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Books on the topic 'Ovarian cancer cell invasion'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Heino, Jyrki, and Veli-Matti Ka ha ri. Cell invasion. Georgetown, Tex: Landes Bioscience, 2002.

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2

Wells, Alan, ed. Cell Motility in Cancer Invasion and Metastasis. Berlin/Heidelberg: Springer-Verlag, 2006. http://dx.doi.org/10.1007/b103440.

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3

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

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4

Farghaly, Samir A. Adoptive Cell Immunotherapy for Epithelial Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0005.

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The standard management for epithelial ovarian cancer (EOC) is a combination of aggressive debulking surgery with residual tumor of less than 1 cm and platinum-based chemotherapy. However, a high percentage of patients experience disease recurrence. Extensive efforts to find new therapeutic options have been made, albeit cancer cells develop drug resistance and malignant progression occurs. Novel therapeutic strategies are needed to enhance progression-free survival and overall survival of patients with advanced EOC. Several preclinical and clinical studies investigated feasibility and efficacy of adoptive cell therapy (ACT) in EOC. The aim of this chapter is to present an overview of ACT in EOC, focusing on Human Leukocyte Antigen (HLA)-restricted tumor infiltrating lymphocytes and MHC-independent immune effectors such as natural killer and cytokine-induced killer. The available data suggest that ACT may provide the best outcome in patients with low tumor burden, minimal residual disease, or maintenance therapy. Further preclinical studies and clinical trials are needed.

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5

Stashwick, Caitlin, Brian J. Czerniecki, and Janos L. Tanyi. Dendritic Cell Vaccine Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0008.

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Dendritic cell vaccine therapy has emerged as an exciting new field in immunotherapy in ovarian cancer over the past two decades. This chapter reviews the biology of dendritic cells, including dendritic cell subsets, development, activation, and maturation as well as strategies for clinical use of dendritic cell vaccines. While there is encouraging data in preclinical work for dendritic cell vaccine, the outcomes of clinical trials have not shown robust responses. A summary of the clinical trials using dendritic cell vaccines in ovarian cancer is reviewed. Treatment-related toxicities and potential therapies to increase clinical efficacy are also discussed.

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6

Lavoué, Vincent, Patrick Legembre, Jean Levêque, Fabrice Foucher, Sébastien Henno, and Florian Cabillic. Ovarian Cancer Immunity. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0003.

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Epithelial ovarian cancer (EOC) is a significant cause of cancer-related mortality in women, and there has been no substantial decrease in the death rates due to EOC in the past three decades. Thus, basic knowledge regarding ovarian tumor cell biology is urgently needed to allow the development of innovative treatments for EOC. Traditionally, EOC has not been considered an immunogenic tumor, but there is evidence of an immune response to EOC in patients. Clinical data demonstrate that an anti-tumor immune response and immune evasion mechanisms are correlated with a better and lower survival, respectively, providing evidence for the immunoediting hypothesis in EOC. This chapter focuses on the immune response and immune suppression in EOC.

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7

Farghaly, Samir A., ed. Ovarian Cancer Immunotherapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.001.0001.

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Ovarian Cancer Immunotherapy provides a broad overview of several aspects of basic sciences and clinical and therapeutic aspects of immunotherapy for ovarian cancer, as well as state-of-the-art information on molecular genetics and biology. Chapters are written by a team of expert contributors from around the world and explore topics such as antibody therapeutics for ovarian carcinoma, emerging serum biomarkers, ovarian cancer immunity, adoptive cell immunotherapy, the biology of dendritic cells, the role of growth factors, and more. Readers will also gain a better understanding of the molecular and cellular events that underlie ovarian cancer immunology. This book is an ideal reference for clinicians and medical students caring for patients with ovarian cancer, including attending surgeons and physicians, and clinical fellows and residents in the disciplines of gynecologic oncology, medical oncology, and surgical oncology.

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8

1950-, Brodt Pnina, ed. Cell adhesion and invasion in cancer metastasis. Austin: R.G. Landes Co., 1996.

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9

Wells, Alan. Cell Motility in Cancer Invasion and Metastasis. Springer, 2010.

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10

Chapman, Hannah, and Christine Elwell. Ovarian and testicular cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0328.

