16
Cancer
Susan Doyle-Lindrud
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Cellular Regulation Health Promotion
Coping
LEARNING OUTCOMES
1. Describe the incidence, survival, and mortality rates of 8. Distinguish between external beam radiation and
cancer in the United States. brachytherapy.
2. Discuss the processes involved in the biology of cancer. 9. Describe the effects of radiation therapy and
3. Outline the stages of cancer development. chemotherapy on normal tissues.
4. Describe the role of the immune system related to cancer. 10. Identify the types and effects of immunotherapy and
5. Discuss the role of the nurse in the prevention, detection, targeted therapy.
and diagnosis of cancer. 11. Describe the nursing management of patients receiving
6. Explain the use of surgery, chemotherapy, radiation chemotherapy, radiation therapy, immunotherapy, and
therapy, immunotherapy, targeted therapy, and hormone targeted therapy.
therapy in treating cancer. 12. Describe nutrition therapy for patients with cancer.
7. Identify the classifications of chemotherapy drugs and 13. Identify complications associated with cancer.
methods of administration. 14. Describe support interventions for cancer patients,
survivors, and their caregivers.
KEY TERMS
angiogenesis immunotherapy
brachytherapy malignant neoplasms
cancer metastasis
carcinogens oncogenes
carcinoma in situ (CIS) peripheral stem cell transplantation (PSCT)
chemotherapy protooncogenes
external beam radiation staging
hematopoietic stem cell transplantation (HSCT) targeted therapy
histologic grading vesicants
immunologic surveillance
Cancer is a group of diseases characterized by uncontrolled and attitudes about cancer. You can help people decrease their risk
unregulated cell growth. The resulting problems may be directly for cancer and take part in cancer screening. You need to know
related to the cancer, a consequence of cancer treatment, or a about types of cancer, treatment options, managing side effects
combination of both. The shared physiologic, psychologic, and of therapy, and supportive therapies. By supporting patients and
social impact of cancer on patients and their caregivers is con- caregivers as they cope with the effects of cancer and treatment,
siderable. A lot of anxiety and fear are associated with a cancer you are helping them adhere to cancer management plans and
diagnosis. improve quality of life.
Educating health care professionals and the public is essen- We often consider cancer a disease of aging. Most cases
tial to promote realistic attitudes about cancer and cancer treat- are diagnosed in those over age 55 years. However, it occurs
ment. You are in a key position to lead efforts for changing in people of all ages. An estimated 1.8 million people in the
265
,266 SECTION 3 Problems Related to Homeostasis and Protection
BOX 16.1 BIOLOGIC SEX CONSIDERATIONS TABLE 16.2 Cancer Deaths by Site and
Cancer Gender
MALE FEMALE
Men
• More die from cancer-related deaths each year Type % Type %
• Have a higher mortality rate from lung cancer Lung and bronchus 21 Lung and bronchus 21
• Prostate cancer has the highest incidence among men Prostate 11 Breast 15
• More likely to develop liver cancer Colon/rectum 9 Colon/rectum 8
• More likely to be diagnosed with invasive cancer over their lifetime Pancreas 8 Pancreas 8
Liver and intrahepatic bile 6 Ovary 4
Women ducts
• Lung cancer has the highest death rate among women Leukemia 4 Uterus 4
• Breast cancer has the highest incidence among women Esophagus 4 Liver and intrahepatic bile 4
• Thyroid cancer is more prevalent in women ducts
• Cancer incidence is higher in females during early adulthood (ages 20–49) Urinary bladder 4 Leukemia 3
Non-Hodgkin lymphoma 4 Non-Hodgkin lymphoma 3
Brain & other nervous 3 Brain and other nervous 3
system system
TABLE 16.1 Cancer Incidence by Site and
Gendera Source: National Cancer Institute: Cancer stat facts. Retrieved from
https://seer.cancer.gov/statfacts.
MALE FEMALE
Type % Type %
Prostate 27 Breast 13 BIOLOGY OF CANCER
Lung 12 Lung 13
Colon/rectum 8 Colon/rectum 8 Two major dysfunctions present in the process of cancer devel-
Urinary bladder 6 Uterus 7 opment are defective cell proliferation (growth) and defective
Melanoma 6 Melanoma 5 cell differentiation.
