Biological Sciences
Cancer
Cancer is a disease characterized by the uncontrolled growth and spread of abnormal cells in the body. These cells can form tumors and interfere with normal bodily functions. Cancer can arise from various factors, including genetic mutations, environmental exposures, and lifestyle choices, and it can affect any part of the body. Treatment options for cancer include surgery, chemotherapy, radiation therapy, and targeted therapies.
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10 Key excerpts on "Cancer"
eBook - PDF- Caterina A. M. La Porta, Stefano Zapperi(Authors)
- 2017(Publication Date)
- Cambridge University Press(Publisher)
2 The Biology of Cancer Cancer results from abnormal cellular growth. It is considered to be benign when localised in situ while it is defined to be malign and metastatic when it is invasive and spreads inside the body through blood or lymphatic vessels. Cancer progres- sion can be interpreted as an evolutionary process, as we discuss in Section 2.1. In spite of the increasing knowledge gained on the molecular mechanisms involved in the deregulation of Cancer cells, such as the identification of many oncogenes and oncosuppressors (discussed in Section 2.2), many open questions still exist about the origin of Cancer cells. In Section 2.3, we introduce a key oncosuppressor gene which is of fundamental importance for Cancer development: P53, also known as the “guardian of the genome.” While important oncogenes and oncosuppressors clearly exist, Cancer involves a multitude of different genes requiring an integrative data-based approach (Section 2.4). Another important issue that is still under investigation is the presence of a sub- population of more aggressive Cancer cells, usually described as Cancer stem cells (Section 2.5) (CSCs). The molecular aspects related to the capability of Cancer cells to receive nutrients from the environment through existing vessels, and the ability of the same Cancer cells to induce vessel formation (angiogenesis), are two critical aspects of the biology of Cancer that we illustrate in Section 2.6. Further- more, in Section 2.7, we illustrate the spread of Cancer cells inside the body in the metastatic process. All together these aspects will be discussed here, combining biological and physical viewpoints. In this perspective, the Cancer ecosystem is the combination of physical forces and biochemical ingredients. Finally, the new diag- nostic tools for the identification of a Cancer cell are also discussed and critically reviewed (Section 2.8).
eBook - ePubBiomaterials for Cancer Therapeutics
Diagnosis, Prevention and Therapy
- Kinam Park(Author)
- 2013(Publication Date)
- Woodhead Publishing(Publisher)
2Cancer cell biology
R. Mrsny, University of Bath, UKAbstract:
Cancer remains the most challenging of diseases to treat for a variety of reasons. While Cancer cells are derived from normal cells of the body, and thus would not normally be considered dangerous, their unregulated growth and dissemination to multiple vital organs provide these cells with the ability to induce significant morbidity and ultimately mortality. Challenges to successfully treat Cancer cells include the fact that they utilize endogenous mechanisms of cell growth and division, and that they are genetically unique to each patient and to each form of Cancer. In order to identify successful pharmacotherapies to selectively target and treat Cancer cells, an improved understanding of cellular processes involving oncogenesis as well as Cancer cell growth and metastasis must be obtained.Key words Cancer cell biology genetic drivers of Cancer environmental factors affecting Cancer2.1 Introduction
Cancer is a poorly defined term used to describe a hugely diverse set of cellular modifications that result in uncontrolled cell growth and their aberrant distribution in the body. Traditionally, strategies to treat a particular type of Cancer have been based upon the tissue and cell type of its origin. With the advent of personalized medicine and an improved ability to examine genetic and biological changes that occur when cells become Cancerous, it has become clear that no two Cancers are identical and that these traditional groupings and the associated approved therapies may not necessarily lead to an effective outcome. While many valid generalizations are made every day by oncologists when dealing with patients with a particular type of Cancer, effective Cancer treatments for many patients are still not available. The goal of this chapter is to highlight the disparate nature of cells that are commonly termed Cancerous and to examine some cellular processes that may more accurately define these cells. It is hoped that with a sufficient appreciation of cell biology events that affect and control Cancer cells, Cancer will one day be treated as a chronic or transient condition rather than a death sentence. Each section of this chapter highlights Cancer cell biology aspects that can affect the potential for such treatments.
