Offers a broad audience a concise presentation of the most up-to-date knowledge about the biology and treatment of cancer; Full coverage of. Whether you have cancer or know someone who does, this booklet has many ideas about ways . For example, you can donate money, books, or clothing that . PDF Drive is your search engine for PDF files. As of today we . This book summarizes the latest findings about the role of cancer stem cells (CSCs) in cancer.
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Download free books at Causes of cancer (aetiology of cancer) Cancer can be defined as a disease in which a group of abnormal cells grow uncontrollably. We would appreciate hearing from you after you read this book. Drop us a note. We care about you! Annette Bloch. Bloch Cancer Hot Line. One H&R Block Way. Travel of cancer cells from a primary tumor to a site of potential metastasis depends on a series of complex biological steps. Figure The Biology of Cancer.
Leukemic cells, in contrast, fail to undergo terminal differentiation Figure For some cell types, particularly fibroblasts, the availability of serum growth factors is the principal determinant of their proliferative capacity in culture. The Cell: Support Center Support Center. This failure of cancer cells to undergo programmed cell death contributes substantially to tumor development.
He has been instrumental in defining functional interrelationships between the subnuclear organization of regulatory proteins and gene expression and has made seminal contributions to mechanisms that direct transcription factors to each nuclear site that supports activation or suppression.
His recent work has linked fidelity of intranuclear localization of gene regulatory machinery with leukemogenesis and metastasis of breast and prostate cancer. A cancer survivor himself, Dr. Please check your email for instructions on resetting your password. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account.
If the address matches an existing account you will receive an email with instructions to retrieve your username. Skip to Main Content. The Biology and Treatment of Cancer: Understanding Cancer Editor s: Pardee Gary S.
First published: Print ISBN: About this book Offers a broad audience a concise presentation of the most up-to-date knowledge about the biology and treatment of cancer Full coverage of cancer prevention and control Clear, thorough discussion of current and possible future therapies Edited by two of the most eminent and widely recognized scholars of cancer research and therapeutics in the world, with contributions from top researchers and clinicians from across North America.
This book is written with the cancer patient and their families in mind. Malignant carcinomas then arise from the benign adenomas, indicated by invasion of the tumor cells through the basal lamina into underlying connective tissue. The cancer cells then continue to proliferate and spread through the connective tissues of the colon wall. Eventually the cancer cells penetrate the wall of the colon and invade other abdominal organs, such as the bladder or small intestine.
In addition, the cancer cells invade blood and lymphatic vessels, allowing them to metastasize throughout the body. Development of colon carcinomas. A single initially altered cell gives rise to a proliferative cell population, which progresses first to benign adenomas of increasing size and then to malignant carcinoma. The cancer cells invade the underlying connective more Substances that cause cancer , called carcinogens , have been identified both by studies in experimental animals and by epidemiological analysis of cancer frequencies in human populations e.
Since the development of malignancy is a complex multistep process, many factors may affect the likelihood that cancer will develop, and it is overly simplistic to speak of single causes of most cancers.
Nonetheless, many agents, including radiation, chemicals, and viruses, have been found to induce cancer in both experimental animals and humans.
Radiation and many chemical carcinogens Figure These carcinogens are generally referred to as initiating agents, since the induction of mutations in key target genes is thought to be the initial event leading to cancer development.
Some of the initiating agents that contribute to human cancers include solar ultraviolet radiation the major cause of skin cancer , carcinogenic chemicals in tobacco smoke, and aflatoxin a potent liver carcinogen produced by some molds that contaminate improperly stored supplies of peanuts and other grains. The carcinogens in tobacco smoke including benzo a pyrene, dimethylnitrosamine, and nickel compounds are the major identified causes of human cancer.
In total, it is estimated that smoking is responsible for nearly one-third of all cancer deaths—an impressive toll for a single carcinogenic agent. Other carcinogens contribute to cancer development by stimulating cell proliferation, rather than by inducing mutations. Such compounds are referred to as tumor promoters , since the increased cell division they induce is required for the outgrowth of a proliferative cell population during early stages of tumor development. The phorbol esters that stimulate cell proliferation by activating protein kinase C see Figure Their activity was defined by studies of chemical induction of skin tumors in mice Figure Tumorigenesis in this system can be initiated by a single treatment with a mutagenic carcinogen.
Tumors do not develop, however, unless the mice are subsequently treated with a tumor promoter usually a phorbol ester to stimulate proliferation of the mutated cells. Induction of tumors in mouse skin. Tumors are initiated by mutations induced by a carcinogen. Development of a tumor then requires treatment with a tumor promoter to stimulate proliferation of the mutated cells. Hormones, particularly estrogens, are important as tumor promoters in the development of some human cancers.