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Ovarian cancer is the fifth most common cancer in females in the UK. In contrast, testicular cancer is a rare disease: there were 2138 new cases of testicular cancer diagnosed in 2008 in the UK, and only 70 deaths. Ninety per cent of all ovarian cancers are of epithelial origin, although germ cell and sex cord–stromal cell tumours also occur. In contrast, 95% of testicular cancers are germ cell tumours, with stromal cell tumours and lymphomas making up the remaining 5%. This chapter discusses ovarian cancer and testicular cancer, including definitions of the diseases and their etiologies, typical symptoms, uncommon symptoms, demographics, natural history, complications, diagnostic approach, other diagnoses that should be considered, prognosis, and treatment.

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11

Heino, Jyrki, and Veli-matti Kahari. Cell Invasion (Medical Intelligence Unit). Landes Bioscience, 2002.

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12

Brodt, Pnina. Cell Adhesion and Invasion Mechanisms in Cancer Metastasis. Landes Bioscience, 1996.

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13

Brodt, P. Cell Adhesion and Invasion Mechanisms in Cancer Metastasis. Springer, 1996.

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14

Wells, Alan. Cell Motility in Cancer Invasion and Metastasis (Cancer Metastasis - Biology and Treatment). Springer, 2006.

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15

Alharbi, Yousef, Manish S. Patankar, and Rebecca J. Whelan. Antibody-Based Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0006.

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With their role in connecting disease-associated antigens to the cellular immune response, antibodies hold considerable promise as therapeutic agents. This chapter discusses three classes of therapeutic antibodies that have been developed for use in ovarian cancer therapy. The first includes antibodies selected against tumor-associated antigens such as MUC16/CA125, mesothelin, epithelial cell adhesion molecule, and folate receptor α‎. Antibodies in the second class target proteins such as CTLA-4 and PD1 that act as immune response checkpoint receptors. The third class of antibodies target secreted factors that promote tumor growth: targets in this class include vascular endothelial growth factor, cytokines, and chemokines. The development of each of these is described. The chapter also discusses the complications presented by soluble antigens, which serve to limit the applicability of antigens (such as MUC16/CA125) that are both cell-surface associated and circulating and the prospects for the combination of antibody-based immunotherapy and chemotherapy.

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16

Abe, Hiroyuki, Amane Sasada, Shigeki Tabata, and Minako Abe. Heat Shock Protein Vaccine Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0009.

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Despite advances in chemotherapeutic regimens, ovarian cancer has a poor prognosis. Therefore important effective treatments are urgently needed. Many studies have reported that the immune system plays a critical role in disease progression and overall survival. One known effective immunotherapy is the dendritic cell (DC)-based vaccine pulsed with tumor-associated antigens. This chapter reports on a method of production of a novel DC-based vaccine. The key technologies are (a) monocyte collection without leukapheresis, (b) monocyte expansion, (c) production of dendritic cells, (d) multiple overlapping long peptides with heat shock protein 70, and (e) combination immunotherapy approach. The next generation of immunotherapy for ovarian cancer will be focused on combination approaches that simultaneously augment immunity while preventing local immune suppression. Possible combinations which might be useful to help patients with ovarian cancer are summarized in this chapter.

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17

Moerdler, Scott, and Xingxing Zang. PD-1/PDL-1 Inhibitors as Immunotherapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0010.

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Programmed death 1 (PD-1), a member of the B7-CD28 immunoglobulin superfamily, and its ligands PD-L1/PD-L2 inhibit T-cell activation. They also play a key role in the tumor microenvironment, allowing for cancer immune escape. PD-1 is induced on a variety of immune cells, including tumor-infiltrating lymphocytes (TILs), while PD-L1 is found on many types of solid tumors including ovarian cancer and some TILs. The use of immunocheckpoint inhibitors like anti-PD-1 and anti-PD-L1 therapies has been shown to reactivate the immune system to attack tumor cells. Ovarian cancers have been shown to be responsive to anti-PD-1 and anti-PD-L1 therapies, though immunocheckpoint inhibitors are not enough. Current research is evaluating combination therapies to improve response rates.

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18

Ajithkumar, Thankamma, Ann Barrett, Helen Hatcher, and Natalie Cook. Clinical management of cancer: flowcharts. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235636.003.0021.

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Bladder cancer 670Breast cancer 671Cervical cancer 672Colon cancer 673Endometrial cancer 674Epithelial ovarian cancer 675Hepatocellular cancer 676Small-cell lung cancer 677Non-small cell lung cancer 678Oesophageal cancer 679Pancreatic cancer 680Prostate cancer 681Rectal cancer 682Stomach cancer ...

