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Books on the topic 'Metastatic progression'

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Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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1

1921-, Franks L. M., and Hart I, eds. Tumour progression and metastasis. Oxford: Oxford University Press for the Imperial CancerResearch Fund, 1988.

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2

Károly, Lapis, Eckhardt S, and International Union Against Cancer, eds. Carcinogenesis and tumour progression. Budapest: Akadémiai Kiadó, 1987.

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3

Kaiser, Hans E., and Aejaz Nasir, eds. Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7.

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4

1928-, Kaiser Hans E., Nasir Aejaz, and Nasir Nelly Adriana, eds. Selected aspects of cancer progression: Metastasis, apoptosis and immune response. [Dordrecht]: Springer, 2008.

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5

1928-, Kaiser Hans E., ed. Cancer growth and progression. Dordrecht: Kluwer Academic Publishers, 1989.

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6

L, Nicolson Garth, Fidler Isaiah J. 1936-, Triton Biosciences Inc, Smith, Kline & French Laboratories., and University of California, Los Angeles., eds. Tumor progression and metastasis: Proceedings of a Triton Biosciences-Smith, Kline & French-UCLA symposium held in Keystone, Colorado, April 6-12, 1987. New York: A.R. Liss, 1988.

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7

S, El-Deiry Wafik, ed. Tumor progression and therapeutic resistance. New York, NY: New York Academy of Sciences, 2005.

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8

service), ScienceDirect (Online, ed. Bone cancer: Progression and therapeutic approaches. Amsterdam: Academic, 2010.

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9

1952-, Dickson Robert B., and Lippman Marc E. 1945-, eds. Mammary tumorigenesis and malignant progression: Advances in cellular and molecular biology of breast cancer. Boston: Kluwer Academic Publishers, 1994.

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10

1943-, Harris Curtis C., Liotta L. A, Genentech Inc, and University of California, Los Angeles., eds. Genetic mechanisms in carcinogenesis and tumor progression: Proceedings of a Genentech-UCLA symposium held at Keystone, Colorado, January 21-27, 1989. New York: Wiley-Liss, 1990.

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11

Tumor dormancy, quiescence, and senescence: Aging, cancer, and noncancer pathologies. Dordrecht: Springer, 2014.

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12

Metastatic Progression and Tumour Heterogeneity. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03928-854-0.

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13

Zannetti, Antonella, Gennaro Ilardi, and Wolfgang Link, eds. Tumor Microenvironment: Molecular Mechanisms and Signaling Pathways Involved in Metastatic Progression. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-448-3.

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14

Healey, John H., and David McKeown. Orthopaedic surgery in the palliation of cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0125.

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Metastatic spread of cancer to bone is frequent and causes pain, disability, and functional limitation. New understanding of the homing method of cancer cells to bone and the mechanism of cancer production of pain raise possible new treatment strategies. Non-surgical treatments such as chemotherapy and hormone therapy are effective in early disease. Bisphosphonates and inhibition of osteoprotegerin prevent progression of bone lesions and avoid pain, radiation, and surgery. Radiotherapy arrests disease and relieves pain in many cases. Surgery is needed when the bone is weak or fractured. It effectively relieves pain and preserves function. It usually requires replacing or bypassing the deficient bone with site-specific reconstructive surgery. Surgery should be selected based on projections of patient survival. New tools to make these projections have been validated and are now available. New targeted drug therapies appear to be changing metastatic bone disease into a more chronic condition. This will alter the management of local disease in many histological subtypes of metastatic cancers.
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15

O’Brien, Tim, and Amit Patel. Kidney cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0088.

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Despite advances in imaging techniques, many patients with renal cancer still present with locally advanced or metastatic disease. Surgical resection remains the main stay of treatment for locally advanced disease, but is technically challenging and survival remains limited. Progression free and overall survival following nephrectomy are dependent on many factors including pathological T-stage, lymph node status, and Fuhrman grade. Patients presenting with metastatic disease still have a poor prognosis and the use of multimodal therapy has yet to deliver dramatic improvements in outcomes, with just 15% of patients surviving in the long term. Understanding the potential but also the limitations of surgery is very important when the overall prognosis may be so limited in this challenging group of patients.
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16

Lasfar, Ahmed, and Karine Cohen-Solal, eds. Tumor Progression and Metastasis. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.77832.

