Cancer: Part 1 Biology, Classification, Diagnosis

Cancer: Part 1 Biology, Classification, Diagnosis
Chapter 16 Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.
Cancer Group of more than 200 diseases Characterized by uncontrolled and unregulated growth of cells Occurs in people of all ages 77% of cases are diagnosed in those over age 55. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cancer More than 1.6 million persons are expected to be diagnosed with invasive carcinoma in 2013. Excluding basal and squamous cell skin cancers Incidence has been declining since the 1990s. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cancer Mortality rates are declining. Incidences of lung, colorectal, breast, and oral cancer have ↓ Largely due to preventive efforts Other cancers have ↑ Leukemia, liver cancer, skin cancers The mortality rate for the most common cancers (prostate, breast, lung, and colorectal) is declining. The incidence of melanoma rose faster than any other malignancy in the United States. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cancer Higher in men than women Second most common cause of death in the United States after heart disease Leading cause of death in people less than 85 years of age Gender differences in incidence and in death rates for specific cancers are presented in Tables 16-1 and 16-2 and the Gender Differences box. Annually about 580,350 Americans are expected to die as a result of cancer, which is more than 1500 people per day. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cancer 5-Year survival rate is now 68% for those who are Disease free In remission Under treatment Does not include number of people who are “cured” of cancer More than 13.7 million Americans are alive today who have a history of cancer. The survival rate represents an increase of 19% over the past 30 years. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cancer Statistics are helpful in describing the scope of cancer as a public health problem, but they cannot describe the combined physiologic, psychologic, and social impact of cancer on individual patients and their caregivers and families. There is considerable apprehension associated with a cancer diagnosis, proportionally more so than with other chronic diseases such as heart disease. Despite advances in treatment and care, there continues to be a great deal of anxiety and fear associated with a diagnosis of cancer. Education of health care professionals and the public is essential to promote realistic attitudes about cancer and cancer treatment. You are in a strategic position to lead efforts at changing attitudes about cancer. You can also (1) assist individuals to decrease their risk of cancer development; (2) help patients comply with cancer management regimens; and (3) support patients and their families as they cope with the effects of cancer and related treatment. You need to be knowledgeable about specific types of cancer, treatment options, management of side effects of therapy, and supportive therapies for cancer. Comstock/Thinkstock Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study George Doyle/Stockbyte/Thinkstock L.M. is a 18-year-old friend of yours. She is trying to get into nursing school and comes to you with a “spot” on her back. She is very worried because her mother died of cancer. She wants to know what you know about cancer. Cancer is a group of more than 200 diseases characterized by uncontrolled and unregulated growth of cells. Cancer affects people of all ages and affects men more than women. It is the 2nd most common cause of death in the United States after heart disease. More people are surviving cancer. Some forms of cancer, including skin cancer, are on the rise. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Biology of Cancer Two major dysfunctions in the process of cancer development: Defective cell proliferation (growth) Defective cell differentiation Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Defective Cell Proliferation
Stem cells Undifferentiated cells Ultimately differentiate and become mature, functioning cells of only that tissue Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cell Life Cycle and Metabolic Activity
Cell proliferation originates in the stem cell and begins when the stem cell enters the cell cycle. Time from when a cell enters the cell cycle to when it divides into two identical cells is called the generation time of the cell. A mature cell continues to function until it degenerates and dies. Generation time is the period from M phase to M phase. Cells not in the cycle but capable of division are in the resting phase (G0). Copyright © 2014 by Mosby, an imprint of Elsevier Inc. 11

Defect in Cellular Proliferation
