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Cancer: A Beginner's Guide (Beginner's Guides), by Paul Scotting
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Cancer is the second biggest killer in the world, but few of us understand how it works or how it is treated. In this illuminating introduction, Paul Scotting explains the science behind the disease and explores why some of us are more likely to develop it than others. Arguing that we’re in a new age of understanding that will revolutionize the fight againtst cancer, Scotting maps out the promising future strategies for its prevention, treatment, and cure.
- Sales Rank: #1252070 in eBooks
- Published on: 2012-12-01
- Released on: 2012-12-01
- Format: Kindle eBook
Review
"Easy to read and interesting. I would recommend it to anybody interested in acquiring a general understanding of the disease." --Nick La Thangue, Chair of Cancer Biology, University of Oxford; Fellow of the Academy of Medical Sciences; and Fellow of The Royal Society of Edinburgh
"Great. There is so much interesting information throughout the book. Filled with depth and breadth." --Melinda Irwin, Associate Professor of Epidemiology, Director of the Cancer Survivorship Program, and Co-director of the Cancer Prevention and Control Research Program, Yale Cancer Center, Yale University
About the Author
Paul Scotting is Associate Professor at the Institute of Genetics at the University of Nottingham.
Most helpful customer reviews
10 of 10 people found the following review helpful.
Perhaps the best available "beginner's guide" to cancer
By Irfan A. Alvi
This book by Paul Scotting is perhaps the best available "beginner's guide" to cancer biology and treatment. The book is clearly written, is reasonably short at only about 200 pages, and the price can't be beat. The technical level of the book is managable for general readers comfortable with science, and yet also sophisticated enough to offer new insights to people with biomedical background.
Here are highlights of some important points which probably aren't known to most people:
(1) There are many types of cancer, and the extent to which they're curable with current treatments varies widely.
(2) Generally, many factors contribute to cancer incidence, including genetic predisposition, environmental exposures, obesity, diet, exercise, and other lifestyle factors. A degree of randomness is involved in how these factors affect each individual. Cancers which are strongly genetically determined (eg, retinoblastoma) are relatively rare. Poor diet (eg, cooked red meat, alcohol, and lack of fruits and vegetables) may be substantially responsible for about a third of all cancer cases. Smoking accounts for about 90% of lung cancer, along with contributing to other types of cancer and other diseases. Radiation typically acts as a carcinogen by causing DNA strand breaks, resulting in chromosomal abnormalities. Only one type of bacteria and a few types of viruses are known to contribute to human cancer, but these pathogens are still responsible for a significant percentage of cancer cases.
(3) The evidence indicates that cancer has always been present in animals and humans, but some types of cancer have become much more common in the past few centuries, partly because of people of living longer, and partly because of negative trends in the factors noted above.
(4) The incidence of various types of cancer varies widely between countries, primarily due to the non-genetic factors noted above. In Western countries, the most common types of cancer are breast, lung, colorectal, and prostate.
(5) It often takes about 10 to 30 years for cancer to appear after initial exposure to a carcinogen.
(6) Gene expression and corresponding phenotype of cells is normally greatly influenced by external signals (eg, growth factors). In tumor cells, these signals are often either ignored or responded to abnormally, and the signals that tumor cells send out are likewise abnormal.
(7) Genetic mutations are clearly linked with cancer. However, (although not mentioned in this book) the extent to which these mutations are cause and/or effect is debated. For example, the dominant somatic mutation theory (SMT) of carcinogenesis argues that mutations are the primary cause of cancer. By contrast, the tissue organization field theory (TOFT) argues that abnormal signaling at the tissue level, especially related to control of proliferation, is primarily responsible for carcinogenesis, with mutations following as an effect.
(8) If the SMT is accepted, it's estimated that several mutations are typically required to produce a tumor cell (with fewer mutations typically corresponding to benign tumors). Mutations in DNA repair genes are nearly universal, and result in genetic instability and a mutator phenotype. Therefore, as a tumor progresses, many additional mutations tend to develop, including extensive chromosomal abnormalities.
(9) The vast majority of cancer deaths are due to carcinomas, which arise from epithelial tissues.
(10) Only about 1% to 3% of our genome codes for proteins, which means that most mutations don't contribute to cancer or other problems. Also, over 90% of tumors show telomerase activity.
(11) Apoptosis is a relatively "clean" cell death process which doesn't promote inflammation, whereas necrosis does promote inflammation. Inflammation in turn inhibits cell death and promotes cell division, and thus may significantly contribute to many types of cancer.
(12) Decreased cell adhesion is a factor contributing to tumor invasion and metastasis.
(13) The probability that a given tumor cell will complete the metastatic process is very low, but having a typically large number of tumor cells makes it likely that metastasis will occur, often at multiple sites.
(14) There are many commonalities between developmental biology and cancer biology, such as similar transcription factors involved in cell motility.
(15) It appears that the immune system is very effective in eliminating most microtumors, but not all of them, so cancer still commonly occurs.
(16) Though childhood cancers are much less common than adult cancers, cancer is still the most common cause of mortality among children. Childhood cancers often appear during the first three years of life, with incidence tapering off with greater age. Childhood cancers usually are biologically different from adult cancers, and tend to be simpler than adult cancers in terms of their genetic damage (and are thus more commonly curable). Leukemias are the most common childhood cancers and are associated with chromosomal abnormalities rather than DNA mutations. Scotting suggests (I think plausibly) that occurence of childhood cancers may be related mainly to higher rates of cell division and/or more intense growth signaling during embryonic and early childhood development, rather than exposure to environmental carcinogens.
(17) "From the earliest times, it has been recognized that the best way to deal with cancer is to catch it early and hit it hard." This is because such tumors (or "precancers") have less tumor cells to eliminate, are biologically simpler, are less heterogeneous, and are less likely to have invaded or metastasized.
(18) Radiotherapy and cytotoxic chemotherapy are usually mutagenic, so they can have at least three adverse effects with respect to malignancy: (a) contributing to development of secondary cancers, (b) selecting for tumor cells which are inherently resistant to treatment, and (c) adding mutations to existing cancers which make these cancers more aggressive. A double-edged sword indeed.
1 of 1 people found the following review helpful.
HIGHLY RECOMMENDED READ
By BLUE FISH
This is a gem of a book, its has in depth information explaining in detail how cancer has evolved and why, how our genes work and grow and what happens when they go wrong, causing the initiation of cancer, how in women HRT and the contraception pill can increase the risk of cancer.
Provides in depth information about skin cancer and sunlight and how since people now live longer into their 70/80s cancer has time to grow.
0 of 0 people found the following review helpful.
Beginner's Guide
By patricia king
This is a very good basic introduction to understanding cancer.
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