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17

Gorelik, Elizier L. Metastasis/Dissemination (Cancer Growth and Progression). Springer, 2007.

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18

Mukherji, Deborah, Aurelius Omlin, Carmel Pezaro, and Johann De Bono. Novel therapies and emerging strategies for the treatment of patients with castration-resistant prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0069.

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Castration-resistant prostate cancer (CRPC) represents a final stage of this malignancy for many men and is defined as the progression of prostate cancer despite castrate levels of testosterone. CRPC may present as a rising PSA, the development of new metastases, or worsening of known metastases. Recent advances have resulted in five new treatments for CRPC: the immunotherapy sipuleucel-T; the cytotoxic cabazitaxel; the androgen biosynthesis inhibitor abiraterone acetate; the radioisotope radium-223; and the antiandrogen enzalutamide. These have all improved overall survival in randomized phase III studies for patients with metastatic CRPC. Furthermore, multiple agents and combinations are currently in late-stage clinical testing. Men with advanced prostate cancer represent an important population for clinical and translational research and clinical trial participation should be considered as part of standard care.
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19

Lemieux, Julie. An exploration of responsiveness to change of psychosocial, quality of life and pain measures to supportive-expressive group therapy intervention, improvement in mood and progression of disease in women with metastatic breast cancer. 2005.

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20

Lemieux, Julie. An exploration of responsiveness to change of psychosocial, quality of life and pain measures to supportive-expressive group therapy intervention, improvement in mood and progression of disease in women with metastatic breast cancer. 2005.

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21

Montironi, Rodolfo, Liang Cheng, Antonio Lopez-Beltran, Roberta Mazzucchelli, Matteo Santoni, and Marina Scarpelli. Prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0060.

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The incidence of prostate cancer (PCa) has risen dramatically in the last years. This event may be partially explained by the employment of digital rectal examination (DRE), serum prostate-specific antigen (PSA), and transrectal ultrasonography. In developed countries, PCa is the most frequent non-skin malignancy in males. It is estimated that one in six males will be diagnosed with PCa during their lifetime, the risk of death due to metastatic PCa being 1 in 30. Multiple factors contribute to the development of PCa, as well as to its progression to an androgen-independent state: dietary factors, inherited susceptibility factors, gene defects, and androgens and their receptors. The chapter will discuss the following topics: high-grade prostatic intraepithelial neoplasia (PIN); atypical small acinar proliferation; morphological criteria for the identification of PCa; reporting of PCa biopsies; prognostic factors in radical prostatectomies (RPs); and specimens.
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22

Liver Cancer - Genesis, Progression and Metastasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100845.

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23

NICHOLSON, GL. Nicolson: Tumor Progression & Metastasis (Proc Keystone Colorado April 1987). John Wiley & Sons Inc, 1988.

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24

Clarke, Noel W. Metastatic disease in prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.

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Metastases are the predominant cause of morbidity and death from prostate cancer (CaP). The tendency for cells to migrate from the primary site, enter the vascular/lymphatic circulation, and implant/grow at secondary sites is the principal discriminator of aggressive form indolent disease. But this process is poorly understood. Cells enter the circulation in increasing number as the disease progresses, impinging on endothelial surfaces, particularly in red bone marrow where they bind and transmigrate, forming early cell colonies. This requires chemo-attractants and nutrients enabling cellular survival. Established metastases thrive independently, disrupting local tissue, as characterized by progressive replacement of red bone marrow and disruption of skeletal architecture. Bone disruption includes massive overstimulation of both osteoblasts and osteoclasts, inducing synchronous over-production of abnormal bone and gross osteolysis.
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25

Merakos, Peter. Role of Proprotein Convertases in Cancer Progression and Metastasis. Morgan & Claypool Life Science Publishers, 2014.

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26

Galluzzi, Lorenzo, and Clement Thomas. Actin Cytoskeleton in Cancer Progression and Metastasis - Part B. Elsevier Science & Technology, 2020.

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27

Actin Cytoskeleton in Cancer Progression and Metastasis – Part C. Elsevier, 2021. http://dx.doi.org/10.1016/s1937-6448(21)x0004-4.

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28

Actin Cytoskeleton in Cancer Progression and Metastasis - Part A. Elsevier, 2020. http://dx.doi.org/10.1016/s1937-6448(20)x0007-4.

