Biological Sciences
Cancer Cells
Cancer cells are abnormal cells that divide uncontrollably and can invade other tissues. They differ from normal cells in their ability to ignore signals that regulate cell growth and death. These cells can form tumors and spread to other parts of the body, leading to the development of cancer.
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7 Key excerpts on "Cancer Cells"
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Index pages curate the most relevant extracts from our library of academic textbooks. They’ve been created using an in-house natural language model (NLM), each adding context and meaning to key research topics.
eBook - ePub- John E. Niederhuber, James O. Armitage, James H Doroshow, Michael B. Kastan, Joel E. Tepper(Authors)
- 2019(Publication Date)
- Elsevier(Publisher)
- • Our understanding and treatment of cancer have always relied heavily on parallel developments in biologic research. Molecular biology provides the basic tools to study genes involved with cancer growth patterns and tumor suppression. An advanced understanding of the molecular processes governing cell growth and differentiation has revolutionized the diagnosis, prognosis, and treatment of malignant disorders.
- • This introductory chapter relates basic principles of molecular biology to emerging perspectives on the origin and progression of cancer and explains newly developed laboratory techniques, including whole-genome analysis, expression profiling, and refined genetic manipulation in and use of genetically diverse animal models, providing the conceptual and technical background necessary to grasp the central principles and new methods of current cancer research.
Since the last edition of this book was published, advances in our understanding of the basic mechanisms of cancer have continued to inform and refine clinical approaches to prevention and therapy. New prognostic and predictive markers derived from molecular biology can now pinpoint specific genetic changes in particular tumors or detect occult malignant cells in normal tissues, leading to improved technologies for tumor screening and early detection. Diagnostic approaches have expanded from morphologic criteria and single-gene analysis to whole-genome technologies and single-cell genomics imported from other biologic disciplines. A new systemic vision of cancer is emerging, in which the importance of individual mutation has been superseded by an appreciation for higher-order organization and individual genetic background, disrupted by complex interactions of disease-associated factors and gene-environmental parameters that affect tumor cell behavior. Results from these cross-disciplinary investigations underscore the complexity of carcinogenesis and have profoundly influenced the design of strategies for both cancer prevention and advanced cancer therapy.
eBook - ePub- Charles A. Kelsey, Philip H. Heintz, Gregory D. Chambers, Daniel J. Sandoval, Natalie L. Adolphi, Kimberly S. Paffett(Authors)
- 2013(Publication Date)
- Wiley-Blackwell(Publisher)
Another trait common to normal cells is the ability to maintain their differentiation. That is, cells always retain their specialty categories whether they are designed for structural support, filtration, protein production, or whatever. This is the way tissues and organs normally function.Cancer Cells and Their Characteristics
Cancer is a collection of diseases characterized by cells with uncontrolled growth and the ability to spread throughout the body. The name “cancer” comes from ancient physicians who noted that cancers removed from the body had crab-like extensions from the main body of the cancer. Figure 8.2 shows an example of a cancer cell.Figure 8.2Example of extensions from a breast cancer. From a scanning electron microscope image from the National Cancer Institute.Normal cell growth is strictly regulated and controlled. In Cancer Cells, this control is lost. The cause of cancer is believed to be a series of mutations in cellular DNA. There is strong evidence that each cell in the human body experiences more than 100,000 DNA breaks every day. The vast majority are correctly repaired or sent to apoptosis. Only a tiny fraction of these DNA lesions are repaired incorrectly and survive. Only a small fraction of the surviving lesions are in genes related to cellular repair. Mutations in the cell repair mechanisms are unusually devastating because the repair mechanism is designed to stop mutations.Damage to the DNA is extremely common and the repair mechanisms are very effective in correcting mistakes in DNA replication. However, given the high frequency of lesions per day in each cell, mistakes in repair are inevitable. Some mutated cells may be able to bypass the cell cycle checkpoints and survive. Most survivors die within a few reproductive cycles but Darwin's law comes into play and a few of these survive.Cancer Cells result from a failure of the delicate balance system between growth and antigrowth signals. Almost all Cancer Cells have at least nine major differences from normal cells. The major difference between benign and cancerous tumors is that cancers spread throughout the body.