eBook - PDFAdvances in Nuclear Oncology
Diagnosis and Therapy
- Emilio Bombardieri, John Buscombe, Giovanni Lucignani, Otmar Schober, Emilio Bombardieri, John Buscombe, Giovanni Lucignani, Otmar Schober(Authors)
- 2007(Publication Date)
- CRC Press(Publisher)
1 What is Cancer? Uwe Haberkorn At first sight Cancer is a disease induced by the failure of control mechanisms. The Cancer cell does not respond to control signals because of damage to its DNA, the presence of oncogene products, or because the homeostatic control mechanisms themselves are disturbed. Biologically this corresponds to uncontrolled proliferation occurring at the wrong place and time driven by oncogenic signals, impaired differentiation, and invasion of other tissues lead-ing to metastases. In a recent review, Hanahan and Weinberg mentioned six essential alterations in cell physiology which are seen as the hallmarks of Cancer: self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of programmed cell death (apoptosis), limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. These alterations are interpreted as results of genetic changes in the Cancer cell. However, mutations in the tumor genome may not be the only cause. 1 Genetic and epigenetic background Cancer has been viewed as a multistep process of genetic alterations that result in the transformation of benign cells into malignant ones. These genetic abnormalities include mutations in tumor-suppressor genes and oncogenes, and chromosomal abnormalities such as chromosomal gain, loss, and/or rearrangement (Table 1.1). 1,2 Such events are thought to be followed by a clonal selection of variant cells that show increasingly aggressive behavior. 3 Although it is still commonly thought that aneuploidy occurs as a late-stage effect rather than as a cause of Cancer development, this might not always be true, as carcinogens such as asbestos and arsenic initially do not cause gene mutations, but rather lead to aneuploid lesions. Further-more, normal cells exposed to chemical carcinogens can become aneuploid long before they show signs of being Cancerous.
eBook - PDF- John Roboz(Author)
- 2002(Publication Date)
- CRC Press(Publisher)
81 Relevant Concepts of Cancer Medicine and Biology 3.1 CLASSIFICATION AND EPIDEMIOLOGY The words tumor (Latin, tumere = to swell) and neoplasm (neo = new, plasma = formation) are used synonymously to describe abnormal tissues characterized by unregulated cellular growth to form a mass without a defined structure. The pathologic process that results in the formation and growth of neoplasms is called neoplasia. Cancer (Latin, for crab) is a general term used to describe any of various types of malignant neoplasms causing over 200 diseases of multicellular organisms. Cancers share several characteristics, including that they originate from mutant, genetically dys- functional cells; they escape normal growth controls; and they invade and colonize normal tissues. On its way to becoming a full-fledged malignant tumor, a nascent neoplastic clone must prevail through a remarkable series of events and must undertake a number of exceptional maneuvers. These include bypassing programmed cell death, circumventing growth restraining signals, growing without growth factors from other cells, evading immunological surveillance, appropriating a vascular supply, burrowing into surrounding tissues, traversing blood or lymph vessels to travel to distant sites, recognizing an appropriate environment for crossing out of the vessels, and finally establishing secondary tumors. Only about 0.1% of the breakaway cells survive after entering the circulation, and most of those are captured in the first capillary bed encountered. In the specific case of cells in the lymph system, those cells arrested in the subcapsular sinuses of the lymph nodes may begin to grow. Other lymph borne-malignant cells may enter the blood vascular system via the lymphatic interconnections in the venous system. 3.1.1 S OLID T UMORS All solid neoplasms have a parenchyma that comprises the neoplastic proliferating cells and a stroma that consists of the supporting connective tissue and blood supply required for growth.
eBook - PDF- Kathleen A. Ireland(Author)
- 2018(Publication Date)
- Wiley(Publisher)
Only a scant few mistakes creep through. Despite the fact that a few of these cells become Cancerous, due to our incredibly adept immune surveillance system, barely one-third of us will develop Cancer in our lifetimes. Cancer is not a single disease. Actually, more than 100 specific diseases are lumped together under the term Cancer. Each form of Cancer requires a specific form of treatment. As we learn more about various Cancers, we are continually refining treatment regimens, to the point where each individual’s treatment regimen is truly a “per- sonal” plan designed to fight a personal Cancer. Medicine has moved beyond the three pillars of previous Cancer therapy—surgery, che- motherapy, and radiation—to embrace such techniques as immuno- therapy, anti-hormone therapy, and genetic and molecular therapy, in an effort to fight Cancerous cells more precisely. The more we learn about the genetic component of Cancer, the closer we come to being able to treat Cancers before they occur by replacing defective genes. Cancer Cells Have Certain Characteristics Cancer describes a series of diseases that all have common charac- teristics. The most striking of these is that Cancer cells lose control over their own growth. Unlike normal cells, Cancer cells either disre- gard or don’t receive the chemical signals that tell them it is time to stop dividing and die. They break away from nearby cells and begin a cycle of uncontrolled, often rapid division and replication. In general terms, Cancer can be defined as uncontrolled cell replication that occurs because of a breakdown in the normal mechanisms of cell regulation. Along with this lack of growth control, all Cancers have other common characteristics: • Cancer cells lack differentiation. A Cancer cell is not differenti- ated, meaning that it has no specified function and therefore can make no contribution to the overall functioning of a particular body part.
