(Relates to Chapter 16, “Cancer,” in the textbook) Copyright © 2011, 2007 by Mosby, Inc., an...

(Relates to Chapter 16, “Cancer,” in the textbook)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

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Group of more than 200 diseases

Characterized by uncontrolled and unregulated growth of cells

Occurs in people of all ethnic groups and all ages


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~1,450,000 persons diagnosed with cancer in 2006 Excluding basal and squamous cell skin cancers▪ More than 1 million cases of basal and squamous cell skin cancer annually


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Incidences of lung, colorectal, and oral cancer have ↓

Other cancers have ↑ Non-Hodgkin’s lymphoma Skin cancer


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Higher in men than womenIncidence and death rates

are higher in African Americans than in whites and other minorities.

Second most common cause of death in the United States after heart disease


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5-Year survival rate is now 66% for those who are Disease free In remission Under treatment Does not include number of people who are “cured” of cancer


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Most human tissues contain predetermined, undifferentiated stem cells.

Predetermined stem cells give rise to mature cells of the type of tissue where they reside.


Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.8

Fig. 16-1. Cell life cycle and metabolic activity. 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).

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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


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Cancer cells respond differently than normal cells to intracellular signals regulating equilibrium. Divide indiscriminately


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Stem cell theory Loss of intracellular control of proliferation results from mutation of stem cells.

DNA is substituted or permanently rearranged.


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Once mutated Cells can die from damage or by initiating programmed cellular suicide (apoptosis).

Can recognize damage and repair itself


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Once mutated (cont’d) Can survive and pass on damage to two or more daughter cells

Surviving mutated cells have potential to become malignant.


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Orderly process progressing from a state of immaturity to a state of maturity

Stable and will not changeExact mechanism of normal

cellular differentiation is not completely understood.


15Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Fig. 16-2. Normal cellular differentiation.

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Two types of genes that can be affected by mutation are

1. Protooncogenes ▪ Regulate normal cellular

processes such as promoting growth

2. Tumor suppressor genes ▪ Suppress growth


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Protooncogenes Genetic locks that keep cells functioning normally

Mutations that alter their expression can activate them to function as oncogenes.


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Tumor suppressor genes Function to regulate cell growth

Suppress growth of tumors Mutations render them inactive.

Result in loss of suppression of tumor growth


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Tumors can be classified as benign or malignant neoplasms

Benign neoplasm Well differentiated Usually encapsulated Expansive mode of growth


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Benign neoplasm (cont’d) Characteristics similar to parent cell

Metastasis is absent. Rarely recur


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Malignant neoplasm May range from well differentiated to undifferentiated

Able to metastasize Infiltrative and expansive growth

Frequent recurrence


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Malignant neoplasm (cont’d) Moderate to marked vascularity Rarely encapsulated Becomes less like parent cell


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Likely to be multifactorialOrigin of cancer may be

Genetic Chemical Environmental Viral or immunologic May arise from causes not yet identified



Fig. 16-3. Process of cancer development.

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Initiation Mutation of cell’s genetic structure▪ From inherited mutation▪ From exposure to a chemical, radiation, or viral agent

Mutated cell has the potential to develop into clone of neoplastic cells.


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Initiation (cont’d) Once initiated, mutation is irreversible.

Not all mutated cells form a tumor.

Mutated cells become tumors only when they establish the ability to self-replicate and grow.


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Initiation (cont’d) Carcinogens may be

▪ Chemical▪ Radiation▪ Viral

Carcinogens can be ▪ Detoxified ▪ Harmlessly excreted


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Initiation (cont’d) Cells damaged by carcinogens may ▪ Self-repair▪ Die▪ Replicate into daughter cells with same genetic alteration


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Chemical carcinogens Long latency period makes identification of carcinogens difficult.

Animal studies may not apply to humans.

Certain drugs have been identified as carcinogens.


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Radiation Ionizing radiation can cause cancer in almost any human tissue.

Dose of radiation needed to cause cancer is unknown.

Ultraviolet radiation is associated with melanoma and squamous and basal cell carcinoma.


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Viral carcinogensVirus 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


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Promotion Characterized by reversible proliferation of altered cells

Activities of promotion are reversible.▪ Obesity▪ Smoking, alcohol▪ Dietary fat


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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.


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Progression Characterized by

▪ Increased growth rate of tumor▪ Invasiveness▪ Metastasis

Most frequent sites of metastasis are lungs, brain, bone, liver, and adrenal glands.



Fig. 16-4. Main sites of metastasis.


Fig. 16-5. The 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.

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Progression (cont’d) Metastasis process begins with rapid growth of primary tumor.▪ Develops its own blood supply

▪ Critical for survival and growth of tumor▪ Tumor angiogenesis is formation of blood vessels within tumor.

▪ Certain segments of primary tumor can detach and invade surrounding tissues.


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Progression (cont’d) Metastasis process (cont’d)

▪ 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.


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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)



Fig. 16-6. Tumor-associated antigens appear on the cell surface of malignant cells.

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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 lymphocytes


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Cytotoxic T cells Kill tumor cells directly Produce cytokines

Natural killer cells and activated macrophages can lyse tumor cells.

B cells produce antibodies directed to tumor surface antigens.


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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.


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Immunologic escape (cont’d)▪ 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



Fig. 16-7. Blocking antibodies prevent T cells from interacting with tumor-associated antigens and from destroying the malignant cell.

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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


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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


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Examples of oncofetal antigens (cont’d) CA-125 CA-19-9 Prostate-specific antigen (PSA) CA 15-3, CA 27-29 kRAS HER-2


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Tumors can be classified by Anatomic site Histology

▪ Grading severity Extent of disease

▪ Staging


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Classification systems provide a standardized way to Communicate with health care team

Prepare and evaluate treatment plan

Determine prognosis Compare groups statistically


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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)


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Anatomic site classification (cont’d) Sarcomas originate from

▪ Embryonal mesoderm (connective tissue, muscle, bone, and fat)

Lymphomas and leukemias originate from ▪ Hematopoietic system


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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.


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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.


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Four grades (cont’d) 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.


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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


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TNM classification system Anatomic extent of disease is based on three parameters:▪ Tumor size and invasiveness (T)▪ Spread to lymph nodes (N)▪ Metastasis (M)


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Lifestyle habits to reduce risks: Avoid or reduce exposure to known or suspected carcinogens. ▪ Cigarette smoke, excessive sun exposure

Eat a balanced diet. Exercise regularly. Obtain adequate rest.


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Habits to reduce risks (cont’d) Have a regular health examination. Change perceptions of stressors. Know seven warning signs of cancer.

Practice recommended cancer screenings.

Practice self-examination. Seek medical care if cancer is suspected.


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Patient may experience fear and anxiety.

Nurse should Give clear explanations, repeat if necessary

Give written information for reinforcement

Actively listen to patient’s concerns


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Diagnostic plan includes Health history Identification of risk factors Physical examination Specific diagnostic studies


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Indicated diagnostic studies depend on site 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


(Relates to Chapter 16, “Cancer,” in the textbook) Copyright © 2011, 2007 by Mosby, Inc., an...

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