Practice nursing care to clients with Altered Cell Growth and Cancer Development

Practice nursing care to clients with Altered Cell Growth and Cancer Development

 

Most people experience some form of altered cell growth. Tire most common types of altered cell growth are harmless (benign) and do not require intervention. Malignant cell growth or cancer, however, is serious and, without intervention, leads to death.

Cancer is a common health problem in the United States and Canada, and approximately 1.5 million people are newly diagnosed with cancer each year (American Cancer Society, 2001).

Some types of cancer can be prevented, and others have better cure rates if diagnosed early. The nurse can have a vital impact in educating the public about cancer prevention and early detection methods.

 

 

Cancer’s Seven Warning Signals

 

 

 

HISTORICAL PERSPECTIVE

Although cancer is very prevalent today, it is not a new disorder. Research has determined that even prehistoric humans experienced cancer. Some types of cancer are more prevalent today, especially among industrialized societies, than in centuries past.

Two reasons for this increase are the longevity of people in industrialized countries and increased environmental exposure to substances that stimulate cancer development.

Cancer will occur in approximately 1 out of every 3 persons currently living in North America (American Cancer Society, 2001), although cancer risk differs for each person.

Cancer prevention is a major health focus for the United States (see the Meeting Healthy People 2010 Objectives box on p. 408). More than 10 million Americans with a history of cancer are alive today, nearly 5 million of whom can be con­sidered cured (American Cancer Society, 2001).

 

OVERVIEW

The continuous growth of cells and tissues is expected during infancy and childhood, and many human body cells continue to “grow” by cell division (mitosis) long after development and maturation are complete.

Such cells are located in tissues where constant damage or wear is likely and where continued cell growth is necessary to replace dead tissues.

Cells of the skin, hair, mucous membranes, bone marrow, and linings of glandular organs (lungs, stomach, intestines, bladder, uterus), as well as support cells of the brain (glial cells), among others, maintain the ability to divide throughout a person’s life span. The growth of these cells is well controlled, ensuring that only the right number of cells is always present in any tissue or organ.

Some tissues and organs stop growing by cell division after development is complete. For example, heart muscle cells no longer divide after fetal life; the number of heart muscle cells is fixed at birth. The size of the heart increases as the person grows because each of the cells gets larger, but the number of muscle cells in the heart does not increase.

 

Reduce cancer deaths to a rate of no more than 103 per 100,000 people

•  Assess all clients for current and past exposures to carcinogens.

•  Help clients to identify personal cancer risks.

•  Help clients to avoid known environmental carcinogens.

•  Assess all clients for a family history of cancer to identify clients at a genetic high risk for cancer.

•  Refer identified clients at a genetic high risk for cancer to an appropriate-level counselor.

•  Teach clients to avoid excessive sun exposure and to use protective clothing, hats, and sun-screening agents when sun exposure is not avoidable.

•  Teach clients about tobacco-related cancers.

•  Help clients who smoke to reduce or quit smoking.

•  Teach clients about alcohol-related cancers.

•  Teach clients about the importance of limiting dietary fat,smoked meats, and red meats.

•  Teach clients about the importance of increasing dietary fiber.

•  Encourage clients to see a health care provider at least once per year for cancer screening.

•  Teach clients the correct technique for breast self-examination or testicular self-examination.

•  Encourage clients to engage in self-screening measures, such as whole-body skin examination, breast self-examination, or testicular self-examination, on a monthly basis.

•  Instruct clients who have any of the seven warning signs of cancer to follow up with their primary care provider as soon as possible.

•  Encourage female clients to follow American Cancer Society guidelines for cervical, breast, and colorectal cancer screening appropriate for age and risk categories.

•  Encourage male clients to follow American Cancer Society guidelines for prostate and colorectal cancer screening appropriate for age and risk categories.

 

Growth that causes tissue to increase in size by enlarging individual cells is called hypertrophy.

Growth that causes tissue to in­crease in size by increasing the number of cells is called hyperplasia (Figure 24-1).

 

 

Figure 24-1 • Tissue growth by hypertrophy and hyperplasia.

 

Any new or continued cell growth not needed for normal development or replacement of dead and damaged tissues is called neoplasia and is always considered abnormal even if it causes no harm.

Whether the new cells are benign or malignant, neoplastic cells develop from normal cells (parent tissues or cells). Thus cancer or any neoplastic cells were once normal cells but changed to no longer look, grow, or function normally. The strict processes controlling normal growth and function have been lost or suppressed. To understand how cancer cells grow, it is first necessary to understand the regulation and function of normal cells.

 

Biology of Normal Cells

Different types of normal cells work together to make the whole person function at an optimal level. To achieve optimal function, each individual cell must perform in a predictable manner.

 

TERMINOLOGY COMMONLY ASSOCIATED WITH ABNORMAL CELL GROWTH

 

anaplastic   Without shape or differentiation, small and round

benign   New, nonmalignant cell growth not needed for normal growth or replacement

carcinogenesis   The transformation of a normal cell into a cancer cell

doubling time   The amount of time it takes for a tumor to double in size by mitotic cell divisions

fibronectin   A large, extracellular, transformation-sensitive cell-surface protein present oormal cells that allows nor­mal cells to adhere tightly together

gene expression   The activation, or “turning on,” of a specific gene to the extent that it synthesizes a specific protein that influences the activity of a cell or group of cells

gene repression   The deactivation, or “turning off,” of a spe­cific gene so that it is silent and does not synthesize a protein

generation time   The period of time necessary for one cell to enter and complete one round of cell division by mitosis

initiation   The damage of a normal cell’s DNA by a carcinogen

latency   The period of time between when a carcinogenic agent or substance damaged the DNA of a normal cell (initi­ated it) and when an overt cancer is present

malignant   Cancerous, new growth of cells by invasion that is not needed for normal development or tissue replacement

metastasis   Invasive growth of cancer cells from the original tumor into distant areas

mitosis   Cell division by exact duplication

morphology   Appearance or shape

multipotent An undifferentiated cell that has multiple poten­tials for maturation and differentiation (also called totipotent and pluripotent)

neoplasia   New cell growth not needed for normal body growth or replacement of dead or missing tissue

oncogene   A developmental gene (proto-oncogene) ex­pressed at an inappropriate time, capable of transforming a normal cell into a cancer cell

ploidy   The chromosome content of a cell aneuploid ploidy   The chromosome content of a cell that is greater or lesser than the normal chromosome number for the species

diploid (euploid) ploidy The normal chromosome content of a cell for the species (e.g., human cells have 46 chromo­somes [23 pairs] per cell)

primary tumor   A tumor formed in a specific tissue as a re­sult of a carcinogenic agent or event

promotion Enhancement of cell division in a cell initiated by a carcinogen

proto-oncogene   A developmental gene expressed during early embryonic development

secondary tumor   A tumor formed as a result of breaking off from a primary tumor and spreading to distant sites (metastasis)

transformation The changing of a normal cell into a cancer cell by a carcinogenic agent or event 

 

Show specific morphology.