Kidney and renal pelvis 5 Non-Hodgkin lymphoma 4
Non-Hodgkin lymphoma 4 Thyroid 3 Defect in Cell Proliferation
Oral cavity and pharynx 4 Kidney and renal pelvis 3 Normally, most tissues have a population of undifferentiated
Leukemia 4 Pancreas 3
cells known as stem cells. These stem cells ultimately differen-
Pancreas 3 Leukemia 3
tiate and become mature, functioning cells of a specific tissue.
aNumbers are estimates and exclude basal and squamous cell skin Cell proliferation starts in the stem cell and begins when the
cancers and carcinoma in situ. stem cell enters the cell cycle (Fig. 16.1). The time from when a
Source: National Cancer Institute: Cancer stat facts. Retrieved from
cell enters the cell cycle to when the cell divides into 2 identical
https://seer.cancer.gov/statfacts.
cells is the generation time of the cell. A mature cell continues to
function until it degenerates and dies.
United States are diagnosed each year with cancer. This number All the body’s cells are controlled by an intracellular mech-
excludes basal and squamous cell skin cancers and carcinoma in anism that determines when cell proliferation is necessary. A
situ of any site except the bladder.1 state of dynamic equilibrium is present under normal condi-
Overall, both the incidence and mortality rates of cancer tions. This means cell proliferation equals cell degeneration
have been declining.2 The incidence of many cancers, such as or death. Normally, the process of cell division and prolifer-
colorectal, lung, and laryngeal cancers, have declined largely ation is activated only in the presence of cell degeneration or
because of preventive efforts. The incidence of other cancers, death (apoptosis). Cell proliferation also occurs if the body
such as kidney, pancreas, liver, uterus, melanoma, multiple has a physiologic need for more cells. For example, a nor-
myeloma, and oropharyngeal, is increasing.3 mal increase in white blood cell (WBC) count occurs with
Overall cancer incidence is higher in men than women. infection.
Differences in incidence and death rates for specific cancers are Another means of proliferation control in normal cells is
shown in Box 16.1 and Tables 16.1 and 16.2. contact inhibition. Normal cells respect the boundaries and ter-
Although mortality rates from all cancers combined are on ritory of the cells around them. They will not invade a territory
the decline, it is still the second most common cause of death in that is not their own. We think the neighboring cells inhibit cell
the United States. Cancer is the leading cause of death of people growth through the physical contact of their cell membranes.
40 to 79 years of age. Each year about 606,520 Americans die Cancer cells grown in tissue culture have a loss of contact inhi-
from cancer. This is more than 1600 people per day.1,2 bition. They have no regard for cell boundaries. They grow on
We have made great progress in controlling cancer for long top of one another and on top of or between normal cells.
periods. More than 16.9 million Americans with a history of The rate of cell proliferation from the time of cell birth to the
cancer are alive today. This includes those who have cancer and time of cell death differs in each body tissue. In some tissues,
are undergoing treatment, are disease free, or are in remission.2 such as bone marrow, hair follicles, and epithelial lining of the
, CHAPTER 16 Cancer 267
Continuously cycling labile cells
(e.g., epidermis, GI tract epithelium)
Some RNA
synthesized
S G2
DNA is synthesized. RNA and
protein synthesis continue
CELL
CYCLE
Relatively dormant with some
RNA and protein synthesized
M Mitosis (cellular
division)
G1
Resting phase: Cells are not
in the process of cellular division
Cell
G0 division
Permanent cells
(e.g., neurons,
cardiac myocytes)
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). (Adapted from Kumar V, Abbas AK, Fausto
N, et al.: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
gastrointestinal (GI) tract, the rate of cell proliferation is rapid. Think of the protooncogene as the genetic lock that keeps the
In other tissues, such as myocardium and cartilage, cell prolifer- cell in its mature functioning state. When this lock is “unlocked,”
ation does not occur or is slow. which can occur through exposure to carcinogens (agents that
Cancer cells proliferate at the same rate as the normal cells of cause cancer) or oncogenic viruses, genetic alterations and
the tissue from which they arise. However, cancer cells respond mutations occur. Thus oncogenes can change a normal cell to a
differently to the intracellular signals that regulate cell prolif- malignant one. This cell regains a fetal appearance and function.
