Authors: Corwin, Elizabeth J.
Title: Handbook of Pathophysiology, 3rd Edition
Copyright 2008 Lippincott Williams & Wilkins
> Table of Contents > Unit I - Fundamental Mechanisms of Health and Disease > Chapter 3 - Cancer
Cancer is the growth of abnormal
Although all cells reproduce during embryogenesis, only certain cells continue to do so after the first few months following an
Rates of Cellular Reproduction
Cells that reproduce go through the cell cycle at some inherent rate. This rate may be increased or decreased. Cells that reproduce slowly, or not at all, spend most of their time in the gap stages (G1 or G0) of interphase. Cells that divide continually
Control of Cellular Reproduction
Cell cycling is controlled by the contributions of a variety of genes that respond to cues on cell crowding, tissue
The following discussion describes the external cues controlling cell growth and provides an example of an important second messenger system. Finally, the two broad categories of genes whose end products ultimately control the cell cycle are presented: the tumor
Hormones and Growth Factors That Control Cellular Reproduction
Various hormones and growth factors may stimulate cells to increase or decrease their rate of reproduction. Epidermal growth factor (EGF), fibroblast growth factor, erythropoietin (EPO, which stimulates red blood cell proliferation), and
Chemicals That Control Cellular Reproduction
Various chemicals may stimulate cells to increase or decrease their rate of reproduction. These chemicals may be released by injured or infected
Physical Cues That Control Cellular Reproduction
Neighboring cells appear to communicate with each other about tissue crowding and tissue type by releasing locally active chemicals, and by passing ions and other small molecules through channels called gap junctions. Normal cells respond to physical and chemical cues put out by a large number of similar cells by
Cytoplasmic Second Messenger System Controlling Cellular Reproduction
The cytoplasmic signal cascade begins after a protein hormone, growth factor, or other chemical binds to a cell membrane receptor and turns on a specific second messenger system. Activated second messenger proteins relay the growth-controlling signal to the
Tumor Suppressor Genes
Several different genes, called
tumor suppressor genes
, control cell cycling by coding for proteins that inhibit cellular growth and reproduction. Tumor suppressor genes are vitally important in all normally functioning cells. As described later, although cancer results from many
Tumor suppressor genes act by producing proteins that slow down or stop the second messenger brigade, including proteins that interfere with the functioning of the stimulatory ras protein. Tumor suppressor genes may also code for proteins that make up surface receptors that bind growth-inhibiting hormones or factors. Other tumor suppressor genes, when activated, stimulate a damaged cell to undergo apoptosis (programmed cell death). Finally, some tumor suppressor genes produce proteins that code for important brakes that act directly on cells about to
The Rb Gene
The RB gene codes for the pRB protein, the master brake of the cell cycle. Without this protein, the cell cycle is constantly in the on mode, and cellular reproduction can occur nonstop. Mutations in this gene have been identified in a variety of human cancers including bone, bladder, small cell lung, and
The P53 Gene
The p53 gene codes for the p53 protein, which normally
are genes found in all cells that, when activated, stimulate a cell to go through the cell cycle, resulting in cellular growth and proliferation. These genes may stimulate cell cycling at all levels, including (1) producing proteins that make up membrane receptors for growth-stimulating hormones and chemicals, (2) increasing the production of second messenger proteins, including the
protein, that transfer growth signals to the nucleus, and (3) producing transcription factors that turn on
The MYC Genes
The MYC genes are a family of proto-oncogenes that code for transcription factor proteins that drive cellular reproduction. In healthy cells, myc genes are activated only in response to growth factors acting on the cell surface. In many types of cancer, however, the myc gene is turned on constantly, even in the absence of growth factors. Cellular proliferation can occur without control when this gene is damaged.
When normal proto-oncogenes become overactive and cause uncontrolled cell division, they are called
, or cancer-
Normal cells differentiate during development. Differentiation means that a given cell becomes specialized in structure and function, and aggregates with similar differentiated cells. For example, some embryonic cells are destined to become cells of the
Differentiation appears to occur from selective suppression of certain genes in some cells, whereas in other cells those same genes are active. Differentiation of each cell and tissue appears to affect differentiation of neighboring cells and tissues. Cells release specific growth factors that initiate or guide differentiation of neighboring cells.