Each normal cell type has a distinct and recognizable appearance, size, and shape as shown in Figure 24-2.

 

Have a small nuclear-cytoplasmic ratio.

As shown in Fig­ure 24-2, the space that the nucleus occupies inside a nor­mal cell is small compared with the size of the cell. The nuclear space is small in proportion to the cytoplasmic space.

Perform specific differentiated functions.

Every normal cell must perform at least one special function to contribute to whole-body homeostasis. For example, skin cells make keratin, liver cells make bile, cardiac muscle cells contract rhythmically, nerve cells generate and conduct impulses, and red blood cells make hemoglobin to carry oxygen.

 Adhere tightly together.

 Normal cells make and secrete proteins that protrude from the cell surface, allowing cells to bind closely and tightly together. In the presence of a pro­tein called fibronectin, normal cells composing most nor­mal tissues are bound tightly to each other. Exceptions are blood cells. Erythrocytes and leukocytes produce no fi­bronectin and do not adhere to one another under normal circumstances.

Are nonmigratory.

Because normal cells are tightly bound together, they do not wander from one tissue to the next (with the exception of erythrocytes and leukocytes).

Grow in an orderly and well-regulated manner.

Normal cells capable of mitosis do not divide unless all internal body conditions are optimal for cell division. These condi­tions include the need for more cells, adequate space, and sufficient nutrients and other resources. Cell division, oc­curring in a well-recognized pattern, is described by the cell cycle.

 CHARACTERISTICS OF NORMAL CELLS

• Have limited cell division.

Normal cells divide (undergo mitosis) for one of two reasons: (1) to develop normal tissue or (2) to replace lost or damaged normal tissue. Even when they are capable of mitosis, normal cells divide only when all internal body conditions and nutrition are just right to promote cell division.

 

Show specific morphology.

 Each normal cell type has a distinct and recognizable appearance, size, and shape,

 

Have a small nuclear-cytoplasmic ratio.

The space that the nucleus occupies inside a normal cell is small compared with the size of the cell. The nuclear space is small in proportion to the cytoplasmic space.

 

Perform specific differentiated functions.

Every normal cell must perform at least one special function to contribute to whole-body homeostasis.

For example, skin cells make keratin, liver cells make bile, cardiac muscle cells contract rhythmically, nerve cells generate and conduct impulses, and red blood cells make hemoglobin to carry oxygen.

 

Adhere tightly together.

 Normal cells make and secrete proteins that protrude from the cell surface, allowing cells to bind closely and tightly together. In the presence of a protein called fibronectin, normal cells composing most normal tissues are bound tightly to each other. Exceptions are blood cells. Erythrocytes and leukocytes produce no fibronectin and do not adhere to one another under normal circumstances.

 

Are nonmigratory.

 Because normal cells are tightly bound together, they do not wander from one tissue to the next (with the exception of erythrocytes and leukocytes).

 

Grow in an orderly and well-regulated manner.

Normal cells capable of mitosis do not divide unless all internal body conditions are optimal for cell division. These conditions include the need for more cells, adequate space, and sufficient nutrients and other resources. Cell division, occurring in a well-recognized pattern, is described by the cell cycle.

 

 

 

Living cells not actively reproducing are not in the cell cycle but in a reproductive resting state termed G_o. During the G_o period, cells actively carry out specific functions but do not divide. Most normal cells spend most of their exis­tence in the G_o state, just like most humans spend the ma­jority of their lives in a nonpregnant state.

Mitotic cell division makes a cell divide into two cells. These two cells are identical to each other and to the origi­nal cell that started the mitotic cell division. The processes of entering and completing the cell cycle are rigidly con­trolled.

The activities occurring during the phases of the cell cycle:

G,. The cell is preparing for division by taking on extra nutrients, generating more energy, and making extra membrane. The amount of cell fluid (cytoplasm) also increases.

S. Because making one cell into two cells requires twice as much of everything, including deoxyri-bonucleic acid (DNA), the cell doubles its DNA content through DNA synthesis.

G₂. The cell makes important proteins that will be used in actual cell division and in normal physiologic function after cell division is complete.

M,  The single cell splits apart into two cells (actual mitosis).

 

 

 

 

 

Neuron

Skin fibroblast

 

Mature red blood cell

 

Figure 2 4 – 2 • Distinctive  morphology of some normal cells.

 

Figure 24-3 • The cell cycle.

 

Figure 24-4      Cellular events during mitotic cell division.

 

 

Are contact inhibited.

Among normal cells capable of cell division, each individual cell will divide only as long as it has some surface not in direct contact with another cell. Once a normal cell is in direct contact on all surface areas with other cell membranes, it no longer undergoes mitosis. Thus normal cell division is contact inhibited.

Contact inhibition is also called density-dependent inhibition of cell growth.

Each normal, mature cell has a specific structure and function, which is an interesting concept, considering that all humans started life as a single cell. The function and be­havior of that first single cell and its daughter cells for sev­eral generations are quite different from those of normal differentiated human cells. Knowledge about some of their differences and control processes has helped in the under­standing of cancer development.

 

 CHARACTERISTICS OF EARLY EMBRYONIC CELLS

•        Demonstrate rapid and continuous cell division.

 Early embryonic cells (from conception to the eighth day) spend most of their time within the cell cycle, actively reproduceing. The generation time for these cells ranges from 2 to 8 hours.

 

·                                     Show anaplastic morphology.

The term anaplasia means “without structural shape or differentiation.” Early embryonic cells do not look like the mature cells they will eventually become. They all have the same anaplastic appearance—small and rounded (Figure 24-5).

•      Have a large nuclear-cytoplasmic ratio.

The nucleus of an early embryonic cell takes up most of the space inside the cell. The ratio of nuclear space to cytoplasmic space is larger than that of a normal differentiated cell.

·                                     Perform no differentiated functions.