eration and death. The result is that cancer cell proliferation is For example, some cancer cells make new proteins character-
indiscriminate and continuous. Sometimes they produce more istic of the embryonic and fetal periods of life. These proteins,
than 2 cells at the time of mitosis. In this way, there is continu- found on the cell membrane, include carcinoembryonic antigen
ous growth of a tumor mass: 1 × 2 × 4 × 8 × 16 and so on. We (CEA) and α-fetoprotein (AFP). They can be found in the blood
call this the pyramid effect. The time needed for a tumor mass to by laboratory studies. Other cancer cells, such as small cell lung
double in size is known as its doubling time. cancer, make hormones that are usually made by cells arising
from the same embryonic cells as the tumor cells.
Defect in Cell Differentiation Tumor suppressor genes suppress growth. They prevent cells
Cell differentiation is normally an orderly process that pro- from going through the cell cycle. Mutations can change tumor
gresses from a state of immaturity to a state of maturity. Because suppressor genes and make them inactive. This results in a loss
all body cells are derived from the fertilized ova, all cells have of their tumor-suppressing action. Examples of tumor suppres-
the potential to perform all body functions. As cells differen- sor genes are BRCA1 and BRCA2. Alterations in these genes
tiate, this potential is repressed. The mature cell can perform increase a person’s risk for breast and ovarian cancer. Another
only specific functions. With cell differentiation, there is a stable tumor suppressor gene is the APC gene. APC mutations increase
and orderly phasing out of cell potential. Normally, the differ- a person’s risk for familial adenomatous polyposis, a precursor
entiated cell is stable and will not dedifferentiate or return to its for colorectal cancer (see Chapter 47). Mutations in the p53
previous undifferentiated state. tumor suppressor gene have been found in many cancers. These
include bladder, breast, colorectal, esophageal, liver, lung, and
Genetic Link ovarian cancers.
Cancer involves the malfunction of genes that control differen-
tiation and proliferation. Two types of normal genes that can be Development of Cancer
affected by mutation are protooncogenes and tumor suppressor The following is a theoretical model of cancer development.
genes. Protooncogenes are normal cell genes that are important The cause and development of each type of cancer are likely to
regulators of normal cell processes. Protooncogenes promote be multifactorial. A common misbelief is that cancer develop-
growth. Mutations that change the expression of protoonco- ment is a rapid, haphazard event. However, cancer is usually an
genes can cause them to function as oncogenes (tumor-induc- orderly process that occurs over time. There are 3 stages: initia-
ing genes). tion, promotion, and progression (Fig. 16.2).
, 268 SECTION 3 Problems Related to Homeostasis and Protection
alter deoxyribonucleic acid (DNA). Carcinogens may be
Initiation Viruses
Target chemical, radiation, or viral.
Hormones cell Chemical carcinogens. Many chemicals are carcinogens
Radiation (e.g., benzene, arsenic, formaldehyde). People exposed to
Chemicals these chemicals over time have a greater incidence of certain
cancers. The long latency period from the time of exposure to
Genetic factors cancer development makes it hard to identify cancer-causing
Altered
Unknown factors cell chemicals.
Radiation. Radiation can cause cancer in almost any body
Dysfunction in tissue. When cells are exposed to a source of radiation, damage
differentiation occurs to DNA. A higher incidence of cancer may occur in
and proliferation
people exposed to radiation in certain occupations, such as
radiologists, radiation chemists, aircrews, and uranium miners.
Ultraviolet (UV) radiation has long been associated with
Cancer melanoma and squamous and basal cell skin cancers. Skin can-
cell cer is the most common type of cancer among whites in the
United States. Sunlight exposure is the main source of UV expo-
Promotion sure, giving off UVA and UVB rays. UV radiation from tanning
beds also causes skin cancer.4
Viral carcinogens. Certain DNA and ribonucleic acid
(RNA) viruses, termed oncogenic, can alter the cells they infect
and induce malignant transformation. These viruses have been
Proliferation identified as causative agents of cancer in animals and humans.