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19

Brinton, Louise A., Mia M. Gaudet, and 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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20

Shrestha, Prashanta, and Masahiko Mori. Tenascin: Expression and Functional Role in Cellular Growth and Adhesion-Implications in Cancer Cell Invasion and Metastasis (Molecular Biology Intelligence Unit). R G Landes Co, 1997.

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21

Josephs, Debra H., Heather J. Bax, Giulia Pellizzari, James F. Spicer, Ana Montes, and 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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22

Bagrodia, Aditya, and Yair Lotan. Low and intermediate risk non-muscle-invasive bladder cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0076.

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Bladder cancer is a common disease that affects more males than females. Most bladder tumours are histologically typed as urothelial cell carcinoma, and these are best divided into cancers invading the muscularis propria and non-invasive malignancies confined to the bladder. The latter are the majority of cancers and include low risk, indolent cancers that may recur within the bladder but not progress to invasion or metastases, and a proportion that subsequently progress to muscle invasion. The risk of intravesical recurrence or progression to invasion from a non-invasive bladder cancer can be stratified as low, intermediate, and high using various pathological factors (such as tumour grade, stage, size, multiplicity, and the presence of carcinoma in situ). In this chapter, we will give an overview of bladder cancer and focus upon tumours at low or intermediate risk of developing future progression to invasion.

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23

Bower, Mark, Louise Robinson, and Sarah Cox. Endocrine and metabolic complications of advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0142.

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Cancer produces endocrine and metabolic complications in two ways. Firstly, the primary tumour or its metastases may interfere with the function of endocrine glands, kidneys, or liver by invasion or obstruction. Secondly, tumours may give rise to remote effects without local spread and these actions are termed paraneoplastic manifestations of malignancy. Generally, these paraneoplastic syndromes arise from secretion by tumours of hormones, cytokines, and growth factors, but also occur when normal cells secrete products in response to the presence of tumour. This chapter reviews the pathogenesis, epidemiology, and management of the commonest paraneoplastic endocrinopathies including hypercalcaemia, Cushing’s syndrome, the syndrome of inappropriate antidiuresis, non-islet cell tumour hypoglycaemia, enteropancreatic hormone syndromes, Carcinoid syndrome, phaeochromocytoma, gonadotrophin secretion syndromes, prolactin and oxytocin secretion, and paraneoplastic pyrexia. The chapter concludes with a brief discussion of the management of metabolic disease in the context of advanced malignancy including hyperglycaemia, thyroid dysfunction, metabolic bone disease, renal failure, liver failure, and lactic acidosis.

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24

Woolf, Eric C., and Adrienne C. Scheck. Ketogenic Diet as Adjunctive Therapy for Malignant Brain Cancer. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0013.

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Malignant brain tumors are devastating, and increased survival requires new therapeutic modalities. Metabolic dysregulation results in an increased need for glucose in tumor cells, suggesting that reduced tumor growth could be achieved with decreased glucose availability either through pharmacological means or use of a high-fat, low-carbohydrate ketogenic diet (KD). KD provides increased blood ketones to support energy needs of normal tissues and has been shown to reduce tumor growth, angiogenesis, inflammation, peritumoral edema, migration, and invasion. Furthermore, this diet can enhance the activity of radiation and chemotherapy in a mouse model of glioma, thus increasing survival. In vitro studies indicate that increasing ketones in the absence of glucose reduction can also inhibit cell growth and potentiate the effects of radiation. Thus, emerging data provide strong support for the use of KD in the treatment of malignant gliomas and thus far has led to a limited number of clinical trials.

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25

Dean, Michael, and Karobi Moitra. Biology of Neoplasia. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0002.

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The term “cancer” encompasses a large heterogeneous group of diseases that involve uncontrolled cell growth, division, and survival, culminating in local invasion and/or distant metastases. Cancer is fundamentally a genetic disease at the cellular level. Tumors occur because clones of abnormal cells acquire multiple lesions in DNA, nearly always involving mutations, chromosomal rearrangements, and extensive alteration of the epigenome. Up to 10% of cancers also involve inherited germline mutations that are moderately to highly penetrant. Cancers begin as localized growths or premalignant lesions that may regress or disappear spontaneously, or progress to a malignant primary tumor. The somatic changes that drive abnormal growth involve activating mutations of specific oncogenes, inactivation of tumor suppressor genes, and/or disruption of epigenetic controls. The latter can result from methylation or the modification of histones and other proteins that affect the remodeling of chromosomes. Numerous non-inherited factors can cause cancer by accelerating these events.

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