- Narayan S Hosmane, John A Maguire, Yinghuai Zhu(Authors)
- 2012(Publication Date)
- World Scientific(Publisher)
Chapter What Is Cancer? 2.1. Historical Background Everyone is linked to Cancer in some manner, whether it is through their own personal experiences and battles, having a family history of the disease, or having observed a friend struggle through the process. The word “Cancer” is a general term that is used in reference to over 100 different dis-eases. In 2008, there were about 8 million deaths worldwide attributed to Cancer and it is estimated that the number will rise to approximately 12 mil-lion by 2030. Normal cells in the body grow, divide, and die. Cancerous cells, however, result when cells begin to grow out of control; they become “immortal.” Normal cells become Cancerous due to mutations caused by damage/change in DNA. This happens more often than one would realize; it is estimated that in human cells the average number of DNA damages per person is about 800/hr. The DNA repair enzymes remove most DNA dam-ages, but unfortunately these enzymes are not 100% effective. Some genes control critical cell functions such as cell growth or programmed cell death (apoptosis); these are called proto-oncogenes. When these are altered by mutation, they can give rise to oncogenes that can lead to Cancer. In the case of Cancer, the damaged DNA is not properly repaired; the cell is allowed to generate with its abnormalities existing. The abnormal cells then continue to replicate, passing its damaged DNA code onto its daughter cells. While the damaged DNA that can result in Cancer is sometimes inher-ited, in many cases, the resulting abnormal cells are due to the environment and lifestyle choices. For instance, cigarette smoking increases the risk of 7 2 abnormal cell growth in the lungs. Cancerous tissue can form in any region of the body. In most cases, a solid tumor (mass of cells) is formed. The out-of-control growth of Cancerous cells poses many threats.
eBook - PDF- Janice Gabriel(Author)
- 2006(Publication Date)
- Wiley(Publisher)
JAG 1 P ART I UNDERSTANDING Cancer 3 CHAPTER 1 What is Cancer? JANICE GABRIEL Cancer is not just one disease, but a generic term used to encompass a group of more than 200 diseases sharing common characteristics. Cancers (carcinomas) are characterized by their unregulated growth and spread of cells to other parts of the body (LeMarbre and Greon- wald, 2000). Management of an individual diagnosed with Cancer is dependent not only on which type of malignancy they have, but also on the extent of its spread, together with its sensitivity to treatment (Gabriel, 2001). It is estimated that one in three people in the United Kingdom will develop a malignancy by the time they reach the age of 70, with the incidence increasing with age. This means that about 270 000 individuals receive a Cancer diagnosis each year in the UK, with more than 7.5 million affected worldwide (Cornwell, 1997; DoH, 2000a; Corner, 2001). Sadly, the UK incidence of Cancer is expected to increase by 2025 (Cornwell, 1997). This chapter attempts to provide a clearer understanding of what Cancers are, and how they spread (metastasize) throughout the body (British Medical Association (BMA), 1997; O’Mary, 2000). It also looks at the importance of staging an individual’s disease before determining their most appropriate management (DoH, 2000a, 2000b). The definition of Cancer As humans we are made up of many millions of cells. Some cells are specific to certain tissues, e.g. epithelial cells are found throughout the gastrointestinal tract, bladder, lungs, vagina, breast and skin. It is this group of cells that accounts for about 70% of Cancers (Venitt, 1978; Corner, 2001). However, any cell has the potential to undergo malignant changes and lead to the development of a carcinoma. The ‘tumour’ cells are not only confined to localized ‘overgrowth’ and infiltration of surrounding tissue, but can also spread to other parts of the body via
eBook - PDF- Cecie Starr, Beverly McMillan(Authors)
- 2015(Publication Date)
- Cengage Learning EMEA(Publisher)
Intensive research is rapidly increasing our understanding of the causes of many kinds of Cancer. As you’ll read in this chapter, today most Cancers are treatable, and many are curable if the disease is caught early. 425 GENES AND DISEASE: Cancer 22 Science Source Copyright 2016 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 426 CHAPTER 22 n As genes switch on and off, they determine when and how fast the cell will grow and divide, when it will stop dividing, and even when it will die. Cancer can result when controls over cell division are lost. n Links to Cell structure 3.2, Cell differentiation 17.1, Mutations in DNA 21.2 Some tumors are Cancer, others are not If cells in a tissue overgrow—an abnormal enlargement called hyperplasia —the result is a defined mass of tissue called a tumor . Technically, a tumor is a neoplasm , which means “new growth.” A tumor may not be “Cancer.” As Figure 22.1A shows, the cells of a benign tumor are often enclosed by a capsule of connective tissue, and inside the capsule they are organized in an orderly way. They also tend to grow slowly and to be well differentiated (structurally specialized for a particular func-tion), much like normal cells of the same tissue (Section 17.1). Benign tumors usually stay put in the body, push aside but don’t invade surrounding tissue, and generally can be easily removed by surgery. Benign tumors can threaten health, as when they occur in the brain. Nearly every-one has at least several of the benign tumors we call moles. Most of us also have or have had some other type of benign neoplasm, such as a cyst.