Cell Recognition and Adhesion to Like Cells
Other adhesion molecules exist between cells and the underlying tissue matrix. These connections anchor cells to one location. When normal cells become detached from each other or experience a loosening of their attachment to underlying tissue, they respond by initiating apoptosis, which prohibits cells from floating free of their tissue of origin.
The Cell Clock
Normal human cells reproduce a predictable number of times, after which they stop and become senescent. This predictability implies that cells possess some counting system that
Telomeres, described in
, are the end pieces of chromosomes that shorten with each division. When the telomere length becomes sufficiently short (indicating that it has divided a certain number of times) the cell stops dividing. Putting the brakes on cell division in response to telomere shortening requires that the cell has functioning RB and p53 proteins. Occasionally, a cell continues to divide after the telomere reaches its threshold length; usually these cells soon self-destruct as their chromosomes begin to chaotically fuse and
Cell crowding also results in neighboring cells releasing signals that inhibit the further replication of cells. This is called contact inhibition .
Uncontrolled Cellular Reproduction
Cancer cells do not respond to the normal cues controlling cellular reproduction. Instead, they go through the cell cycle more often than normal, resulting in an overabundance of abnormal cells. Cancer cells spend little time in the gap stages of interphase and are frequently found in the M (mitosis) and S (DNA copying) stages.
Uncontrolled cellular reproduction occurs when cells become independent of normal growth control signals. This characteristic of cancer cells is called
. Autonomy results when cells do not respond to the cues controlling contact inhibition ”for example, growth
When placed in an
experimental setting, cancer cells aggressively grow on top of each other and produce
Anaplasia refers to regression of a differentiated cell to a less differentiated stage. Cancer cells
Because the immune system poorly responds to embryonic antigens, the presence of highly anaplastic cells may interfere with the host's immune response to the tumor and usually indicates a particularly
Loss of the Cell Clock
Many cancer cells secrete an
Nuclear and Cytoplasmic Derangement
Cancer cells often demonstrate multiple derangements of the nucleus, cytoplasmic organelles, and cytoskeleton. The nucleus is frequently enlarged and deformed, with obvious chromosomal breaks, deletions, additions, and translocations. The rate of mitosis is usually increased. In the cytoplasm, intracellular structures show disorganization and changes in
Tumor Cell Markers
Some cancer cells release tumor cell markers, which are specific substances secreted by a tumor into the blood, urine, or spinal fluid of an individual with a particular cancer. Tumor cell markers may be specific antigens present on the cancer cells. Some tumor antigens are similar to fetal antigens and are called oncofetal antigens ( onco refers to cancer). Because fetal antigens often do not provoke an immune response, they may mask the tumor against the host's immune system. Tumor cell markers may even include
Clinical Implications of Tumor Cell Markers
Tumor cell markers are clinically important because they offer a means of identifying certain cancers as well as a cancer's progression before, during, and after treatment. For instance, if a specific tumor cell marker is identified in a patient, it suggests that cancer may exist in the person, and further diagnostic evaluation is necessary. Furthermore, in
Examples of Tumor Cell Markers
Examples of tumor cell markers include:
Alpha-fetoprotein for liver and yolk sac (ovarian and testicular) cancers
Carcinoembryonic antigen for colorectal cancer
Human chorionic gonadotropin (hCG) for many tumors, including choriocarcinoma (usually cancer of the uterus)
Acid phosphatase and prostate-specific antigen (PSA) for prostate cancer
Monoclonal immunoglobulin (one subtype of antibody) for multiple melanoma
CA-125, a protein released from
Although the presence of a tumor cell marker may
Tumor Growth Rate
Each tumor grows at a certain rate dependent on characteristics of both the host and the tumor itself. Important characteristics of the host that affect a tumor's growth rate include the person's age, sex, and overall health and nutritional status. The status of the host's immune system is also important. An individual who is immunosuppressed may be unable to recognize a tumor as foreign, or may be unable to respond to a tumor that he or she recognizes. Certain hormonal states (e.g.,
Important characteristics of a tumor that affect its growth rate include its location in the body and its blood supply. The degree of cellular anaplasia and the presence or absence of tumor growth factors are also important characteristics. Many tumors depend on
Tumor Angiogenesis Factors
Tumor angiogenesis factors are substances secreted by tumor cells that stimulate the development of new blood vessel formation. To survive, all cells require an adequate blood supply for the delivery of
Measuring tumor angiogenesis factors in the blood or urine may allow for early diagnosis of some cancers. Even more exciting are new
Descriptions of Tumor Growth and Spread
Growth and spread of a tumor is often described clinically; some of the different terms used are listed below. Tumor treatment often depends on the grade and stage of the cancer.