eBook - ePubUnderstanding Cancer
An Introduction to the Biology, Medicine, and Societal Implications of this Disease
- J. Richard McIntosh(Author)
- 2019(Publication Date)
- Garland Science(Publisher)
Cell reproduction is under tight control. The number of cell divisions in each adult tissue matches the number of cell deaths and/or losses, thereby maintaining a healthy tissue. The transformation of a cell from normal to cancerous begins when that cell loses proper growth control, so it divides when it should not. Progression from this initial event into a dangerous cancer involves additional changes in cell behavior: first a loss in the ability to differentiate, then a loss in the fidelity of gene transmissions from one cell generation to the next, and finally a loss of the ability to stay attached to neighboring cells. These changes result in cells that can wander through the body, forming unwanted growths at sites distant from the original site of excess growth. This behavior, called metastasis, is at the heart of what can make cancer both lethal and difficult to treat.Cancer diagnosis is commonly achieved by noticing a growth of cells where they don’t belong, either through tactile detection of a lump or visualization of an inappropriate growth. Cancer can then be treated, either by cutting out the unwanted cells or by killing them. The latter can be achieved by exposing the Cancer Cells to radiation or to chemicals that interfere with their growth and induce them to die. However, none of these treatments is entirely satisfactory because they damage a body’s healthy cells as well as the cancerous ones. Modern medical scientists are working to find treatments that are truly specific for Cancer Cells, but this task is difficult for at least two reasons: (1) Cancer Cells are derived from our own cells by mutation, so even though they have lost normal control, they are still quite similar to normal cells, making it difficult to find treatments that are cancer cell specific; and (2) Cancer Cells are genetically unstable, so they can change from one cell generation to the next. A treatment that kills unwanted growths one day may not work only a little while later. For these reasons, cancer is a hard disease to cure, and it will probably be many years before modern medicine is really in control of the cancer problem.ESSENTIAL CONCEPTS
• A cell is the minimum unit of life. Each cell is able to take in food, which provides materials and energy for the synthesis of the molecules it needs to grow, divide, and form two daughter cells.•
eBook - ePub- Nessar Ahmed, Maureen Dawson, Chris Smith, Ed Wood(Authors)
- 2007(Publication Date)
- Taylor & Francis(Publisher)
Cancer Cells fail to respond to the usual controling signals and their growth becomes unregulated. Indeed, the name cancer comes from a Latin word meaning ‘a crab’, and describes the manner in which the pattern of penetration into normal tissues by the abnormal growth bears a superficial resemblance to a crab’s claw. These abnormal cells may invade nearby tissues and may enter the blood and lymph systems and spread to remoter areas. Figure 17.1 Some intrinsic and extrinsic factors that influence cell division. Today, the term cancer is used popularly to describe what is known as a malignant tumor. Oncology, derived from the Greek word oncos, a lump, is the branch of medicine involved with the study of the development of tumors, their epidemiology, diagnosis and treatment. A tumor is an abnormal mass of cells that may be benign or malignant. Benign tumors generally grow slowly and do not spread to other tissues, though they may continue to grow in situ. Such tumors are only harmful if they interfere with the normal function of a tissue, or if they cause pressure by growing within a confined space, such as in the brain. A malignant tumor is one that spreads from its initial site, where it is known as the primary tumor, through the blood and lymph to establish secondary tumors in other organs. Such movement from the primary tumor and the formation of secondary tumors is known as metastasis. A term that is often used in the context of cancer is neoplasm. This means, literally, a new tumor or new mass, but is generally used to describe a cancer. The causes of cancer are complex and varied. Some arise from environmental agents called carcinogens, others are brought about by oncogenic, that is cancer-inducing, viruses. Most cancers arise, ultimately, from mutations in DNA
eBook - ePub- Jeffrey S. Tobias, Daniel Hochhauser(Authors)
- 2013(Publication Date)
- Wiley-Blackwell(Publisher)
Cancer Cells are not fully responsive to the normal constraints in the parent tissue. The restriction point in the cell cycle marks the point at which cells are irreversibly committed to proceeding with DNA replication. This depends on the presence of exogenous nutrients and growth factors in normal cycling cells. An important property of Cancer Cells is their ability to continue the cell cycle in the presence of nutrient deprivation. Additionally, cancers always show a degree of anaplasia, which is a failure of the mechanism of cellular differentiation. Critically, cancers have the ability to metastasize, that is the ability to spread from the site of origin to distant tissues.While these features are present in most human cancers, some of these properties are not absolutely distinct from normal tissues. Thus it is true that the normal regulatory mechanisms controlling growth are defective in cancer, but there often remains a check or constraint on the pattern of growth of human neoplasms (see below). Similarly, although we regard the most anaplastic of cancers as ‘undifferentiated’ in the sense that they seem to have arisen from the more primitive precursors of the differentiated tissue, many cancers nonetheless do retain some of the functions of the mature tissues. Metastasis, however, is a property unique to cancer. Furthermore, it is metastasis which in most instances kills the patient, and understanding the biology of metastasis is one of the central problems of cancer research.The following section is concerned with the events that follow the carcinogenic event and which lead to the development of an invasive, metastasizing malignancy.Monoclonality and heterogeneity in cancer
It is probable that most human neoplasms are monoclonal in origin. This means that the original oncogenic events affected a single cell and that the tumour is the result of growth from that one cell. There are two major lines of evidence which have led to this conclusion. First, certain women are heterozygotes for two forms of the enzyme glucose 6-phosphate dehydrogenase (G6PD). The gene for the enzyme is carried on the X chromosome and, in female heterozygotes, either the maternal or paternal form is present on either one of the X chromosomes. In a female, each cell loses activity of one or other X chromosome and therefore, in a heterozygote for this enzyme, every cell in the body will have either one form of the enzyme or the other. In studies on haematological malignancies arising in heterozygotes for G6PD, the cancers are found to contain either the maternal or the paternal form of the enzyme, implying that the original cancer arose from one cell which either had one form of the enzyme or the other. In chronic granulocytic leukaemia, the restriction of enzyme expression is found in cells of the granulocyte series and, importantly, in red cells and platelets as well, implying that a stem cell is affected by the malignant process.