All cells are controlled by an intracellular mechanism that determines proliferation. Cancer cells grown in culture are characterized by loss of contact inhibition. Grow on top of one another and on top of or between normal cells Under normal conditions, a state of dynamic equilibrium is constantly maintained (i.e., cell proliferation equals cell degeneration or death). Normal cells respect the boundaries and territory of the cells surrounding them. They will not invade a territory that is not their own. The neighboring cells are thought to inhibit cell growth through the physical contact of the surrounding cell membranes. In contact inhibition, cancer cells have no regard for cell boundaries. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Cancer cells respond differently than normal cells to intracellular signals regulating equilibrium. Divide indiscriminately Divide haphazardly Can produce > 2 cells during mitosis A common misconception regarding the characteristics of cancer cells is that the rate of proliferation is more rapid than that of any normal body cell. In most situations, cancer cells proliferate at the same rate as the normal cells of the tissue from which they originate. In some tissues, such as bone marrow, hair follicles, and epithelial lining of the gastrointestinal (GI) tract, the rate of cell proliferation is rapid. In other tissues, such as myocardium and cartilage, cell proliferation does not occur or is slow. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Pyramid effect Exponential growth of cancer cells from continuous and indiscriminate proliferation 1 X 2 X 4 X 8 X 16 X 32……. The time required for a tumor mass to double in size is known as its doubling time. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Normal Cellular Differentiation
Because all body cells are derived from the fertilized ova, all cells have the potential to perform all body functions. As cells differentiate, this potential is repressed, and the mature cell is capable of performing only specific functions. With normal cell differentiation, there is a stable and orderly phasing out of cell potential. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Normal Cellular Differentiation
Orderly process progressing from a state of immaturity to a state of maturity Stable and will not change Under normal conditions, the differentiated cell is stable and will not dedifferentiate (i.e., revert to a previous undifferentiated state). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Defect in Cellular Differentiation
Two types of genes that can be affected by mutation are Protooncogenes Regulate normal cellular processes such as promoting growth Tumor suppressor genes Suppress growth Cancer involves the malfunction of genes that control differentiation and proliferation. Protooncogenes are normal cell genes that regulate normal cell processes to keep them in their mature, functioning state. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Protooncogenes Genetic locks that keep cells functioning normally Mutations that alter their expression can activate them to function as oncogenes. When this lock is “unlocked,” as may occur through exposure to carcinogens or oncogenic viruses, genetic alterations and mutations occur. The abilities and properties that the cell had in fetal development are again expressed. When protooncogenes are mutated, they can begin to function as oncogenes (tumor-inducing genes). Oncogenes can change a normal cell to a malignant one. This cell regains a fetal appearance and function. For example, some cancer cells produce new proteins, such as those characteristic of the embryonic and fetal periods of life. These proteins, located on the cell membrane, include carcinoembryonic antigen (CEA) and α-fetoprotein (FP). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Tumor suppressor genes Function to regulate cell growth Prevent cells from going through the cell cycle Mutations make them inactive. Result in loss of suppression of tumor growth Examples of tumor suppressor genes are BRCA-1 and BRCA-2. Another tumor suppressor gene is the APC gene. Alterations in this gene increase a person’s risk for familial adenomatous polyposis, which is a precursor for colorectal cancer. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study Because you are already a nursing student, L.M. asks you to explain the biology of cancer to her. What do you tell her? George Doyle/Stockbyte/Thinkstock Two major dysfunctions in the process of cancer development are defective cell proliferation and defective cell differentiation. Cell proliferation, or growth, originates in the stem cell and begins when the stem cell enters the cell cycle. Normally, cells differentiate and become mature, functioning cells of a certain kind of tissue. There is an equilibrium between cell proliferation and cell degeneration. In cancer, cells respond differently and divide indiscriminately and haphazardly. When they produce more than 2 cells at the time of mitosis, there is continuous growth of a tumor mass, called the pyramid effect. Cell differentiation is normally a stable, orderly process that progresses from a state of immaturity to a state of maturity. Cancer results in malfunction in that process. Cancer involves the malfunction of genes that control differentiation and proliferation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Process of Cancer Development