Grading: An assessment of the tumor based on the degree of anaplasia it
Staging: A clinical decision concerning the size of a tumor, the degree of local invasion it has produced, and the degree to which it has spread to distant sites in a given individual.
Doubling time: An estimate of the mean amount of time required for the division of the tumor cells. Tumor cells that rapidly divide have a short doubling time.
Tumors may grow only locally, or may spread to distant sites in the process called metastasis . It is the metastasis of tumors that may ultimately lead to death of the individual.
Local Growth of a Tumor
The term cancer refers to the crab-like projections put out by a growing tumor into the local tissue. Tumors spread locally when these crab-like projections injure and kill neighboring cells. Growing tumors injure and kill neighboring cells both by compressing the cells and blocking off their blood supply. Tumor cells also appear to release chemicals or enzymes that destroy the integrity of a neighboring cell's membrane, causing the cell to
Metastasis is the movement of cancer cells from one part of the body to another. Metastasis usually occurs through the spread of cancer cells from the original (primary) site in the blood or lymph to a new, secondary site. The term malignancy refers to the ability of a tumor to metastasize. See page C1 for illustrations.
The Process of Metastasis
Steps involved in the metastasis of a primary tumor to a distant site include detachment, invasion,
Figure 3-1. Tumor detachment, invasion, dissemination, and seeding.
To metastasize, cancer cells must first detach from their primary cluster. Recall that normal cells are linked to neighboring cells and underlying matrix tissue, and thus detach with difficulty. In addition, if a normal cell senses that it has become detached from its neighbors, it undergoes apoptosis. Cancer cells, in contrast, lose adhesion with like cells and the extracellular matrix, allowing for relatively easy detachment. Likewise, a cancer cell may produce chemicals that
To spread to distant sites, detached tumor cells must gain
Dissemination and Seeding
Movement of tumor cells in the blood or lymph is called dissemination. Eventually, and especially if they are traveling in clumps, some tumor cells will get caught in a capillary or lymph network downstream from the primary site. Although many cells may die, a few tumor cells at this new site may survive and begin to seed the area. The more cells that detach from the primary tumor, the more likely it is that at least one will survive the journey and start a new tumor growth elsewhere.
When the secondary site has reached a critical size, the tumor cells will again begin to produce tumor angiogenesis factor and new blood vessel formation will be initiated to support growth of this secondary site.
Progress of a Metastasizing Tumor
Because cancer cells tend to be large, most lodge in the
Figure 3-2. Spread of tumor cells from a primary site to a secondary site. Note: most tumors spread through blood or lymph to the lungs; GI tumors spread in portal flow to the liver; prostate tumors frequently spread to the bone.
The Immune System and Cancer
The presence in the blood of antibodies, T cells, and natural killer (NK) cells produced against specific tumor antigens has been confirmed in individuals with cancer. In addition, individuals who are immunocompromised, including those with AIDS or those taking immunosuppressant drugs, have an increased chance of developing cancer. Potent anti-cancer cytokines, including tumor necrosis factor alpha (TNF±), have been identified that assist the immune system in identifying and destroying cancer cells. All of these findings demonstrate clearly that the immune and inflammatory systems have important roles in fighting and preventing cancer.