In the early embryonic period, cells do not have any differentiated functions. They have not yet committed to a specific cell type. Each early embryonic cell is totally flexible and can mature to become any body cell. This flexibility is called pluripotency, multipotency, or totipotency because each cell has an unlimited potential for maturation.

 

Figure 24-5       Embryonic cells at about 5 days after conception.

 

Adhere loosely together.

Early embryonic cells do not make fibronectin and are not tightly bound together.

 

Are able to migrate.

Because early embryonic cells are not tightly bound together, they do not remain in one place within the embryo but migrate throughout the early embryo.

 

Are not contact inhibited.

 Having all sides or areas of an early embryonic cell in continuous contact with the mem­brane surfaces of other cells does not inhibit embryonic cell division.

 

 

COMMITMENT

At some point in early embryonic development, cells become differentiated. In response to an unknown signal, each cell commits itself to a specific differentiated maturational outcome.

The cell has not yet taken on any differentiated features or functions; rather, it positions itself within a group of cells that will eventually become only one specific organ or tissue

Commitment involves turning off specific early embryonic genes that controlled or regulated early rapid growth. These genes, called proto-oncogenes, have no apparent normal function at any other point in life.

After the early embryonic regulatory genes are “turned off’ (repressed or suppressed), other specific genes that con­trol the expression of specific differentiated functions must be “turned on” (expressed) selectively in different cell types.

For example, the gene for insulin is actively expressed only in fe­tal pancreatic beta cells and is repressed in all other cells. This selective gene expression directs the normal growth and dif­ferentiation of specific body cells.

 

Biology of Abnormal Cells

Body cells do not exist in isolation but are exposed to personal and environmental changes, which can alter how the cells grow or function. When either cell growth or cell function is changed, the cells are considered abnormal.

 

 CHARACTERISTICS OF BENIGN CELLS

 

Benign tumor cells are normal cells growing in the wrong place, at the wrong time, or at the wrong rate. Examples in­clude moles, uterine fibroid tumors, skin tags, endometriosis, and nasal polyps. Benign cells:

 

Demonstrate   continuous   or   inappropriate   cell growth.

 Benign tumors are tissues unnecessary for nor­mal function, growing too much or in the wrong place.

 

 Show specific morphology.

Benign tumors strongly re­semble their parent tissues, retaining the specific mor­phologic features of parent tissue.

 

 Have a small nuclear-cytoplasmic ratio.

Just like com­pletely normal cells, benign tumor cells have a small nu­cleus compared with the rest of the cell.

• Perform differentiated functions.

Not only do benign tumors look like their parent tissues, but they also per­form the same differentiated functions. For example, in endometriosis, one type of benign tumor, the normal lin­ing of the uterus (endometrium) grows in an abnormal place (such as on an ovary, on the peritoneum, or in the chest cavity). This displaced endometrium acts just like normal endometrium by increasing vascularity and tis­sue thickness each month under the influence of estro­gen and progesterone. When these hormone levels drop and the normal endometrium sheds from the uterus, the displaced endometrium, wherever it is, also sheds.

 

•  Adhere tightly together.

•  Benign tumor cells make and secrete fibronectin, and benign tumor cells bind tightlyto one another. In addition, many benign tissues are “encapsulated,” or surrounded with fibrous connective tissue, helping to hold the benign tissue together.

 

•  Are nonmigratory.

•   Benign tissues do not wander but remain tightly bound and do not invade other body tissues.

 

•  Grow in an orderly manner.

 

•  Benign tumor cells follow normal cell growth patterns even though their growth is not needed. Growth may continue beyond an appropriate
time, but the rate of growth is normal for the parent tissue. The benign tumor grows by hyperplastic expansion.

 

 CHARACTERISTICS OF MALIGNANT CELLS

 

Cancer (malignant) cells are abnormal, serve no useful func­tion, and are harmful to normal body tissues. Malignant tu­mors commonly:

•        Demonstrate rapid or continuous cell division. Some cancer cells have a short generation time (2 to 4 hours); others have a generation time even longer than that of normal cells. Most cancer cells have a generation time similar to that of the parent tissue.

A major distinction betweeormal and cancer cells is that cancer cells divide nearly continuously. Almost as soon as one round of mitosis is complete, the daughter cells begin a new round.

•        Show anaplastic morphology. Cancer cells lose the specific appearance of their parent cells, becoming anaplastic. As a cancer cell becomes even more malignant, it becomes smaller and rounder. This loss of specific appearance can make diagnosis of cancer type difficult, because many types of cancer cells look alike.

■ Have a large nuclear-cytoplasmic ratio. The nucleus of a cancer cell is larger than that of a normal cell, and the cancer cell is small. The nucleus occupies much of the space within the cancer cell, creating a large nuclear-cytoplasmic ratio.

Lose some or all differentiated functions. Along with losing the appearance of the parent cell, cancer cells lose some differentiated functions the parent tissue per­formed. Cancer cells serve no useful purpose.

Adhere loosely together. Cancer cells make little, if any, fibronectin. As a result, they adhere poorly to each other, and little pressure is needed to allow some cancer cells to break off from the primary tumor.

Are able to migrate. Because cancer cells do not bind tightly together and have many enzymes on their cell surfaces, they are able to slip through blood vessels and tissues and spread from the original tumor site to many other body sites. This ability to spread (metastasize) is a key characteristic of cancer cells and a frequent cause of death among people with cancer.

 Grow by invasion. Cancer cells expand and extend into other tissues, both close by and more remote from the original tumor, by invasion or metastasis. Together with persistent growth, metastasis makes untreated cancer deadly.

Are not contact inhibited. Cancer cells continue to di­vide even when contacted on all surface areas by other cells; thus their growth is not contact inhibited. The per­sistence of cancer cell division, even under adverse con­ditions, is one factor making the disease so difficult to control.

CANCER DEVELOPMENT

 Carcinogenesis/Oncogenesis

Carcinogenesis and oncogenesis are synonyms for cancer development.

The process of changing a cell with a nor­mal appearance and function into a cell with malignant char­acteristics is called malignant transformation. Malignant transformation occurs through the steps of initiation, promo­tion, progression, and metastasis.

  INITIATION

 

The first step in carcinogenesis is initiation.