eBook - ePubComputational Immunology
Basics
- Shyamasree Ghosh(Author)
- 2019(Publication Date)
- CRC Press(Publisher)
10Cancer Biology
10.1 INTRODUCTION
The daughter cells of a dividing parent cell that has lost the controlled cell division form a tumour and when they migrate and grow in the other tissues, it is called cancer. Malignant tumours differ from the benign tumours by their growth and evasiveness. Metastatic Cancer Cells secrete matrix metalloproteinases that degrades the extracellular matrix proteins. The malignant cells then migrate by chemotaxis through the blood vessels into different sites of the body giving rise to the secondary tumour. Growth of metastatic cancer is stimulated by adequate blood supply for nutrients and oxygenation and removal of cellular waste through angiogenesis [1 ,2 ]. The hypoxic environment of cancers induces expression of hypoxia-inducible factor-1alpha (HIF-1α) which regulates angiogenic growth factors like vascular endothelial growth factor (VEGF) [1 ,2 ,3 ]. Cytokines, interleukins, and other growth factors contribute to angiogenesis for cancer proliferation [1 ,2 ,3 ].In 2000, Hanahan and Weinberg listed six significant alterations essential for malignant growth (a) self-sufficient growth signals, (b) insensitivity to antigrowth signals, (c) replicative potential, (d) ability to evade apoptosis, sustained angiogenesis, (e) ability to invade the tissues, and (f) metastasis Recent studies have revealed that exploitation of immune mechanisms and evasion of immune surveillance are hallmarks in cancer cell development [138 ].Tumours are classified based on the tissue of their origin. Carcinomas develop from endodermal or ectodermal tissues like skin, glands, as in breast cancer, colon cancer, and lung cancer. The cancers originating in the mesodermal tissue of bone, blood vessels and cartilage are called the sarcomas. Malignant hematopoietic cells give rise to leukemia that originate from myeloid and lymphoid lineages. They are of two types: acute leukaemias originating from less mature cell and chronic leukaemias originating from mature cells in adults. Hematopoietic cells growing as solid tumours lead to lymphomas growing in bone marrow or lymph nodes including Hodgkin’s and non-Hodgkin’s lymphoma. Melanomas arise from darkly pigmented cells, mostly originating in the skin. Neuroblastoma arise from neuroblasts of adrenal medulla, Retinoblastoma, originates in the retina of the eye, nephroblastoma generate in the embryonic kidney cells. Gliomas are cancers of the nerve tissue.
eBook - ePub- William T. Blows(Author)
- 2006(Publication Date)
- Routledge(Publisher)
- Many cells in a tumour are dividing to form different cell lines, i.e. cell colonies all derived from the same parent cell and having the same characteristics.
- The word cancer must only be used in the context of a malignant infiltrative tumour, but never used for tumours that are non-malignant and non-infiltrative.
- Benign tumours are common, the cells are the same as the tissue of origin, they grow slowly by expansion, the tumour is encapsulated and does not produce metastases.
- Malignant tumours are rarer, but more common in the elderly. The cells are different from the tissue of origin, they grow fast by infiltration and metastases and the tumour has no capsule.
References
Blows W. T. (2001) The Biological Basis of Nursing: Clinical Observations, Routledge, London.Blows W. T. (2003) The Biological Basis of Nursing: Mental Health, Routledge, London.King R. J. B. (2000) Cancer Biology (2nd edn), Prentice Hall, London.Kumar V., Cotran R. S. and Robbins S. L. (1997) Basic Pathology (6th edn), W. B. Saunders Company, Philadelphia.Martini F. H. (2004) Fundamentals of Anatomy and Physiology (6th edn), Benjamin Cummings, Pearson Education International, San Francisco.Strachan T. S. and Read A. P. (2001) Human Molecular Genetics