Cancer Cell Evasion of the Immune Response
Despite an apparent immune response to tumors, cancer cells are frequently able to evade the immune system. Highly anaplastic cells that primarily express oncofetal antigens are most likely to evade immune detection and are especially malignant. Other cancer cells may demonstrate changes in the expression of the major histocompatibility (MHC) antigens that normally stimulate a cell-mediated immune response, which may also allow cancer cells to evade the immune system. Cancer cells may also survive a host immune response by producing blocking antibodies that capture all host antibodies built against the tumor, allowing the tumor to continue to grow. These and other means by which tumor cells may escape immune recognition or destruction are being investigated. Experiments to boost the immune response to a tumor are also underway.
Cancer Cell Stimulation by the Immune Response
A too robust immune or inflammatory response also has been implicated in the development of cancer. For example, about 25% of cancers appear to be related to chronic infection. Liver cancer often develops after
Conditions of Disease
There are several categories of cancer, and several
Categories of Cancer
Tumors are identified based on the tissue from which they develop. The suffix oma is usually added to the tissue term to identify it as a tumor, either
Lymphoma is a cancer of the lymphatic tissue, including the lymph capillaries, lacteals, spleen, various lymph nodes, and lymph vessels. The thymus and bone marrow may also be affected. Specific lymphomas include Hodgkin lymphoma (cancer of the lymph nodes and spleen, formerly called Hodgkin's disease) and malignant lymphoma.
Sarcoma is a cancer of the connective tissue, including cells found in the muscle and bone.
Glioma is a cancer of the glial (support) cells of the central nervous system.
is a term used to describe abnormal epithelial cells that are as yet confined to a certain area and thus
The Theory of Carcinogenesis
Cancer development is a
The theory of carcinogenesis suggests that in certain individuals, an error in DNA copying may not be noticed, the cell cycle may not stop in time for repair, or the defective cell may not self-destruct. If the DNA error is not identified and corrected, the genetic change becomes a permanent mutation and is passed on to all daughter cells. This step is irreversible and is called cellular initiation. For a cancer to develop from this first, irreversible event, years of additional interactions with the cell by endogenous (internally-produced) and exogenous (environmental) factors that cause additional genetic changes must occur, and all must lead to the production of a cell that proliferates aggressively and without quality control. These additive effects are called promoting events. If the promoting events have significance related to a cell becoming autonomous, they may cause the cell to become cancerous ( Fig. 3-3 ). Factors that promote the acceleration of the cell cycle through stimulation of oncogenic genes and those that allow an abnormal cell to avoid detection by the immune system are most likely to result in a mutated cell becoming carcinogenic.
An uncorrected mutation
A key point in this scenario is that the failure to detect or repair a DNA error is the first step of the cascade. This failure usually occurs in an individual who inherited a mutation in a tumor suppressor gene from one parent and developed a mutation in the other gene later in life, or in an individual who developed, over the course of a lifetime, mutations in both of the genes coding for a particular tumor suppressor,
Effect of Frequent Cell Cycling on Transcription Errors
The more times DNA is
Monoclonal Tumor Development
When a tumor develops, it appears to do so from a mistake passed on from a single cell. This results in a monoclonal tumor from one ancestral cell. This theory is consistent with there being one mutated cell that eventually develops into a cancer.
Promoters of DNA Replication Errors
Although some mistakes in DNA replication occur randomly, certain physical agents, chemicals, and microorganisms are known to cause DNA errors. Such agents include ionizing radiation, ultraviolet radiation,
Certain viruses have been identified that can cause DNA mutations. These viruses may damage the DNA directly by causing a transcription error, or may insert into the host DNA and turn on cellular proliferation. Cancers known to be caused
by a virus include Burkitt's lymphoma, caused by the Epstein-Barr virus, cervical cancer, caused by certain strains of the human papilloma virus, and liver cancer, caused by the hepatitis B virus. Kaposi's sarcoma also may be caused by a virus and occurs especially in those suffering from
As mentioned previously, in addition to directly altering the DNA and causing cancer, viruses and other microorganisms may irritate the cell and cause chronic inflammation. Inflammation associated with the release of pro-inflammatory cytokines may stimulate cellular proliferation and angiogenesis.