Normal cells can become cancer cells if their proto-oncogenes are turned back on at any time after early embryonic development is complete. Anything that can penetrate a cell, get into the nu­cleus, and damage the DNA can damage the genes, turning on genes that should remain suppressed and turning off nor­mal genes (Cooper, 1995). Substances that can change the activity of a cell’s genes so that the cell has malignant char­acteristics are called carcinogens. Carcinogens may be chemicals, physical agents, or viruses. Table 24-4 lists com­mon carcinogens and the types of cancer they are known to cause. Chapters presenting the care of clients with specific cancers discuss specific carcinogens (when known) within the Etiology sections.

Pure carcinogens initiate mutational changes in a cell’s genes and are thus called initiators. Initiation is an irre­versible event that can lead to cancer development if it does not interfere with the cell’s ability to divide.

Once a cell has been initiated, it can become a cancer cell if the cellular changes that occurred during initiation are enhanced by promotion. One cancer cell is not signifi­cant, however, unless it can divide. If it cannot divide, it cannot form a tumor. If growth conditions are right, how­ever, widespread metastatic disease can develop from just one cancer cell.

 KEY CONCEPTS RELATED TO CANCER DEVELOPMENT

 

•  Neoplastic cells originate from normal body cells.

•  Transformation of a normal cell into a cancer cell involves mutation of the genes (DNA) of the normal cell.

•  Early embryonic genes activated at an inappropriate time can cause a cell to develop into a tumor.

•  Only one cell has to undergo malignant transformation for cancer to begin.

•  Benign tumors grow by expansion, whereas malignant tumors grow by invasion.

•  Most tumors arise from cells that are capable of cell division.

•  Primary prevention of cancer involves avoiding exposure to known causes of cancer.

•  Secondary prevention of cancer involves screening for early detection.

•  Tobacco use is a causative or permissive factor in 30% of all malignant neoplasms.

 

KNOWN ENVIRONMENTAL CARCINOGENS

 

 PROMOTION

Once a normal cell has been initiated by a carcinogen and has cancer cell characteristics, it can become a tumor if its growth is enhanced. The time between a cell’s initiation and develop­ment of an overt tumor is called the latency period, which can range from months to years and depends on the type of cell initiated and the presence of promoters.

Promoters are substances that promote or enhance initi­ated cell growth (Weinberg, 1996). They can also shorten the latency period. Promoters may be hormones, drugs, or a wide variety of industrial chemicals.

■ PROGRESSION

After cancer cells have grown to the point that a detectable tu­mor is formed (a 1-cm tumor has at least 1 billion cells in it), other events must occur for this tumor to become a health problem. First, the tumor must establish its own blood supply. In the early stages, the center cells of the tumor receive nutri­tion only by diffusion from the surrounding fluids. After the tumor reaches 1 cm, however, diffusion is not efficient, and cells in the center of the tumor become hypoxic and start to die. To continue to grow and survive, the tumor makes tumor angiogenesis factor (TAF). TAF stimulates capillaries and other blood vessels in the area to grow new branches into the tumor (Pitot, 1986). These blood vessels ensure the tumor’s continued nourishment.

As tumor cells continue to divide, some of the new cells experience more changes from the original, initiated cancer cell. Actual colonies or subpopulations within the tumor be­gin to appear. These subpopulations differ from the original cancer cell. Some of the differences provide these subpopulations with advantages that allow them to live and divide no matter how the environmental conditions around them change; these differences are thus called “selection advan­tages.” Changes that a tumor undergoes at this time allow it to become more malignant. Over time, the tumor cells come to have fewer and fewer normal cell characteristics.

The original tumor formed from transformed normal cells is called the primary tumor. It is usually identified by the tis­sue from which it arose (parent tissue), such as in breast can­cer or lung cancer. When primary tumors are located in vital organs, such as the brain or lungs, they can grow to such an extent that they either lethally damage the vital organ or “crowd out” healthy organ tissue and interfere with that or­gan’s ability to perform its vital function. At other times, the primary tumor is located in soft tissue that can expand with­out damage as the tumor grows. One such site is the breast. The breast is not a vital organ, and even if it had a large tumor in it, the primary tumor would not cause the client’s death. When the tumor spreads from the original site into vital areas, life functions can be disrupted.

■ METASTASIS

In metastasis, cancer cells move from their original location by breaking off from the original group and establishing re­mote colonies. These additional tumors are called metastatic or secondary tumors. Even though the tumor is now in an­other organ, it is still a cancer from the original altered tissue. For example, when breast cancer spreads to the lung and the bone, it is breast cancer in the lung and bone, not lung cancer and not bone cancer. Metastasis occurs through several pro­gressive steps, as shown in Figure (Liotta, 1992).

 

 

1                                          2                                                               3                                4

1. Malignant transformation

2. Tumor vascularization

3. Blood vessel penetration

4. Arrest and invasion

Figure 24-6 • The steps of metastasis

 

1. Malignant transformation

Some normal cuboidal cells have undergone malignant transformation and have divided enough times to form a tumorous area within the cuboidal epithelium.

 

2. Tumor vascularization

Cancer cells secrete tumor angiogenesis factor (TAF), stimulating the blood vessels to bud and form new channels that grow into the tumor.

 

3. Blood vessel penetration

Cancer cells have broken off from the main tumor. Enzymes on the surface of the tumor cells make holes in the blood vessels, allowing cancer cells to enter blood vessels and travel around the body.

 

4. Arrest and invasion

Cancer cells clump up in blood vessel walls and invade new tissue areas. If the new tissue areas have the right conditions to support continued growth of cancer cells, new tumors (metastatic tumors) will form at this site.

 

EXTENSION INTO SURROUNDING TISSUES

Tumors secrete enzymes that open up areas of surrounding tissue. Mechanical pressure, created as the tumor increases in size, forces tumor cells to invade new territory.

 

PENETRATION INTO BLOOD VESSELS

The same enzymes that open up areas of surrounding tissue make large pores in the client’s blood vessels, allowing tumor cells to enter the blood and circulate throughout the body.

 

 RELEASE OF TUMOR CELLS

Because tumor cells are loosely held together, clumps of cells break off of the primary tumor into blood vessels for transport.

 

 INVASION OF TISSUE AT THE SITE OF ARREST

Tumor cells circulate through the blood and enter tissues at remote sites. When conditions in the remote site are appropriate for the tumor, the cells stop circulating (arrest) and invade the surrounding tissues, creating secondary tumors. Three routes responsible for metastatic spread are local seeding, bloodborne metastasis, and lymphatic spread.

