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Książki na temat „Cancer cells – Proliferation”

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Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 lutego 2022

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1

Enders, Greg H. Cell cycle deregulation in cancer. New York: Springer, 2010.

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2

M, Soto A., red. The society of cells: Cancer control of cell proliferation. Oxford: Bios Scientific Publishers, 1999.

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Sonnenschein, C. The society of cells: Cancer and control of cell proliferation. Oxford: Bios Scientific Publishers, 1999.

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4

Ito, Takaaki. Differentiation and proliferation of pulmonary neuroendocrine cells. Jena, Germany: Urban & Fischer, 1999.

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5

Cancer Stem Cell Workshop (2007? Berlin-Brandenburg Academy of Sciences and Humanities). Cancer stem cells: Novel concepts and prospects for tumor therapy. Redaktorzy Wiestler O. D. 1956-, Haendler B i Mumberg D. Berlin: Springer, 2007.

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6

Cancer Stem Cell Workshop (2007? Berlin-Brandenburg Academy of Sciences and Humanities). Cancer stem cells: Novel concepts and prospects for tumor therapy. Redaktorzy Wiestler O. D. 1956-, Haendler B i Mumberg D. Berlin: Springer, 2007.

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7

Meridith, Alan T. Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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9

V, Pavlova Lyudmila, i Yakovlev Andrej Yu 1944-, red. Biomathematical problems in optimization of cancer radiotherapy. Boca Raton: CRC Press, 1994.

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10

Ludlow, John W. Tumor suppressors: Involvement in human diseases, viral protein interactions, and growth regulation. Austin: R.G. Landes, 1994.

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11

1943-, Ford Richard J., Maizel Abby L i M.D. Anderson Hospital and Tumor Institute., red. Mediators in cell growth and differentiation. New York: Published for the University of Texas M.D. Anderson Hospital and Tumor Institute at Houston, Houston, Tex., by Raven Press, 1985.

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12

Resende, Rodrigo R., i Henning Ulrich, red. Trends in Stem Cell Proliferation and Cancer Research. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4.

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13

S, Lakshmi M., red. The genetics of cancer: Genes associated with cancer invasion, metastasis, and cell proliferation. San Diego: Academic Press, 1997.

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14

Pereira, Michael A. Effect of dichloroacetic acid and trichloroacetic acid on cell proliferation in B6C3F1 mice. Denver, CO: AWWA Research Foundation and American Water Works Association, 1995.

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15

APOPTOSIS AND CELL CONTROL IN CANCER (Ucl Molecular Pathology). Garland Science, 1995.

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16

Avner, Friedman, i Aguda B, red. Cell cycle, proliferation, and cancer. Berlin: Springer, 2006.

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17

Apoptosis and cell cycle control in cancer: Basic mechanisms and implications for treating malignant disease. Oxford: BIOS Scientific, 1996.

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18

M, García-Caballero, Brandes L. J i Hosoda S, red. Histamine in normal and cancer cell proliferation. Oxford: Pergamon Press, 1993.

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19

Sonnenschein, Pr. The Society of Cells: Cancer and Control of Cell Proliferation. Garland Science, 1998.

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20

L, Boynton Alton, i Leffert H. L, red. Control of animal cell proliferation. Orlando: Academic Press, 1985.

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21

L, Boynton Alton, i Leffert Hyam L, red. Control of animal cell proliferation. Academic, 1987.

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22

P, Briggs Andre, i Coburn Jacob A, red. Handbook of cell proliferation. Hauppauge, NY: Nova Science Publishers, 2009.

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23

Nicolini, Claudio A. Cell Growth. Springer, 2012.

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24

(Editor), O. D. Wiestler, B. Haendler (Editor) i D. Mumberg (Editor), red. Cancer Stem Cells: Novel Concepts and Prospects for Tumor Therapy (Ernst Schering Foundation Symposium Proceedings). Springer, 2007.

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25

L, Pusztai, Lewis Claire E i Yap E, red. Cell proliferation in cancer: Regulatory mechanisms of neoplastic cell growth. Oxford: Oxford University Press, 1996.

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26

Growth, Cancer, and the Cell Cycle: The Molecular, Cellular, and Developmental Biology. Humana Press, 2011.