eBook - PDF- Stella Pelengaris, Michael Khan, Stella Pelengaris, Michael Khan(Authors)
- 2009(Publication Date)
- Wiley-Blackwell(Publisher)
• Expression profiling of tumors (as exemplified by the “poor prognosis signature” defined by van’t Veer and colleagues) may enable more accurate diagnosis/prognosis of Cancers. As this process is ultimately refined to analyses of single cells, such profiling may address numerous unanswered questions in Cancer biology. This chapter is deliberately aimed to be provoc-ative and stimulating. We will introduce and summarize the concepts and topics to be covered in the book, but with continual emphasis on new thinking and key novel models for oncogenesis. Cancer has been recognized throughout recor-ded history and was known to the ancient Egyptians (see Appendix 1.1, history of Cancer) but it was not until the seventeenth century that the formal study of Cancer (oncology) was first documented. As with much of biology, the last 50 years has witnessed spectacular pro-gress in describing the fundamental molecular basis of Cancer following the advent of molecu-lar biology and genetics. What is still a matter of some concern is that such exponential pro-gress in describing the biology of Cancer has, as yet, not translated into an equally impress-ive progress in the treatment of most common Cancers (see Fig. 1.1). At first glance the bio-logy of Cancer appears straightforward: Cancer cells stop obeying the restraints imposed on cells within the adult organism and instead mul-tiply uncontrollably and in places they should not. However, in order to achieve such inde-pendence Cancer cells must overcome numer-ous intrinsic and extrinsic barriers which seek to prevent such selfish behavior before it can threaten the survival of the entire organism. In this book we will describe the means by which normal cells become Cancer cells and the key cellular processes which are disrup-ted along the way. We will also describe how this basic knowledge has been translated into improved diagnostics and therapeutics for Cancer patients.
eBook - PDFMatters of Life and Death
Perspectives on Public Health, Molecular Biology, Cancer, and the Prospects for the Human Race
- John Cairns(Author)
- 2021(Publication Date)
- Princeton University Press(Publisher)
The response to this continual stream of information allows it to modulate its behavior, partly according to pre-set programs and partly to adjust for any unprogrammed chance events. I have described the control of cell behavior in terms of the signals that pass between cells, but that was not the kind of introduction to can-cer research given in most textbooks in the 1960s. Like the early studies of zoology and botany, or biochemistry and biophysics, Cancer research had produced a huge array of undigested facts. Fifty years ago, textbooks of biochemistry gave a detailed description of intermediary metabolism, but could not say how enzymes worked or how cells knew which en-zymes to make and how to make them. Thirty years ago, textbooks on the microscopic anatomy and pathology of human Cancer could be inches thick, yet tell the reader almost nothing about what underlies the behav-ior of Cancer cells. The experimental study of Cancer had generated its own equally voluminous literature. These days, few people have the time Multicellular Systems and Cancer • 141 to work their way through all this stuff. But I think there are often lessons to be learned from the histories of the various sciences. So I will now give a brief recapitulation of the early days of Cancer research. The History of Cancer Research The first attempts to produce Cancers in animals were based on what little was known about the causes of human Cancers. The Industrial Rev-olution had resulted in large numbers of people being exposed to toxic substances that are not part of the normal human environment, and by the end of the nineteenth century, factory workers who were continually exposed to tars and oils had been observed to develop Cancer in the exposed areas of skin. So it was natural to test the effects of these sub-stances in animals. Most animals, however, have much thicker skins than humans, and the results were negative until the experimenters used rabbits and mice.
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