 

TABLE 24-5      COMMON SITES OF METASTASIS FOR DIFFERENT CANCER TYPES
BREAST CANCER Bone*  Lung* Liver Brain	PROSTATE CANCER Bone (especially spine and legs)*  Pelvic nodes
LUNG CANCER Brain* Bone Liver  Lymph nodes Pancreas	MELANOMA Gastrointestinal tract Lymph nodes Lung Brain
COLORECTAL CANCER Liver* Lymph nodes Adjacent structures	PRIMARY BRAIN CANCER Central nervous system

 

*Most common site of metastasis for the specific malignant neoplasm.

 

• LOCAL SEEDING

Local seeding involves distribution of shed cancer cells in the local area of the primary tumor. In ovarian cancer, for example, cells often spill from the primary tumor into the peritoneal cavity and set up multiple seeding sites.

 

. BLOODBORNE METASTASIS

 

Bloodborne metastasis (tumor cell release into the blood) is the most common cause of cancer spread. Combined with seeding, distribution via the bloodstream determines the area of metastases.

Many circulating tumor cells are destroyed by factors in the circulation, immune responses, or unsuitable environments in the organs in which the cells stop. Clumps of tumor cells can become trapped in capillaries. These clumps damage the capillary wall and allow tumor cells to enter the surround­ing tissue.

 

 

■ LYMPHATIC SPREAD

 

Lymphatic spread is related to the number, structure, and lo­cation of lymph nodes and vessels.

Primary sites that are rich in lymphatics are more susceptible to early metastatic spread than are areas with few lymphatics.

 

 

Cancer Classification

Other terms describe the tumor’s biologic behavior, anatomic site, and degree of differentiation.

Approximately 100 different types of cancer arise from various tissues or organs. Figure 24-7 compares cancer distribution by site and gender. Cancers are divided into two major categories: solid and hematologic.

Solid tumors are associated with the organs from which they develop (e.g., breast cancer and lung cancer). Hematologic can­cers (e.g., leukemias and lymphomas) originate from blood cell-forming tissues, which communicate with all organs.

Penetration into Blood Vessels

The same enzymes that open up areas of surrounding tissue make large pores in the client’s blood vessels, allowing tumor cells to enter the blood and circulate throughout the body.

 

 Release of Tumor Cells

Because tumor cells are loosely held together, clumps of cells break off of the primary tumor into blood vessels for transport.

 Invasion of Tissue at the Site of Arrest

Tumor cells circulate through the blood and enter tissues at re­mote sites. When conditions in the remote site are appropriate for the tumor, the cells stop circulating (arrest) and invade the surrounding tissues, creating secondary tumors.

Three routes responsible for metastatic spread are local seed­ing, bloodborne metastasis, and lymphatic spread.

 

Cancer Classification

Terms that describe neoplasia by tissue origin and classify the tumor as benign or malignant:

 

 

Other terms describe the tumor’s biologic behavior, anatomic site, and degree of differentiation.

Approximately 100 different types of cancer arise from various tissues or organs. Cancers are divided into two major categories: solid and hematologic.

Solid tumors are associated with the organs from which they develop (e.g., breast cancer and lung cancer). Hematologic cancers (e.g., leukemias and lymphomas) originate from blood cell-forming tissues, which communicate with all organs.

 

Cancer Grade and Stage

To help standardize cancer diagnosis, prognosis, and treat­ment, classification systems of grading and staging were de­veloped. Grading of a tumor classifies cellular aspects of the cancer. Staging of the client classifies clinical aspects of the cancer.

 

 GRADING

Some cancer cells are “more malignant” than others, varying in their aggressiveness and sensitivity to treatment. Some can­cer cells barely resemble the tissue from which they arose, are aggressive, and rapidly metastasize. These cells are consid­ered more malignant, forming a “high-grade” tumor. On the basis of cell appearance and activity, grading compares the cancer cell with the normal parent tissue from which it arose.

Different groups have established different grading sys­tems for different types of cancer cells, but overall they re­semble the standard system listed in Table 24-7. This system rates tumor cells; the lowest rating is given to those tumors that closely resemble normal cells, and the highest rating is given to those that little resemble normal cells.

Grading the cells is the first step in confirming cancer. Grading provides one means of evaluating the client with can­cer for prognosis and appropriate therapy. It also allows health care professionals to evaluate the results of manage­ment and compare local, regional, national, and international statistics.

 PLOIDY

Another biologic feature describing cancer cells is chromo­some number and appearance, or ploidy. Normal human cells have 46 chromosomes (23 pairs), the normal diploid number. When malignant transformation occurs, changes in the genes and chromosomes also occur. Some tumor cells gain or lose wole chromosomes and may have structural abnormalities of the remaining chromosomes. When a tumor cell has more or less than the normal diploid number, it is said to be aneuploid. The degree of aneuploidy generally increases with the degree of malignant transformation.

 

 

Leading Sites of New Cancer Cases and Deaths, 2006

 

 

STAGING

Staging determines the cancer’s exact location and degree of metastasis present at diagnosis. Staging is important because, for most cancers, the smaller the tumor is at diagnosis and the less it has spread, the greater the chances are that treatment will result in a cure. Tumor stage also influences selection of therapy. Staging is done in three different ways:

1.  Clinical staging. This staging assesses the client’s clinical manifestations and evaluates clinical signs for the tumor size and degree of metastasis. Clinical tests are used, and tumor cells may be obtained for biopsy, but clinical staging does not include major surgery.

2.  Surgical staging. This staging determines the tumor size, number, sites, and degree of metastasis by inspection at surgery.

3.  Pathologic staging. This staging is the most definitive type. The tumor size, number, sites, and degree of metastasis are determined by pathologic examination of tissues obtained at surgery.

Some site-specific staging systems exist, such as Dukes’ staging of colon and rectal cancer and Clark‘s levels method of staging skin cancer.

The American Joint Committee on Cancer (AJCC) developed the TNM (tumor, node, metastasis) system to describe the anatomic extent of cancers.

 

 

 

The stages guide treatment and are useful for prognosis and com­parison of the end results of treatment.

The TNM staging system is based on the concept that similar cancers share similar patterns of growth and extension.

TNM staging systems are specific to each solid tumor site. Table 24-8 gives basic defi­nitions for. the TNM staging system.

TNM staging is not useful for cancers that arise in the bone marrow or lymphoid tis­sues.

