increased incidence in patients with HIV. These include, but are not limited to, Hodgkin’s disease and anal, liver, lung, oropharyngeal, colorectal, and renal cancers. They are generally referred to as “non-AIDS-defining cancers.” The increasing longevity of persons living with HIV as well as concurrent modifiable risk factors such as tobacco use may also influence the epidemiology of these malignancies.
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38

The Official Patient's Sourcebook on Kaposi's Sarcoma: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2003.

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39

AIDS-Related Cancers and Their Treatment. New York: Marcel Dekker, Inc., 2003.

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40

(Editor), C. Boshoff, i R. A. Weiss (Editor), red. Kaposi Sarcoma Herpesvirus: New Perspectives (Current Topics in Microbiology and Immunology). Springer, 2006.

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41

(Editor), R. A. Weiss, red. Cancer, HIV And AIDS (Cancer Surveys, Vol 10) (Cancer Surveys, Vol 10). Cold Spring Harbor Laboratory Pr, 1991.

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42

(Contributor), WHO, red. Epstein-Barr Virus and Kaposi's Sarcoma Herpes Virus/Human Herpesvirus 8 (IARC Monographs on Eval of Carcinogenic Risk to Humans). World Health Organisation, 1997.

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43

President's Cancer Panel Meeting: Transcript of proceedings, March 8, 2000. Bethesda, Md. (31 Center Dr., Room$A48, Bethesda 20892-2473): National Cancer Institute, 2000.

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44

Krown, Susan E., i Dirk P. Dittmer. Molecular Basis for Therapy of AIDS-Defining Cancers. Springer, 2014.

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45

Wong, Germaine, i Angela C. Webster. Cancer after kidney transplantation. Redaktor Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0287.

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Cancer is a major cause of mortality and morbidity after transplantation. The overall risk of cancer among transplant recipients is at least 2.5–3-fold greater than that of the age- and gender-matched general population. The increased risk is also type specific, and is greatest among virus-related neoplasms such as Kaposi sarcoma, post-transplant lymphoproliferative disease, and vulvovaginal cancers, with an excess risk of at least 9–20 times greater than that of the general population. Cancer prognoses are also poor in transplant recipients, with less than 10% surviving 5 years after initial diagnoses. Despite the increased cancer risk, little is known about the efficacy of treatment, the screening strategies, and the outcomes of patients with cancer and kidney transplants. Uncertainties also exist as to how the various types of modern immunosuppression impact on recipients’ overall long-term survival and quality of life. This chapter discusses the incidence and prognoses of patients with de novo cancer after transplantation, the epidemiology of donor cancer transmission, the outcomes of transplanting patients with a prior history of cancer, as well as the different approaches to cancer screening and management after kidney transplantation.
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46

Kuypers, Dirk R. J., i Maarten Naesens. Immunosuppression. Redaktor Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.

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Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids and corticosteroids has been fine-tuned over the last decade, based on empirically derived observations as well as on the results of large multicentre randomized clinical studies. Corticosteroid withdrawal and avoidance are feasible, at least in patients with a low immunological risk, but CNI-free protocols have had few long-term successes. Some minimization strategies have increased risk of developing acute rejection or (donor-specific) anti-HLA antibodies, with deleterious effects on the graft. Mammalian target of rapamycin inhibitors (mTORi) have shown limited benefit in early CNI replacement regimens and their long-term use as primary drug is hampered by intolerance. In the setting of particular malignant disease occurring after transplantation, such as squamous cell carcinoma of the skin and Kaposi’s sarcoma, mTORi seem promising. Induction agents (anti-interleukin 2 receptor monoclonal antibodies, antithymocyte globulins) effectively diminish the risk of early immunological graft loss in recipients with moderate to high immunological risk but at the price of more infectious or malignant complications. While personalized transplantation medicine is only in its early stages of development, attempts are made to quantitatively measure the clinical degree of immunosuppression, to tailor immunosuppressive therapy more specifically to the patient’s individual profile, and to monitor graft status by use of invasive (e.g. surveillance renal biopsies) and non-invasive biomarkers. These scientific endeavours are a necessity to further optimize the current immunosuppressive therapy which will remain for some time to come.
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47

Grant, Warren, i Martin Scott-Brown. Principles of oncogenesis. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.
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