Effect of Any Mutating Agent
Any physical, chemical, or viral agent may cause mistakes in DNA replication or destroy proofreading enzymes. The worst-case scenario is that a mutating agent may deactivate a tumor suppressor gene that controls cell
A mutated cell is not a cancerous cell; many years of promoting events must occur before that cell becomes cancerous. It is suggested that various promoting agents may act to cause a mutated cell to become cancerous by accelerating the proliferation of the cell. Some promoters may stimulate cellular proliferation by stimulating oncogenes or increasing surface receptors for growth factors.
Other promoting agents may not cause an actual mutation in the DNA of a gene, but rather may cause a given tumor suppressor gene to be deactivated or silenced. This type of change in the DNA is referred to as an
Examples of promoters include endogenous hormones such as estrogen, certain food
Some mistakes in DNA replication throughout a lifetime are inevitable. However, certain conditions or behaviors, known as risk factors, can increase or decrease the likelihood of a mutation arising and a mutated cell being promoted until it is cancerous.
Risk factors for cancer include exposure to any physical, chemical, or viral substance that is known to be mutagenic, and prolonged exposure to any promoter. Mutagens may be inhaled or eaten, or may act on the skin, such as in the case of ultraviolet (UV) radiation.
Behavioral Risk Factors
Certain behaviors increase the likelihood that an individual will be frequently exposed to cancer-causing stimuli. Behavioral risk factors
Other behavioral risk factors include those associated with sexual behavior. A high number of sexual
Hormonal Risk Factors
Estrogen may act as a promoter for certain cancers, such as breast and endometrial cancer. Because estrogen levels are high in menstruating women, the risk for developing breast cancer is increased in women who started menstruating early and reached menopause late. Delayed childbearing or choosing not to bear children increases the risk of breast cancer. This increased risk appears to be related to many years of uninterrupted exposure to estrogen. Estrogen replacement therapy in postmenopausal women appears to be associated with an increase in the risk of breast cancer.
Inherited Risk Factors
A family history of cancer, especially clustered as one type, is a risk factor for developing cancer. Genetic tendencies for carcinogenesis may involve fragile or mutated tumor suppressor genes, susceptibility to certain mutagens or promoters, faulty proofreading enzymes, or a poorly functioning immune system. Inherited defects in the p53 gene and the RB gene have been documented to be associated with a high risk of cancer. Certain cancers have a higher tendency to run in families than others. For example, although most cases of colon cancer arise spontaneously, some families carry mutations that increase the risk of this disease.
Likewise, although most cases of breast cancer arise without any clear genetic link, inheritable breast cancer accounts for approximately 5% to 19% of all breast cancers. There have been two genes identified that increase a
Pediatric cancers likely have a genetic component. In children, the development of cancer is accelerated from several decades to only one or two decades. Acceleration may occur if a child inherits in the germ line (egg or sperm) one defective gene controlling a tumor suppressor or proto-oncogene product or develops such a mutation early in embryogenesis. Later, a second gene error would cause early cancer growth. Similarly, inheriting defective genes for proofreading enzymes would increase the risk of early cancer development.
It is likely that each of us has a certain genetic tendency toward developing cancer, which results in a small percentage of individuals developing cancer without exposure to known mutagens or promoters, whereas others with long-term exposures will
Factors That are Protective Against Cancer Development
Studies suggest that women who breastfeed for at least 6 consecutive months have a reduced risk of developing breast cancer. In addition, women who have had multiple pregnancies have a reduced risk of breast cancer. These findings may relate to the decreased number of menstrual periods
There is also a reduced risk of breast cancer in women who exercise even moderately. This finding may be related to reduced estrogen levels or to a decrease in fat consumption and obesity.