 

 

Tumor growth is discussed in terms of doubling time (the amount of time it takes for a tumor to double in size) and mitotic index (the percentage of actively dividing cells within a tumor). The smallest tumor likely to be detected by a physical examination or diagnostic test is about 1 cm in diameter and contains 1 billion cells. To reach this size, a tumor will have undergone at least 30 doublings. A tumor with a mitotic index of less than 10% is a relatively slow growing tumor; a tumor with an index of 85% is fast growing. Tumors have a wide range of growth rates. Fast-growing tumors, such as lym-phomas, may double in 4 weeks; an adenocarcinoma of the lung may double in 21 to 40 weeks.

 

Causes of Cancer Development

 

The causes of serious ill-health in the world are changing. Infection as a major cause is giving way to noncommunicable diseases such as cardiovascular disease and cancer. In 1996 there were 10 millioew cancer cases worldwide and six million deaths attributed to cancer.

In 2020 there are predicted to be 20 millioew cases and 12 million deaths. Part of the reason for this is that life expectancy is steadily rising and most cancers are more common in an ageing population. More significantly, a globalization of unhealthy lifestyles, particularly cigarette  smoking and the adoption of many features of the modern Western diet (high fat, low fibre content) will increase cancer incidence.

Tobacco use and diet each account for about 30% of new cancer cases, with infection associated with a further 15%; thus, much of cancer is preventable. No individual can guarantee not to contract the disease, but it is so strongly linked to diet and lifestyle that there are plenty of positive steps that can be taken to reduce the chances: eat more fruit and vegetables, reduce the intake of red meat and definitely do not smoke. Carcinogens interact with the individual’s constitution, both inherited and acquired, determining vulnerability to cancer induction. This vulnerability is based on how an individual deals with the carcinogens, ideally eliminating them in a harmless form before they do any genetic damage or being able to repair that damage.

The science of classical epidemiology has identified populations at high cancer risk (e.g. users of tobacco products). However, many lifelong smokers do not get cancer, perhaps because of the way they handle potential carcinogens metabolically, and the relatively new science of molecular epidemiology attempts to identify high-risk individuals within populations, such as smokers.

Many issues concerning diet and cancer are controversial (e.g. fat intake and breast cancer). This may be because only certain polyunsaturated fatty acids generate damaging free radicals; furthermore, the intake level of antioxidant vitamins that can scavenge these harmful radicals is a confounding factor.

Reducing infection, particularly in the poorer countries, will lead to reduc ions in cancer incidence. Infectious agents associated with increased cancer risk include hepatitis B virus (liver), certain subtypes of human papillomavirus (cervix), the bacterium Helicobacter pylori (stomach) and human immunodeficiency virus (many sites).

 

Factors Believed to Contribute to Global Causes of Cancer

 

Carcinogenesis or oncogenesis takes years and depends on several tumor and client factors. Essentially, three interacting primary factors influence the development of cancer: envi­ronmental exposure to carcinogens, genetic predisposition, and immune function. These interactions account for varia­tion in cancer development from one person to another, even when each person is exposed to the same hazards.

For some types of cancer, specific causes have been iden­tified, and people at risk can avoid contact with specific agents associated with the development of that cancer type.

This is called primary prevention of cancer and is effective in minimizing the risk for some types of cancer.

For many types of cancer, however, absolute causes remain unknown.

For other cancer types, even though the cause may be known, exposure cannot be avoided. These problems make primary prevention of some types of cancer impossible.

For people with these cancers, early detection, or secondary prevention, can be helpful because treatment outcome is usually better with the diagnosis of small tumors that have not metastasized.

 

 ONCOGENE ACTIVATION

Regardless of specific cause, the mechanism of carcinogene­sis appears to be the same: the activation of proto-oncogenes into oncogenes. When a normal cell is exposed to any car­cinogen (initiator), the normal cell’s DNA can be damaged or mutated. The mutations can cause the early embryonic genes (proto-oncogenes), which should be suppressed forever, to be turned on or activated again. These genes are then oncogenes and can cause the cell to change from normal to malignant (Cooper, 1995).

About 50 different proto-oncogenes that can be activated into oncogenes have been identified so far, and scientists estimate that at least 50 more exist. These oncogenes are not abnormal genes but are part of every cell’s normal makeup and were crit­ically important in early development. Oncogenes become a problem only if they are activated (derepressed) after develop­ment is complete, as a result of exposure to carcinogenic agents or events. Activation of some specific oncogenes causes specific cancers. Table 24-9 lists known oncogenes and the malignancies they have been found to cause. Extrinsic and intrinsic factors are associated with oncogene activation.

 

TABLE 24-9 •  MALIGNANCIES ASSOCIATED WITH ALTERED ONCOGENE ACTIVITY

 

 EXTRINSIC FACTORS INFLUENCING CANCER DEVELOPMENT

Up to 80% of cancer in North America may be the result of en­vironmental, or extrinsic, factors (Trichopoulos, Li, & Hunter, 1996). Environmental carcinogens are chemical, physical, or viral agents that cause cancer.

 

TABLE 24-10   ■ MALIGNANCIES ASSOCIATED WITH TOBACCO USE

 

Data from American Cancer Society. (2001). Cancer facts and figures—2001. Report No. ОО–ЗООМ-No. 5008.01. Atlanta: Author.

 

CLIENT EDUCATION GUIDE

 

Dietary Habits to Reduce Cancer Risk

•  Avoid excessive intake of animal fat.

•  Avoid nitrites (prepared lunch meats, sausage, bacon).

•  Minimize your intake of red meat.

•  Keep your alcohol consumption to no more than one or two drinks per day.

•  Eat more bran.

•  Eat more cruciferous vegetables, such as broccoli, cauliflower, Brussels sprouts, and cabbage.

•  Eat foods high in vitamin A (such as apricots, carrots, and leafy green and yellow vegetables) and vitamin С (such as fresh fruits and vegetables, especially citrus fruits).

  Chemical Carcinogenesis

Many chemicals capable of causing malignant transformation appear to have similar chemical structures. More than 20 organic and inorganic industrial chemicals, drugs, and other products used in everyday life are known to be carcinogenic, and hundreds more are suspected of being carcinogenic.

Some chemicals are complete carcinogens that can both initiate and promote cancer. Others are pure initiating agents, or incomplete carcinogens. Still others are only promoting agents. Some substances, such as tobacco and alcohol, appear to be only mildly carcinogenic; it takes chronic exposure to large amounts before a cancer develops. However, these two substances can act as co-carcinogens; when taken together, they enhance the carcinogenic activity of each other and of other carcinogens.