The proliferation of cells of the uterine endometrium, for example, is stimulated by estrogen , and exposure to excess estrogen significantly increases the likelihood that a woman will develop endometrial cancer. The risk of endometrial cancer is therefore substantially increased by long-term postmenopausal estrogen replacement therapy with high doses of estrogen alone.
Fortunately, this risk is minimized by administration of progesterone to counteract the stimulatory effect of estrogen on endometrial cell proliferation. However, long-term therapy with combinations of estrogen and progesterone may lead to an increased risk of breast cancer.
In addition to chemicals and radiation, some viruses induce cancer both in experimental animals and in humans. These viruses are important not only as causes of human cancer; as discussed later in this chapter, studies of tumor viruses have played a key role in elucidating the molecular events responsible for the development of cancers induced by both viral and nonviral carcinogens.
The uncontrolled growth of cancer cells results from accumulated abnormalities affecting many of the cell regulatory mechanisms that have been discussed in preceding chapters. This relationship is reflected in several aspects of cell behavior that distinguish cancer cells from their normal counterparts. Cancer cells typically display abnormalities in the mechanisms that regulate normal cell proliferation, differentiation, and survival.
Taken together, these characteristic properties of cancer cells provide a description of malignancy at the cellular level. The uncontrolled proliferation of cancer cells in vivo is mimicked by their behavior in cell culture.
A primary distinction between cancer cells and normal cells in culture is that normal cells display density-dependent inhibition of cell proliferation Figure Normal cells proliferate until they reach a finite cell density, which is determined in part by the availability of growth factors added to the culture medium usually in the form of serum.
They then cease proliferating and become quiescent, arrested in the G 0 stage of the cell cycle see Figure The proliferation of most cancer cells, however, is not sensitive to density-dependent inhibition. Rather than responding to the signals that cause normal cells to cease proliferation and enter G 0 , tumor cells generally continue growing to high cell densities in culture, mimicking their uncontrolled proliferation in vivo.
Density-dependent inhibition. Normal cells proliferate in culture until they reach a finite cell density, at which point they become quiescent.
Tumor cells, however, continue to proliferate independent of cell density. A related difference between normal cells and cancer cells is that many cancer cells have reduced requirements for extracellular growth factors.
As discussed in Chapter 13, the proliferation of most cells is controlled, at least in part, by polypeptide growth factors. For some cell types, particularly fibroblasts, the availability of serum growth factors is the principal determinant of their proliferative capacity in culture.
The growth factor requirements of these cells are closely related to the phenomenon of density-dependent inhibition, since the density at which normal fibroblasts become quiescent is proportional to the concentration of serum growth factors in the culture medium. The growth factor requirements of many tumor cells are reduced compared to their normal counterparts, contributing to the unregulated proliferation of tumor cells both in vitro and in vivo.
In some cases, cancer cells produce growth factors that stimulate their own proliferation Figure Such abnormal production of a growth factor by a responsive cell leads to continuous autostimulation of cell division autocrine growth stimulation , and the cancer cells are therefore less dependent on growth factors from other, physiologically normal sources. In other cases, the reduced growth factor dependence of cancer cells results from abnormalities in intracellular signaling systems, such as unregulated activity of growth factor receptors or other proteins e.
Autocrine growth stimulation. A cell produces a growth factor to which it also responds, resulting in continuous stimulation of cell proliferation. Cancer cells are also less stringently regulated than normal cells by cell-cell and cell- matrix interactions. Most cancer cells are less adhesive than normal cells, often as a result of reduced expression of cell surface adhesion molecules.
For example, loss of E-cadherin, the principal adhesion molecule of epithelial cells , is important in the development of carcinomas epithelial cancers. As a result of reduced expression of cell adhesion molecules , cancer cells are comparatively unrestrained by interactions with other cells and tissue components, contributing to the ability of malignant cells to invade and metastasize. The reduced adhesiveness of cancer cells also results in morphological and cytoskeletal alterations: Many tumor cells are rounder than normal, in part because they are less firmly attached to either the extracellular matrix or neighboring cells.
A striking difference in the cell-cell interactions displayed by normal cells and those of cancer cells is illustrated by the phenomenon of contact inhibition Figure Normal fibroblasts migrate across the surface of a culture dish until they make contact with a neighboring cell.
Further cell migration is then inhibited, and normal cells adhere to each other, forming an orderly array of cells on the culture dish surface. Tumor cells, in contrast, continue moving after contact with their neighbors, migrating over adjacent cells, and growing in disordered, multilayered patterns. Not only the movement but also the proliferation of many normal cells is inhibited by cell-cell contact, and cancer cells are characteristically insensitive to such contact inhibition of growth.
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