Dietary factors are important in reducing cancer risk. Diets rich in substances known to scavenge or remove dangerous free radicals, called free-
Cancers may be diagnosed in routine examinations before any clinical manifestations appear. When clinical manifestations develop, they are
Cachexia is a term used to describe the general wasting of fat and protein seen in many patients with cancer. Weight loss
Anemia occurs for many different reasons and in many different types of cancers. Most individuals with metastatic cancer eventually develop anemia. It occurs early in those with cancer of the blood-forming cells of the bone marrow. This is true whether the cancer
Fatigue frequently occurs as a result of poor nutrition, protein malnutrition, and poor oxygenation of tissues resulting from anemia. Certain cytokines produced to support the immune response against cancer also are known to cause fatigue. Growing tumors collapse the blood supply to healthy cells while stimulating their own blood supply. They take over the nutrient and oxygen supply of normal cells, causing widespread fatigue.
Diagnosis of cancer involves reviewing the patient's clinical presentation, gaining information on personal habits such as smoking, and investigating the patient's genetic background for cancer.
Screening tests, such as Pap smears to detect cervical cancer, mammograms to detect breast cancer, and digital examinations of the prostate
Advanced methods to diagnose and localize cancer include radiographs, CAT scans, and magnetic
Non-invasive diagnostic tests for oral cancer are being developed that involve testing for the presence of salivary bacteria not normally present in healthy individuals.
Cancer diagnosis is confirmed by surgically extracting a sample from a suspicious lesion, a procedure known as a biopsy, and performing a microscopic examination of the cells.
Infections are common in those with cancer. Infections develop as a result of protein malnutrition, other dietary deficiencies, and immune suppression (especially bone marrow suppression), which often accompanies conventional therapies. Hormones released in response to the long-term stress of cancer can also cause immune suppression. Complications from surgery also may result in infections in patients with cancer. Infection is a major cause of disability and death in those with cancer.
Pain may occur as a result of the invading tumor pressing on nerves or blood vessels in the area. Compression of the blood vessels can lead to tissue hypoxia, lactic acid accumulation, or cell death. Pain also occurs because the cancer cells release
Pain caused by compression of nerves and blood vessels occurs especially in tissues that exist in space-limiting compartments, such as bone or brain. For example,
Several treatments for cancer are available, as outlined below and shown in Table 3-1 . All have the highest rate of success with early identification of the cancer.
Surgery has long been a treatment for cancer, with the first documented account of breast removal for cancer in 200 A.D. Surgery has a better chance of curing a cancer if used on solid, well-circumscribed tumors. Tumors that have metastasized may be treated with surgery to give the patient relief from pain of the pressure of the growing tumor on surrounding nerves. Surgery is also used to debulk the tumor, which
Radiation therapy uses ionizing radiation to kill tumor cells. Radiation works on the principle that the cells most susceptible to the
Table 3-1. Cancer Therapy, Actions, and Effects
Chemotherapy uses drugs of several different classes to destroy cells in the S, M, or initial G stages of the cell cycle. Tumors grow rapidly and therefore have the most number of replicating and dividing cells and so are most susceptible to chemotherapy. However, healthy cells are also susceptible to the damaging effects of chemotherapy. Chemotherapy is frequently used in addition to surgery or radiation therapy, but may be used alone. It also may be used for
One emerging type of adjuvant chemotherapy involves using reproductive hormone antagonists to fight reproductive cancers. The best example of this type of drug is tamoxifen, used clinically to fight estrogen-dependent breast cancers. Tamoxifen also appears to prevent the development of breast cancer in some women at high risk of the disease. Tamoxifen and similar drugs, collectively known as selective estrogen receptor modulators (SERMs), exert estrogenic effects on some tissues, for example uterine endometrial tissue, bone, and the cardiovascular system, but exert anti-estrogenic effects on the breast. This observation may allow different drugs to be tailored to the specific needs of each woman. Clinical trials to evaluate the use of tamoxifen to prevent the development of breast cancer are continuing.