Cells are not equally susceptible to chemically induced malignant transformation. Normal cells that retain the capac­ity for cell division are at greater risk for cancer development than are normal cells that are not capable of cell division. Cancers commonly arise in bone marrow, skin, lining of the gastrointestinal tract, ductal cells of the breast, and lining of the lungs. All of these cells normally undergo mitotic cell di­vision. Cancers of nerve tissue, cardiac muscle, and skeletal muscle are rare. These cells do not normally undergo mitotic cell division.

Approximately 30% of cancers diagnosed in North Amer­ica are related to tobacco use (American Cancer Society, 2001). Tobacco is the single most important source of preventable chemical carcinogenesis. It contains many different chemical compounds, including complete carcinogens and co-carcinogens. Tobacco use or ingestion can initiate and promote cancer. The risk of cancer development for a person who uses tobacco depends on his or her immune function; amount, depth, and mode of exposure; and tobacco tar con­tent. The type of cancer that develops depends on the suscep­tibility of specific sites to various concentrations of tobacco and its metabolites.

Tissues associated with the greatest risk for cancer are those with direct contact with tobacco smoke. Cigarette smoking and tobacco use are also implicated in the develop­ment of cancers remote from tissues with direct contact with tobacco.

 Physical Carcinogenesis

Physical agents or events may cause cancer by the same mech­anism as for chemical carcinogens (i.e., by induction of DNA damage).

Two types of physical agents suspected of causing cancer are radiation and chronic irritation (Pitot, 1986).

 

•   RADIATION

Radiation is a physical agent capable of carcinogenesis. Even small doses of radiation affect cells. Some effects are temporary and reparable; others are irreversible and may be lethal to the damaged cell. The two types of radiation associated with car-cinogenesis are ionizing and ultraviolet (UV). Ionizing radiation occurs naturally in such minerals as radon, uranium, and ra­dium. Most rocks and soil contain various concentrations of ura­nium and radium. Other sources of ionizing radiation include di­agnostic and therapeutic radiation, as well as cosmic radiation. UV radiation is the most common type of solar radiation. Other sources of UV radiation include tanning beds and germicidal lights. UV rays do not penetrate deeply, and the most common type of cancer associated with UV exposure is skin cancer.

Both ionizing and UV radiation produce gene mutations and chromosomal damage. Although radiation exposure in­duces cancers more frequently among cells that can divide, it can cause cancer among nondividing cells as well.

 

 CHRONIC IRRITATION

 

Chronic irritation and tissue trauma have been suspected as predisposing physical agents to cancer development, but this theory has not yet been supported directly. The incidence of skin cancer is higher in people with burn scars and other tis­sues that have sustained severe injury. Chronically irritated tissues may undergo frequent mitosis and thus are at an in­creased risk for spontaneous DNA mutation (Pitot, 1986).

 

 Viral Carcinogenesis

Relatively few viruses have yet been proved to be carcino­genic to humans, although some are suspected to play major roles in cancer development. When viruses infect body cells, they break the DNA chain and insert their own genetic mate­rial into the human DNA chain. Breaking the DNA, along with viral gene insertion, mutates the normal cell’s DNA and can either activate an oncogene or repress a suppressor gene. Viruses capable of causing cancer are known as oncoviruses. Table 24-11 lists specific cancers of known viral origin.

 

 Dietary Factors Related to Carcinogenesis

Epidemiologic data relate cancer development to many dietary practices or combinations of dietary practices and environ­mental exposures. However, the relationship of diet to car­cinogenesis is poorly understood. Because dietary considera­tions are rarely independent of other possible carcinogenic agents, evidence of dietary contributions to cancer develop­ment is clouded. Suspected dietary factors include low crude fiber intake, high intake of red meat, and high animal fat in­take. Preservatives, contaminants, preparation methods, and additives (dyes, flavorings, and sweeteners) are being assessed for possible carcinogenic effects. Chart 24-1 identifies foods considered to have high carcinogenic potential.

 

 INTRINSIC FACTORS INFLUENCING CANCER DEVELOPMENT

Intrinsic factors, including immune function, age, and genetic predisposition, also affect whether a person is likely to de­velop cancer.

■ Immune Function

The immune system protects the body from foreign invaders and non-self cells (see Chapter 20). Non-self cells include cells made in the body that are no longer normal, such as can­cer cells. The part of the immune system responsible for can­cer protection is cell-mediated immunity. Natural killer (NK) and helper T-cells are most important to immune surveillance. The instrumental role of the immune system in protecting the body from cancer is supported by cancer incidence statis­tics in immunosuppressed people. Children younger than 2 years of age and adults older than 60 years of age have im­mune systems that function at less than optimal levels, and both groups have a higher incidence of cancer compared with that of the general population. Organ transplant recipients tak­ing immunosuppressive drugs to reduce the risk of organ re­jection also have a higher incidence of cancer. In clients with AIDS, incidence may be as high as 70%.

 Age

Advancing age is the single most significant risk factor re­lated to the development of cancer (American Cancer Society, 1991). Of all cancers, 50% occur in people older than 65 years of age (American Cancer Society, 2001). The higher cancer incidence in this age-group may reflect lifelong accu­mulation of DNA mutations that result in cell transformation and cancer. The body may no longer be able to repair these mutations as it once did. The effectiveness of the immune sys­tem, especially cell-mediated immunity, is also reduced in the older adult, resulting in a limited ability to recognize and climinate altered self cells

Manifestations of cancer in older clients may be overlooked and attributed to changes that coincide with normal aging. Older adults must be aware of and report symptoms such as the seven warning signs of cancer to health care providers. Health care providers must treat these reports with respect and thoroughly investigate all manifestations suggestive of disease.