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27

1924-, Frei Emil, i Bristol-Myers Symposium on Cancer Research (10th : 1987 : Boston, Mass.), red. The Regulation of proliferation and differentiation in normal and neoplastic cells. San Diego: Academic Press, 1989.

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HALL, PETER ED. Assessment Of Cell Proliferation In Clinical Practice. Springer, 1992.

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(Editor), Peter A. Hall, D. A. Levison (Editor) i N. A. Wright (Editor), red. Assessment of Cell Proliferation in Clinical Practice. Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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30

(Editor), Lajos Pusztai, C. E. Lewis (Editor) i Eric Yap (Editor), red. Cell Proliferation in Cancer: Regulatory Mechanisms of Neoplastic Cell Growth (Oxford Medical Publications). Oxford University Press, USA, 1995.

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31

T, Meridith Alan, red. Handbook of prostate cancer cell research: Growth, signalling, and survival. Hauppauge, NY: Nova Science, 2009.

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32

B, Kastan M., i Imperial Cancer Research Fund (Great Britain), red. Checkpoint controls and cancer. Plainview, NY: Cold Spring Harbor Laboratory Press, 1997.

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Avner, Friedman, i Aguda B, red. Tutorials in mathematical biosciences. Berlin: Springer, 2006.

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34

Wei, Dai, red. Checkpoint responses in cancer therapy. Totowa, NJ: Humana Press, 2008.

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35

Eisen, Tim. The patient with renal cell cancer. Redaktor Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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36

Josephs, Debra H., Heather J. Bax, Giulia Pellizzari, James F. Spicer, Ana Montes i Sophia N. Karagiannis. Antibody Therapeutics for Ovarian Carcinoma and Translation to the Clinic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0001.

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Despite improvements over the past decade in the treatment of ovarian cancer, many patients are at risk of recurrent disease and emerging drug resistance. The increased selectivity and reduced toxicity of molecularly targeted anti-cancer agents renders them attractive for development in ovarian cancer, and monoclonal antibodies targeting ovarian cancer-specific tumor antigens represent the largest such group investigated in this clinical setting. This chapter describes examples of monoclonal antibodies clinically evaluated for efficacy in ovarian cancer. These agents recognize molecular targets expressed on tumors or within tumor microenvironments that may be essential for tumor cell survival and proliferation. Recently, antibodies targeting checkpoint molecules on immune cells have shown efficacy in modulating anti-tumor immunity, and applications in ovarian carcinomas are evaluated. The chapter focuses on therapeutic agents’ attributes on targeting key cancer growth and progression pathways, and propensity to engender effector functions by activating immune effector cells in tumors and the circulation.
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37

Ajithkumar, Thankamma, Ann Barrett, Helen Hatcher i Natalie Cook. Paediatric malignancies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235636.003.0015.

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Leukaemia is the commonest cancer (accounting for >40% of cases) in children. It is a clonal proliferation of stem cells which leads to bone marrow failure and tissue infiltration.• Acute lymphoblastic leukaemia (ALL): 4/100,000• Acute myeloid leukaemia (AML): 0.7/100,000• Chronic myeloid leukaemia (CML): 0.2/100,000...
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38

Skuse, Gary R., i John W. Ludlow. Tumor Suppressors: Involvement in Human Diseases, Viral Protein Interactions and Growth Regulation (Molecular Biology Intelligence Unit). R G Landes Co, 1995.

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39

Bertolaso, Marta, i John Dupré. A Processual Perspective on Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779636.003.0016.

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This chapter attempts to illuminate the dynamic stability of the organism and the robustness of its developmental pathway by considering the biology of cancer. Healthy development and stable functioning of a multicellular organism require an exquisitely regulated balance between processes of cell division, differentiation, and death (apoptosis). Cancer involves a disruption of this balance, which results in unregulated cell proliferation. The thesis defended in this chapter is that the coupling between proliferation and differentiation, whether normal or pathological (as in cancer), is best understood within a process-ontological framework. This framework emphasizes the interactions and mutual stabilizations between processes at different levels and this, in turn, explains the difficulty in allocating the neoplastic process to any particular level (genetic, epigenetic, cellular, or histological). Understanding these interactions is likely to be a precondition of a proper understanding of how these mutual regulations are disrupted in the processes we call cancerous.
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40

Freifeld, Alison G. An Introduction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199938568.003.0100.