This is a theoretical model of the development of cancer. A common misbelief is that the development of cancer is a rapid, haphazard event. Cause and development of each type of cancer are likely multifactorial: An orderly process occurring over a period of time Comprises several stages Initiation Promotion Progression Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Initiation 1st stage Mutation of cell’s genetic structure Any change in the usual DNA sequence Cancer cells arise from normal cells as a result of changes in genes. The first stage is called initiation. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Gene Mutations Inherited 5% of all cancers or the predisposition to the cancers are inherited. Lead to a very high risk for cancer Acquired Most cancers are acquired. Mutations are discussed in Chapter 13. Most cancers do not result from inherited genes but are acquired from damage to genes occurring during one’s lifetime. An acquired mutation is passed on to all cells that develop from that single cell. The damaged cell may die or repair itself. However, if cell death or repair does not occur before cell division, the cell will replicate into daughter cells, each with the same genetic alteration. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study George Doyle/Stockbyte/Thinkstock L.M. tells you “I knew I would get cancer someday since my mother had it.” What can you tell her about the genetic link in the initiation phase of cancer development? A common misbelief is that the development of cancer is a rapid, haphazard event. However, cancer is usually an orderly process comprising several stages and occurring over a period of time. The first stage, initiation, is a mutation in the cell’s genetic structure. Gene mutations can occur in two different ways: inherited from a parent (passed from one generation to the next) or acquired during a person’s lifetime. About 5% of all cancers or the predisposition to the cancers are inherited from one's parents. These genetic alterations lead to a very high risk of developing a specific type of cancer. However, most cancers do not result from inherited genes but are acquired from damage to genes occurring during one’s lifetime.1 An acquired mutation is passed on to all cells that develop from that single cell. The damaged cell may die or repair itself. However, if cell death or repair does not occur before cell division, the cell will replicate into daughter cells, each with the same genetic alteration. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Carcinogens Cancer-causing agents capable of producing cell alterations Many are detoxified by protective enzymes and are harmlessly excreted. Failure of protective mechanisms allows them to enter the cell’s nucleus and alter DNA. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Chemical carcinogens Many chemicals have been identified as carcinogens over the years. Long latency period makes identification of carcinogens difficult. Certain drugs have been identified as carcinogens. Chemicals were identified as cancer-causing agents in the latter part of the eighteenth century when Percival Pott noted that chimney sweeps had a higher incidence of cancer of the scrotum associated with exposure to soot residues in chimneys. Persons exposed to certain chemicals over a period of time have a greater incidence of certain cancers than others. The long latency period from the time of exposure to the development of cancer makes it difficult to identify cancer-causing chemicals. Drugs that are capable of interacting with DNA (e.g., alkylating agents) and immunosuppressive agents have the potential to cause cancer. The use of alkylating agents (e.g., cyclophosphamide [Cytoxan]), either alone or in combination with radiation therapy, has been associated with an increased incidence of acute myelogenous leukemia in persons treated for Hodgkin’s lymphoma, non-Hodgkin’s lymphomas, and multiple myeloma. These secondary leukemias are resistant to chemotherapy. Secondary leukemia has also been observed in persons who have undergone transplant surgery and who have taken immunosuppressive drugs. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Radiation Radiation can cause cancer in almost any human tissue. Damage occurs to the DNA. Ultraviolet radiation is associated with melanoma and squamous and basal cell carcinoma. Certain malignancies have been correlated with radiation as a carcinogenic agent: Leukemia, lymphoma, thyroid cancer, and other cancers increased in incidence in the general population of Hiroshima and Nagasaki after the atomic bomb explosions. A higher incidence of bone cancer occurs in persons exposed to radiation in certain occupations, such as radiologists, radiation chemists, and uranium miners. Skin cancer is the most common type of cancer among whites in the United States. Of great concern is the increase in the incidence of melanoma. Although the cause of melanoma is probably multifactorial, UV radiation secondary to sunlight exposure is linked to the development of melanoma. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Viral carcinogens Virus Associated Cancer Epstein-Barr virus (EBV) Burkitt’s lymphoma Human immunodeficiency virus (HIV) Kaposi sarcoma Hepatitis B virus Hepatocellular carcinoma Human papillomavirus Squamous cell carcinomas Certain DNA and ribonucleic acid (RNA) viruses, termed oncogenic, can transform the cells they infect and induce malignant transformation. Viruses have been identified as causative agents of cancer in animals and humans. Burkitt’s lymphoma has consistently shown evidence of the presence of the Epstein-Barr virus (EBV) in vitro. Persons with acquired immunodeficiency syndrome (AIDS), which is caused by human immunodeficiency virus, have a high incidence of Kaposi sarcoma. Other viruses that have been linked to the development of cancer include hepatitis B virus, which is associated with hepatocellular carcinoma, and human papillomavirus, which is believed to be capable of inducing lesions that progress to squamous cell carcinomas, such as cervical, anal, and head and neck cancers. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study George Doyle/Stockbyte/Thinkstock L.M. begins to cry and tells you she spends a lot of time in the sun and never used sunscreen, even though she promised her mother she would. What do you know about the role of sun in the development of skin cancer? UV radiation is considered a carcinogen. Carcinogens may be chemical, radiation, or viral. Ultraviolet (UV) radiation has long been associated with melanoma and squamous and basal cell carcinoma of the skin. Skin cancer is the most common type of cancer among whites in the United States. Of great concern is the increase in the incidence of melanoma. Although the cause of melanoma is probably multifactorial, UV radiation secondary to sunlight exposure is linked to the development of melanoma. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Promotion Characterized by reversible proliferation of altered cells Activities of promotion are reversible. Obesity Smoking, alcohol Dietary fat An important distinction between initiation and promotion is that the activity of promoters is reversible. This is a key concept in cancer prevention. Approximately half of cancer-related deaths in the United States are related to tobacco use, unhealthy diet, physical inactivity, and obesity. Some carcinogens are capable of both initiating and promoting the development of cancer. These carcinogens are termed complete carcinogens. Cigarette smoke is an example of a complete carcinogen capable of initiating and promoting cancer. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Latent period May range from 1 to 40 years Length of latent period associated with mitotic rate of tissue of origin and environmental factors For disease to be clinically evident, tumor must reach a critical mass that can be detected. A tumor that is 1.0 cm (0.4 inch) (the size usually detectable by palpation) contains 1 billion cancer cells. A 0.5-cm tumor is the smallest that can be detected by current diagnostic measures, such as magnetic resonance imaging (MRI). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Progression Characterized by Increased growth rate of tumor Invasiveness Metastasis Progression is the final stage in the natural history of a cancer. Metastasis is the spread of the cancer to a distant site. Certain cancers seem to have an affinity for a particular tissue or organ as a site of metastasis (e.g., colon cancer often spreads to the liver). Other cancers are unpredictable in their pattern of metastasis (e.g., melanoma). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Main Sites of Metastasis
Most frequent sites of metastasis are lungs, brain, bone, liver, and adrenal glands. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Pathogenesis of Cancer Metastasis
To produce metastases, tumor cells must detach from the primary tumor and enter the circulation, survive in the circulation to arrest in the capillary bed, adhere to capillary basement membrane, gain entrance into the organ parenchyma, respond to growth factors, proliferate and induce angiogenesis, and evade host defenses. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Progression Metastasis process begins with rapid growth of primary tumor. Develops its own blood supply Tumor angiogenesis Tumor cells can detach and invade surrounding tissues. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Development of Cancer Progression Metastasis process Detached cells can invade lymph nodes and vascular vessels to travel to distant sites. Most mobile tumor cells do not survive. Surviving tumor cells must create an environment conducive to growth and development. Once free from the primary tumor, metastatic tumor cells frequently travel to distant organ sites via lymphatic and hematogenous routes. These two routes of metastasis are interconnected. Thus it is theorized that tumor cells metastasize via both routes. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Immune response is to reject or destroy cancer cells. May be inadequate as cancer cells arise from normal human cells Some cancer cells have changes on their surface antigens. Tumor-associated antigens (TAAs) {See next slide for figure.} Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Tumor-Associated Antigens on Cell Surface