■ Genetic Predisposition

As previously discussed, oncogenes are primarily intrinsic factors related to carcinogenesis. Proto-oncogenes, precursors of oncogenes, are passed on from generation to generation. The development of cancer, however, depends on more than these genes. The proto-oncogene needs to be altered to allow expression of the oncogene. In some people, the location of specific proto-oncogenes is different, which may allow them to be activated more easily (Cooper, 1995). In other people, the position of the oncogene may be ormal, but the gene controlling the oncogene’s activity, the suppressor gene, may be abnormal or out of place. These variations in gene location are inheritable. Table 24-9 lists specific malignancies associated with altered oncogene activity;

 

TABLE 24-13   •  MALIGNANCIES ASSOCIATED WITH ALTERED SUPPRESSOR GENE ACTIVITY

Suppressor Gene       Malignancies

Colorectal, stomach, and pancreatic carcinomas

Colorectal carcinoma

Melanoma; brain tumors; leukemias; sarcomas; breast, bladder, ovarian, lung, and kidney carcinomas

Neurofibroma, colon carcinoma, astrocytoma

Neurofibroma, meningioma, schwannoma

Breast, bladder, colorectal, esophageal, liver, lung and ovarian carcinomas; brain tumors; sarco­mas; leukemias and lymphomas

Retinoblastoma; sarcomas; breast, bladder, esophageal, and lung carcinomas

Renal cell carcinoma, pheochromocy-toma, hemangioblastoma

“Not all breast, prostate, or ovarian cancers are inherited.

Patterns of genetic predisposition for cancer other than oncogenes have also been identified, including the following:

•  Inherited predisposition for specific cancers

•  Inherited conditions associated with cancer

•  Familial clustering

•  Chromosomal aberrations

 

Assessment Consideration

Colorectal cancer

Ask the client whether bowel habits have changed over the past year (e.g., in consistency, frequency, or color).

Is there any obvious blood in the stool?

Test at least one stool specimen for occult blood during the client’s hospitalization.

Encourage the client to have a base­line colonoscopy.

Encourage the client to reduce di­etary intake of animal fats, red meat, and smoked meats.

Encourage the client to increase di­etary intake of bran, vegetables, and fruit.

 

Bladder cancer

Ask the client about the presence of:

·        Pain on urination

·        Blood in the urine

·        Cloudy urine

·        Increased frequency or urgency

 

Prostate cancer

Ask the client about:

·        Hesitancy

·        Change in the size of the urine stream

·        Pain in the back or legs

·        History of urinary tract infections

 

Skin cancer

Examine skin areas for moles or warts.

Ask the client about changes in moles (e.g., color, edges, or sensation).

 

Leukemia

Observe the skin for color, petechiae, or ecchymosis.

Ask the client about:

·        Fatigue

·        Bruising

·        Bleeding tendency

·        History of infections and illnesses

·        Night sweats

·        Unexplained fevers

 

Lung cancer

Observe the skin and mucous membranes for color.

How many words can the client say be­tween breaths?

Ask the client about:

·        Cough

·        Hoarseness

·        Smoking history

·        Exposure to inhalation irritants

·        Shortness of breath

·        Activity tolerance

·        Frothy or bloody sputum

·        Pain in the arms or chest

·        Difficulty swallowing

 

TABLE 24-12 • THE SEVEN WARNING SIGNS OF CANCER

С       Changes in bowel or bladder habits

A       A sore that does not heal

U       Unusual bleeding or discharge

T       Thickening or lump in the breast or elsewhere

I        Indigestion or difficulty swallowing

О       Obvious change in a wart or mole

N       Nagging cough or hoarseness

 

 

CULTURAL CONSIDERATIONS

The incidence of cancer varies among races. American Cancer Society data (2001) show that African Americans have a higher incidence of cancer than Caucasians do, and the death rate is higher for African Americans. Since 1960 the overall incidence among African Americans has increased 27%, whereas for Caucasians it has increased 12%. Cancer sites and cancer-related mortality vary along racial lines as well.

When risks for cancer development are assessed, however, race and genetic predisposition cannot be considered alone. Behavior related to a cultural or ethnic group, geographic lo­cation, diet, and socioeconomic factors must also be assessed. The American Cancer Society (2001) has reported that cancer incidence and survival are often related to socioeconomic fac­tors, such as the availability of health care services or the be­lief that seeking early health care has a positive effect on the outcome of cancer diagnosis (see the Evidence-Based Practice for Nursing box at right).

 

CANCER PREVENTION   

Avoidance of Known or Potential Carcinogens

A very effective means of preventing cancer development is avoidance of known or potential carcinogens. This method of prevention is appropriate when the cause of a specific cancer is known or strongly implicated and avoidance is easily ac­complished. Examples of effective avoidance are using skin protection during sun exposure, avoiding tobacco, and elimi­nating environmental asbestos. As more causes of cancer are identified, the prevention method of avoidance will likely be­come even more effective.

 

Avoidance or Modification of Associated Factors

Absolute causes are not known for many cancers, but specific conditions or exposures appear to have an associated risk. Some examples are the increased incidence of some cancer types among people who consume alcohol; the association of a diet high in fat and low in fiber with colon cancer, breast cancer, and ovarian cancer; and the greater incidence of cer­vical cancer among women with many sexual partners. It is thought that avoidance or reduction of exposure to the associ­ated condition or factor might result in decreased risks for cancer development.

 

Preventing Cancer through Diet and Lifestyle

 

 

Chemoprevention

A new form of cancer prevention, chemoprevention, is cur­rently under study to determine its effectiveness. This strategy uses exogenous chemicals, such as synthetic chemicals, natu­ral nutrients, or other substances found in plant food sources, to disrupt one or more steps important to cancer development. Such agents may be able to reverse existing damage or halt the progression of the transformation process.

Chemopreventive agents have a variety of actions, including the following, that disrupt at least one important step in the process of cancer: Blocking an inactive compound from becoming an ac­tive carcinogen Blocking the direct action of a carcinogen on DNA

•        Enhancing the rate of elimination of a carcinogen from he body

Suppressing the activity of a carcinogen Suppressing the promoting activity of a carcinogen

•        Suppressing the progression of a premalignant or early tage malignancy into a more malignant state

The ultimate goal of chemopreventive strategies is preven­tion of cancer development. Target populations for whom chemoprevention might be effective include the following:

·        Healthy people with no known specific cancer risk

·        People at greater thaormal risk because of increased environmental exposure or decreased immune function

·        People with precancerous lesions

·        •        People with a history of cancer

Gene Alteration as a Potential Form of Cancer Prevention

Because cancer development clearly involves gene changes (either congenital genetic abnormalities or acquired gene damage), researchers have suggested that altering damaged genes could prevent cancer development. At the present stage of scientific development, people can be screened for some gene alterations that will eventually lead to cancer. Such screening can help a genetically susceptible person either alter lifestyle factors or participate in early detection methods to identify a malignancy when cure is more likely. Although it is not yet possible to “fix” or remove an abnormal gene in humans, gene therapy in the future is not out of the realm of possibility.