Burkitt lymphoma is associated with Epstein-Barr virus (EBV).5
People with acquired immunodeficiency syndrome (AIDS),
Progression caused by human immunodeficiency virus (HIV), have a high
Evidence of incidence of Kaposi sarcoma (see Chapter 15). Other viruses
clinical disease
linked to cancer include hepatitis B virus, which is associated
with primary liver cancer (hepatocellular cancer), and human
Evidence of papillomavirus (HPV). HPV can cause lesions that progress to
regional spread squamous cell cancers, such as cervical, anal, and head and neck
and metastasis
cancers.
Fig. 16.2 Process of cancer development.
Promotion
Initiation A single alteration of the cell’s genetic structure is not enough to
Cancer cells arise from normal cells because of changes in genes. cause cancer. However, the odds of cancer development increase
The first stage, initiation, involves a mutation in the cell’s genetic with the presence of promoting agents. Promotion, the second
structure. A mutation is any change in the usual DNA sequence. stage in cancer development, is characterized by the reversible
proliferation of the altered cells. An increase in the altered cell
Genetic Link population increases the likelihood of more mutations.
Gene mutations can occur in 2 ways: inherited from a parent An important distinction between initiation and promotion
(passed from one generation to the next) or acquired during a is that the activity of promoters is reversible. This is a key con-
person’s lifetime. See more about mutations in Chapter 13. cept in cancer prevention. Promoting factors include agents
We think the genetic predisposition to cancer plays a role in such as obesity, cigarette smoking, and alcohol use. Changing
about 5% to 10% of cancers. These genetic alterations lead to a a person’s lifestyle to modify these risk factors can reduce the
high risk for developing a specific type of cancer. However, most chance of cancer development. Around 40% of newly diagnosed
cancers do not result from inherited genes. They are acquired cancers in the United States are potentially avoidable. These
from damage to genes occurring during one’s lifetime. An include cancers caused by obesity, alcohol use, unhealthy diet,
acquired mutation is passed on to all cells that develop from that smoking, and physical inactivity.1
single cell. The damaged cell may die or repair itself. However, Several promoting agents have activity against specific body
if cell death or repair does not occur before cell division, the tissues. These agents tend to promote specific kinds of cancer.
cell will replicate into daughter cells, each with the same genetic For example, cigarette smoke is a promoting agent in lung can-
alteration. cer. In conjunction with alcohol use, it promotes esophageal and
Carcinogens. Carcinogens are cancer-causing agents bladder cancers.
capable of producing cell alterations. Many are detoxified by Some carcinogens, termed complete carcinogens, are capable
protective enzymes and harmlessly excreted. If this protective of both initiating and promoting cancer development. Cigarette
mechanism fails, carcinogens can enter the cell’s nucleus and smoke is an example of a complete carcinogen.
Cancer
Susan Doyle-Lindrud
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Cellular Regulation Health Promotion
Coping
LEARNING OUTCOMES
1. Describe the incidence, survival, and mortality rates of 8. Distinguish between external beam radiation and
cancer in the United States. brachytherapy.
2. Discuss the processes involved in the biology of cancer. 9. Describe the effects of radiation therapy and
3. Outline the stages of cancer development. chemotherapy on normal tissues.
4. Describe the role of the immune system related to cancer. 10. Identify the types and effects of immunotherapy and
5. Discuss the role of the nurse in the prevention, detection, targeted therapy.
and diagnosis of cancer. 11. Describe the nursing management of patients receiving
6. Explain the use of surgery, chemotherapy, radiation chemotherapy, radiation therapy, immunotherapy, and
therapy, immunotherapy, targeted therapy, and hormone targeted therapy.
therapy in treating cancer. 12. Describe nutrition therapy for patients with cancer.
7. Identify the classifications of chemotherapy drugs and 13. Identify complications associated with cancer.
methods of administration. 14. Describe support interventions for cancer patients,
survivors, and their caregivers.