Drugs have been developed that block receptors for growth factors over-expressed on certain cancer cells. The best known of this type of drug is Herceptin (trastuzumab), which binds to and blocks HER2 receptors that are over-expressed in some women with breast cancer. HER2 receptors normally bind circulating epidermal growth factor (EGF); when overabundant, the proliferative effect of EGF is excessive. By binding to the HER2 receptors, Herceptin blocks the effect of EGF. Herceptin also may act to alert the immune system to the abnormal cancer cells, thereby targeting them for destruction. In an exciting development, when patients with metastatic breast cancer positive for over-
Immunotherapy is a form of cancer treatment that takes advantage of the two cardinal features of the immune system: specificity and memory. Immunotherapy may be used to identify a tumor and any sites of hidden metastasis. Immunotherapy may stimulate the host's own immune system to respond more aggressively to a tumor, or tumor cells may be
Fluorescence-labeled antibodies: To identify a tumor, antibodies can be produced in a culture against tumor-specific antigens taken from a patient. The antibodies can then be labeled with a fluorescent isotope and injected into the patient before, or at different times during or after treatment. If the antibodies encounter their specific type of tumor cells, the antibodies will bind to the tumor cells and the resulting fluorescence can be
Immune stimulants: Boosting the host's natural immune response to tumor cells involves activating B and T cells to notice the presence of a growing tumor. This approach has been used in skin tumors by injecting antigens capable of stimulating the immune system. Natural immunostimulants, such as interferon or some interleukins administered to
Attacking antibodies: Antibodies produced against specific tumor antigens are being used to attack and destroy tumor cells. For example, monoclonal antibodies have been developed against malignant B cells and used in patients with lymphoma. Various other attacking antibodies also are available for use in cancer therapy.
Therapies based on the unique molecular biology of tumor cells compared to normal cells are being developed. These treatments take advantage of the recent discoveries of how cancers grow to invade local tissues and metastasize into the blood or lymph. Examples of biologic therapies being developed against tumors include drugs that specifically block tumor angiogenesis factors and enzymes such as collagenase type IV. Tumors make their own growth factors and populate their cell membranes with receptors for these factors and other substances that stimulate their growth. Drugs that block the production of tumor growth factors and the receptors for growth factors also are under development.
Gene therapy is being developed to fight cancer. In gene therapy, pieces of DNA containing special messages are delivered to cancer cells with the hope that the cancer cell will take up the DNA and begin
DNA methyl transferase inhibitors that reverse epigenetic processes associated with the
The World Health Organization has outlined treatment strategies to reduce pain and has devised an analgesic ladder for pain that includes the use of non-opioid analgesia first, followed by a weak opioid and then a strong opioid. The opioid drug morphine is the drug of choice for
Administration of recombinant erythropoietin (EPO) to treat anemia and so reduce the debilitating fatigue experienced by many patients with cancer has proven highly successful. Erythropoietin is a hormone released by the kidney in response to hypoxia, and stimulates the production of red blood cells by bone marrow. It is contraindicated for some patients.
Exercise has been shown to be effective in reducing symptoms and improving the physical and psychosocial functioning of patients with cancer.
Cancer prevention is the ultimate goal. Although cancer will occur in some people regardless of lifestyle or personal behavior, certain types of lifestyles and behaviors increase cancer risk, while others decrease it. Cancer prevention includes the following:
Avoidance of cigarette smoking is the number one behavior that can reduce the risk of cancer, both for the individual who smokes and for family
A diet rich in fruits, vegetables, and fiber and low in animal fat has been associated with a reduction in cancer in some studies.
Avoidance of sexually transmitted diseases reduces the risks of developing cancers related to infectious processes, including cervical and liver cancer.
Early detection of cancer, while not a preventive measure, can lead to containing or destroying a cancer before it has metastasized throughout the body. Early detection depends on identifying risk factors for a specific patient and using appropriate physical examination techniques. Early cancer detection tests include self breast examination and mammography, prostate examination, self testicular examination, and regular skin examination. Some screening tests, including Pap smears, tests for intestinal polyps, and biopsies of abnormal skin lesions, may allow for intervention even before dysplastic cells (cells showing early signs of abnormality) become cancerous.
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