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29

Actin Cytoskeleton in Cancer Progression and Metastasis - Part B. Elsevier, 2020. http://dx.doi.org/10.1016/s1937-6448(20)x0008-6.

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30

Galluzzi, Lorenzo, and Clement Thomas. Actin Cytoskeleton in Cancer Progression and Metastasis - Part A. Elsevier Science & Technology Books, 2020.

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31

Galluzzi, Lorenzo, and Clement Thomas. Actin Cytoskeleton in Cancer Progression and Metastasis - Part C. Elsevier Science & Technology, 2021.

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32

Thomas, Clément, and Lorenzo Galluzzi. Actin Cytoskeleton in Cancer Progression and Metastasis - Part A. Elsevier Science & Technology, 2020.

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33

Tse, Joyce Che Yan. Functional Heterogeneity of Fibroblasts in Cancer Progression and Metastasis. 2011.

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34

Galluzzi, Lorenzo, and Clement Thomas. Actin Cytoskeleton in Cancer Progression and Metastasis - Part C. Elsevier Science & Technology Books, 2021.

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35

Metrakos, Peter, and Majid Khatib. Role of Proprotein Convertases in Cancer Progression and Metastasis. Morgan & Claypool Life Science Publishers, 2012.

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36

Galluzzi, Lorenzo, and Clement Thomas. Actin Cytoskeleton in Cancer Progression and Metastasis - Part B. Elsevier Science & Technology Books, 2020.

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37

Kaiser, Hans E., and Aejaz Nasir. Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response. Springer Netherlands, 2010.

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38

Khatib, Abdel-Majid. Proprotein Convertases: Discovery, Characteristics, and Link to Tumor Progression and Metastasis. Morgan & Claypool Life Science Publishers, 2013.

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39

Khatib, Abdel-Majid, and A.-Majid Khatib. Proprotein Convertases: Discovery, Characteristics, and Link to Tumor Progression and Metastasis. Morgan & Claypool Life Science Publishers, 2013.

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40

Kaiser, H. E. Comparative Aspects of Tumor Development (Cancer Growth and Progression). Springer, 1988.

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41

Ajithkumar, Thankamma, Ann Barrett, Helen Hatcher, and Natalie Cook. Concepts of multidisciplinary management. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235636.003.0003.

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Cancer prevention 18Cancer screening 22Cancer genetics 24Genetic counselling 28Principles of cancer diagnosis and management 32Principles of surgical oncology 38Radiotherapy 42Principles of systemic therapy 46Carcinogenesis is a multistep process consisting of progressive molecular and cellular changes leading to early invasive cancer and finally to distant metastasis and death. The initiation and progression of cancer usually takes years. Attempts are being made to reverse the molecular and cellular changes at an early state of cancer initiation or progression. The World Health Organization (WHO) estimates that at least one-third of all cancers are preventable and cancer prevention is the most cost-effective long-term strategy for the control of cancer....
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42

Gvozdenovic, Ana. The relevance of CD44 and hyaluronan interaction in osteosarcoma progression and metastasis. 2012.

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43

Michelson, S. Mathematical Modeling in Tumor Growth and Progression (Invasion and Metastasis, 4-5). S Karger Pub, 1997.

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44

Simon, M. Celeste. Diverse Effects of Hypoxia on Tumor Progression. Springer, 2011.

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45

Simon, M. Celeste. Diverse Effects of Hypoxia on Tumor Progression. Springer, 2012.

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46

Diverse Effects Of Hypoxia On Tumor Progression. Springer, 2010.

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47

Wang, Xu, Tengchuan Jin, Christopher James Pirozzi, Xueli Zhang, and Shu-Heng Jiang, eds. Inflammatory Tumor Immune Microenvironment: Molecular Mechanisms and Signaling Pathways in Cancer Progression and Metastasis. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-754-2.

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48

Ganapathy, Vadivel, Maria E. Mycielska, Eric Kenneth Parkinson, and Sebastian Haferkamp, eds. Metabolite and Nutrient Transporters in Cancer-Cell Metabolism: Role in Cancer Progression and Metastasis. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-768-7.

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49

Diverse Effects of Hypoxia on Tumor Progression (Current Topics in Microbiology and Immunology Book 345). Springer, 2010.

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50

Eisen, Tim. The patient with renal cell cancer. Edited by 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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