It is believed that one of the functions of the immune system is to respond to TAAs. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Immunologic surveillance Response to TAAs Lymphocytes continually check cell surface antigens and detect and destroy abnormal cells. Involves cytotoxic T cells, natural killer cells, macrophages, and B cells Under most circumstances, immune surveillance will prevent these transformed cells from developing into clinically detectable tumors. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Cytotoxic T cells Kill tumor cells directly Produce cytokines Natural killer cells and activated macrophages can lyse tumor cells. B cells produce antibodies that bind to tumor cells. Cytotoxic T cells play a dominant role in resisting tumor growth. Cytokines (e.g., interleukin-2 [IL-2] and γ-interferon) stimulate T cells, natural killer cells, B cells, and macrophages. Natural killer (NK) cells are able to directly lyse tumor cells spontaneously without any prior sensitization. These cells are stimulated by γ-interferon and IL-2 (released from T cells), resulting in increased cytotoxic activity. Monocytes and macrophages have several important roles in tumor immunity. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Immunologic escape Mechanism by which cancer cells evade immune system Suppression of factors that stimulate T cells Weak surface antigens allow cancer cells to “sneak through” surveillance. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Immunologic escape Develops tolerance to immune system by some tumor antigens Suppresses immune response from products secreted by cancer cells Induction of suppressor T cells Blocking antibodies bind TAAs, preventing recognition. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Tumor Escape Mechanism
Blocking antibodies prevent T cells from interacting with tumor-associated antigens and from destroying the malignant cell. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Oncofetal antigens Found on tumor cell surfaces, inside tumor cells, and fetal cells Appearance of fetal antigens is not well understood. May result as cell regains its embryonic capability to differentiate into many cell types These oncofetal antigens can be used as tumor markers that may be clinically useful to monitor the effects of therapy and indicate tumor recurrence. However, oncofetal antigens are not 100% specific for tumor recurrence. Tumor markers are affected by various factors that need to be accounted for when reviewing these results. For example, the persistence of elevated preoperative CEA titers after surgery indicates that the tumor was not completely removed. A rise in CEA levels after chemotherapy or radiation therapy may indicate recurrence or spread of the cancer and may be affected by chronic lung or liver disease and smoking. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Examples of oncofetal antigens Carcinoembryonic antigen (CEA) On cancer cells of GI tract Normal cells (fetal gut, liver, and pancreas) α-Fetoprotein (AFP) Malignant liver cells and fetal liver cells Normally, CEA disappears during the last 3 months of fetal life. CEA was originally isolated from colorectal cancer cells. However, elevated CEA levels have also been found in nonmalignant conditions (e.g., cirrhosis of the liver, ulcerative colitis, heavy smoking). AFP has diagnostic value in primary cancer of the liver (hepatocellular cancer), but it is also produced when metastatic liver growth occurs. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Role of Immune System Examples of oncofetal antigens CA-125 (ovarian carcinoma) CA-19-9 (pancreatic & gallbladder cancer) PSA (prostate cancer) CA 15-3, CA 27-29, HER-2 (breast cancer) kRAS (colon cancer oncogenes) EGFR (lung cancer) Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study George Doyle/Stockbyte/Thinkstock L.M. asks you how they will tell if her cancer is “bad” or not. Briefly, what can you tell her about how and why cancers are classified? Tumors can be classified as benign or malignant. In general, benign neoplasms are well differentiated, and malignant neoplasms range from well differentiated to undifferentiated. The ability of malignant tumor cells to invade and metastasize is the major difference between benign and malignant neoplasms. Tumors can be classified according to anatomic site, histology (grading), and extent of disease (staging). Tumor classification systems are intended to stratify risk. Classification systems provide a standardized way to (1) communicate the status of the cancer to all members of the health care team, (2) assist in determining the most effective treatment plan, (3) evaluate the treatment plan, (4) predict prognosis, and (5) compare like groups for statistical purposes. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Benign vs. Malignant Neoplasms
Tumors can be classified as benign or malignant. Ability of malignant tumor cells to invade and metastasize is the major difference between benign and malignant neoplasms. In general, benign neoplasms are well differentiated, and malignant neoplasms range from well differentiated to undifferentiated. Other differences between benign and malignant neoplasms are presented in Table 16-3. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Classification of Cancer