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This chapter focuses on solid tumors and how they can be treated. Solid tumors, lymphomas, and leukemias represent a widely diverse array of cancers. Until recently, the general approach to treating all of them was to administer cytotoxic anticancer drugs that damage proliferating cells by interfering with mitosis and other essential steps in cellular replication. Localized solid tumors are largely treated by surgical resection and radiotherapy, with cytotoxic chemotherapy being commonly used adjunctively or in cases of metastatic disease. A major drawback of this approach has been the lack of specificity in that cytotoxic drugs will destroy actively dividing normal cells as well as malignant cells. The “shotgun approach” of using intensive cytotoxic chemotherapies has been the mainstay of cancer treatment for at least 6 decades. The chapter concludes that in addition to the tissue damage and immunomodulating effects of anticancer drugs, it should be remembered that cancers themselves may increase the chances for infection.
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41

Brinton, Louise A., Mia M. Gaudet i Gretchen L. Gierach. Breast Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0045.

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Breast cancer is the most frequently diagnosed cancer in women worldwide, with annual estimates of 1.7 million newly diagnosed cases and 522,000 deaths. Although more breast cancers are diagnosed in economically developed than in developing countries, the reverse is true for mortality, reflecting limited screening and less effective treatments in the latter. Breast cancer incidence has been on the rise in the United States for many years, but in recent years this is restricted to certain subgroups, while internationally there have been continued generalized increases, likely reflecting adoption of more Westernized lifestyles. Breast cancer is widely recognized as being hormonally influenced, with most of the established risk factors believed to reflect the influence of cumulative exposure of the breast to stimulatory effects of ovarian hormones—leading to increased cellular proliferation, which in turn can result in genetic errors during cell division.
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42

Bisen, Prakash S., Zakir Khan i Saurabh Bundela. Biology of Oral Cancer: Key Apoptotic Regulators. Taylor & Francis Group, 2013.

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Bisen, Prakash S., Zakir Khan i Saurabh Bundela. Biology of Oral Cancer: Key Apoptotic Regulators. Taylor & Francis Group, 2017.

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44

Girod, Sabine C., i Sabine Christiane Girod. Tumor Suppressor Genes and Cell Proliferation Control in the Carcinogenesis of the Oral Mucosa. QUINTESSENCE, 1999.

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45

Tutorials in Mathematical Biosciences III: Cell Cycle, Proliferation, and Cancer (Lecture Notes in Mathematics Book 1872). Springer, 2005.

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(Contributor), B. Aguda, M. Chaplain (Contributor), A. Friedman (Contributor), M. Kimmel (Contributor), H. A. Levine (Contributor), G. Lolas (Contributor), A. Matzavinos (Contributor), M. Nilsen-Hamilton (Contributor), A. Swierniak (Contributor) i Avner Friedman (Editor), red. Tutorials in Mathematical Biosciences III: Cell Cycle, Proliferation, and Cancer (Lecture Notes in Mathematics / Mathematical Biosciences Subseries). Springer, 2006.

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47

Hodgkiss, Andrew. Further clinical issues. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0012.

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The clinical challenges arising when a person with a severe mental illness, such as schizophrenia or bipolar disorder, develops a cancer are surveyed. Delayed diagnosis and access to oncological treatment, factors contributing to reduced adherence, and the interruption of specialist community psychiatric care are discussed. Long-term psychotropic medication may complicate end-of-life care, and access to palliative care is usually limited for those in secure mental health inpatient units. The striking inverse relationship between neurodegenerative disorders (Alzheimer-type dementia) and proliferative disorders (cancers) is considered.Psychiatric aspects of haematopoietic stem cell transplantation (HSCT) are reviewed, including psychopathology arising from drugs used to prevent graft-versus-host disease and from infections complicating chronic immunosuppression. Cognitive impairment and suicide after HSCT are considered.
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48

Transforming Growth Factor-Beta in Cancer Therapy: Volume II (Cancer Drug Discovery and Development). Humana Press, 2008.

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49

Grant, Warren, i Martin Scott-Brown. Prevention of cancer. Redaktorzy Patrick Davey i 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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Transforming Growth Factor-Beta in Cancer Therapy: Volume I, Basic and Clinical Biology (Cancer Drug Discovery and Development). Humana Press, 2008.

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