Tumors can be classified by Anatomic site Histology Grading severity Extent of disease Staging Tumor classification systems are intended to stratify risk. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Classification systems provide a standardized way to Communicate with health care team Prepare and evaluate treatment plan Determine prognosis Compare groups statistically. Classification systems provide a standardized way to (1) communicate the status of the cancer to all members of the health care team, (2) assist in determining the most effective treatment plan, (3) evaluate the treatment plan, (4) predict prognosis, and (5) compare like groups for statistical purposes. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Anatomic site classification Identified by tissue of origin Carcinomas originate from Embryonal ectoderm (skin, glands) Endoderm (mucous membrane of respiratory tract, GI and GU tracts) In the anatomic classification of tumors, the tumor is identified by the tissue of origin, the anatomic site, and the behavior of the tumor (i.e., benign or malignant) (see Table 16-4). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Anatomic site classification Sarcomas originate from Embryonal mesoderm (connective tissue, muscle, bone, and fat) Lymphomas and leukemias originate from Hematopoietic system Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Histologic classification Appearance of cells and degree of differentiation are evaluated to determine how closely cells resemble tissue of origin. Poorly differentiated tumors have a worse prognosis than those closer in appearance to normal cells. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Four grades of abnormal cells Grade I Cells differ slightly from normal cells and are well differentiated. Grade II Cells are more abnormal and moderately differentiated. Grade I: Cells differ slightly from normal cells (mild dysplasia) and are well differentiated (low grade). Grade II: Cells are more abnormal (moderate dysplasia) and moderately differentiated (intermediate grade). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Four grades Grade III Cells are very abnormal and poorly differentiated. Grade IV Cells are immature and primitive and undifferentiated. Cell of origin is difficult to determine. Grade III: Cells are very abnormal (severe dysplasia) and poorly differentiated (high grade). Grade IV: Cells are immature and primitive (anaplasia) and undifferentiated; cell of origin is difficult to determine (high grade). Grade X: Grade cannot be assessed. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Clinical staging classifications 0: Cancer in situ 1: Tumor limited to tissue of origin; localized tumor growth 2: Limited local spread 3: Extensive local and regional spread 4: Metastasis Classifying the extent and spread of disease is termed staging. This classification system is based on the anatomic extent of disease rather than on cell appearance. Although there are similarities in the staging of various cancers, there are many differences for specific types of cancer. Clinical staging has been used as a basis for staging a variety of tumor types, including cancer of the cervix and Hodgkin’s lymphoma. Other malignant diseases (e.g., leukemia) do not use this staging approach. The clinical staging classification system determines the anatomic extent of the malignant disease process by stages: Stages 0 – IV. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

TNM classification system Anatomic extent of disease is based on three parameters: Tumor size and invasiveness (T) Spread to lymph nodes (N) Metastasis (M). See Table 16-5 for more information. Examples of the TNM classification system can be found in Tables and 52-6. TNM staging cannot be applied to all malignancies. For example, the leukemias are not solid tumors and therefore cannot be staged by using these guidelines. Carcinoma in situ has its own designation in the system (Tis) since it has all the histologic characteristics of cancer except invasion—a primary feature of the TNM staging system. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Diagnoses of Cancer Patient may experience fear and anxiety. You should Actively listen to patient’s concerns. Manage your own discomfort. Give clear explanations; repeat if necessary. Give written information for reinforcement. When a patient has a possible diagnosis of cancer, it is a stressful time for the patient and the family. Patients may undergo several days to weeks of diagnostic studies. During this time, fear of the unknown may be more stressful than the actual diagnosis of cancer. Patients may also be overwhelmed or confused by the need for multiple diagnostic studies and consultations. Help to coordinate care between multiple specialists and provide explanations of the purpose of required tests as well as any special preparation needed for them. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Diagnoses of Cancer Diagnostic plan includes Health history History of present illness Identification of risk factors Physical examination Specific diagnostic studies Plan of care begins when cancer is suspected. Diagnosis may follow abnormal screening test results or when symptoms appear. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Diagnoses of Cancer Indicated diagnostic studies depend on site of cancer Cytology studies Chest x-ray CBC, chemistry profile Liver function studies Endoscopic examinations Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Diagnoses of Cancer Indicated diagnostic studies depend on site of cancer Radiographic studies Radioisotope scans PET scan Tumor markers Genetic markers Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Diagnoses of Cancer Biopsy involves histologic examination by a pathologist of a piece of tissue. Tissue may be obtained by Needle or aspiration Incisional procedure Excisional procedure. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Case Study George Doyle/Stockbyte/Thinkstock L.M. tells you she wants to be healthier. What can you tell her about lifestyle changes she can adopt to prevent cancer or at least lead to early detection? Reduce or avoid exposure to known or suspected carcinogens and cancer-promoting agents, including cigarette smoke and sun exposure. Eat a balanced diet that includes vegetables and fresh fruits, whole grains, and adequate amounts of fiber. Reduce dietary fat and preservatives, including smoked and salt-cured meats containing high nitrite concentrations. Limit alcohol intake. Participate in regular exercise (i.e., 30 minutes or more of moderate physical activity five times weekly). Maintain a healthy weight. Obtain adequate, consistent periods of rest (at least 6 to 8 hours per night). Eliminate, reduce, or change the perceptions of stressors and enhance the ability to effectively cope with stressors. Have a physical examination on a regular basis that includes a health history. Be familiar with your own family history and your risk factors for cancer. Learn and practice the recommended American Cancer Society cancer screening guidelines for breast, colon, cervical, and prostate cancer. Learn and practice self-examination. Know the seven warning signs of cancer. Seek immediate medical care if you notice a change in what is normal for you and if cancer is suspected. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Prevention and Detection of Cancer
Lifestyle habits to reduce risks: Practice recommended cancer screenings. Practice self-examination. Know seven warning signs of cancer. Seek medical care if cancer is suspected. Learn and practice the recommended American Cancer Society cancer screening guidelines for breast, colon, cervical, and prostate cancer. (See eTable 16-3 on the website for this chapter.) Learn and practice self-examination (e.g., breast or testicular self-examination). See Table 16-6 for the seven warning signs of cancer. (These are signs of advanced cancer.) Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Lifestyle habits to reduce risks: Avoid or reduce exposure to known or suspected carcinogens: Cigarette smoke, excessive sun exposure Eat a balanced diet. Limit alcohol intake. Exercise regularly. As a nurse, you have an essential role in the prevention and early detection of cancer. Eliminating risk factors reduces the incidence of cancer. As part of your goal related to public education, you need to (1) motivate people to recognize and modify behaviors that may negatively affect health and (2) encourage awareness of and participation in health-promoting behaviors. Eat a balanced diet that includes vegetables and fresh fruits, whole grains, and adequate amounts of fiber. Reduce dietary fat and preservatives, including smoked and salt-cured meats containing high nitrite concentrations. Participate in regular exercise (i.e., 30 minutes or more of moderate physical activity five times weekly). Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Lifestyle habits to reduce risks: Maintain a healthy weight. Get adequate rest. Eliminate, reduce, or cope with stress. Have a regular health examination. Be familiar with your family history. Know your risk factors. Obtain adequate, consistent periods of rest (at least 6 to 8 hours per night). Eliminate, reduce, or change the perceptions of stressors and enhance the ability to effectively cope with stressors. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Audience Response Question A nurse plans a community education program related to prevention of the cancer with the highest death rates in both women and men. What should the nurse include in the teaching plan? Smoking cessation Screening with colonoscopy Regular examination of reproductive organs Use of sunscreen as protection from ultraviolet light Answer: a Rationale: The highest number of cancer deaths by site are for cancer of the lung and bronchus. Smoking is the leading cause of lung and bronchial cancer. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

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