KEY TERMS
angiogenesis immunotherapy
brachytherapy malignant neoplasms
cancer metastasis
carcinogens oncogenes
carcinoma in situ (CIS) peripheral stem cell transplantation (PSCT)
chemotherapy protooncogenes
external beam radiation staging
hematopoietic stem cell transplantation (HSCT) targeted therapy
histologic grading vesicants
immunologic surveillance
Cancer is a group of diseases characterized by uncontrolled and attitudes about cancer. You can help people decrease their risk
unregulated cell growth. The resulting problems may be directly for cancer and take part in cancer screening. You need to know
related to the cancer, a consequence of cancer treatment, or a about types of cancer, treatment options, managing side effects
combination of both. The shared physiologic, psychologic, and of therapy, and supportive therapies. By supporting patients and
social impact of cancer on patients and their caregivers is con- caregivers as they cope with the effects of cancer and treatment,
siderable. A lot of anxiety and fear are associated with a cancer you are helping them adhere to cancer management plans and
diagnosis. improve quality of life.
Educating health care professionals and the public is essen- We often consider cancer a disease of aging. Most cases
tial to promote realistic attitudes about cancer and cancer treat- are diagnosed in those over age 55 years. However, it occurs
ment. You are in a key position to lead efforts for changing in people of all ages. An estimated 1.8 million people in the
265
,266 SECTION 3 Problems Related to Homeostasis and Protection
BOX 16.1 BIOLOGIC SEX CONSIDERATIONS TABLE 16.2 Cancer Deaths by Site and
Cancer Gender
MALE FEMALE
Men
• More die from cancer-related deaths each year Type % Type %
• Have a higher mortality rate from lung cancer Lung and bronchus 21 Lung and bronchus 21
• Prostate cancer has the highest incidence among men Prostate 11 Breast 15
• More likely to develop liver cancer Colon/rectum 9 Colon/rectum 8
• More likely to be diagnosed with invasive cancer over their lifetime Pancreas 8 Pancreas 8
Liver and intrahepatic bile 6 Ovary 4
Women ducts
• Lung cancer has the highest death rate among women Leukemia 4 Uterus 4
• Breast cancer has the highest incidence among women Esophagus 4 Liver and intrahepatic bile 4
• Thyroid cancer is more prevalent in women ducts
• Cancer incidence is higher in females during early adulthood (ages 20–49) Urinary bladder 4 Leukemia 3
Non-Hodgkin lymphoma 4 Non-Hodgkin lymphoma 3
Brain & other nervous 3 Brain and other nervous 3
system system
TABLE 16.1 Cancer Incidence by Site and
Gendera Source: National Cancer Institute: Cancer stat facts. Retrieved from
https://seer.cancer.gov/statfacts.
MALE FEMALE
Type % Type %
Prostate 27 Breast 13 BIOLOGY OF CANCER
Lung 12 Lung 13
Colon/rectum 8 Colon/rectum 8 Two major dysfunctions present in the process of cancer devel-
Urinary bladder 6 Uterus 7 opment are defective cell proliferation (growth) and defective
Melanoma 6 Melanoma 5 cell differentiation.
Kidney and renal pelvis 5 Non-Hodgkin lymphoma 4
Non-Hodgkin lymphoma 4 Thyroid 3 Defect in Cell Proliferation
Oral cavity and pharynx 4 Kidney and renal pelvis 3 Normally, most tissues have a population of undifferentiated
Leukemia 4 Pancreas 3
cells known as stem cells. These stem cells ultimately differen-
Pancreas 3 Leukemia 3
tiate and become mature, functioning cells of a specific tissue.
aNumbers are estimates and exclude basal and squamous cell skin Cell proliferation starts in the stem cell and begins when the
cancers and carcinoma in situ. stem cell enters the cell cycle (Fig. 16.1). The time from when a
Source: National Cancer Institute: Cancer stat facts. Retrieved from
cell enters the cell cycle to when the cell divides into 2 identical
https://seer.cancer.gov/statfacts.
cells is the generation time of the cell. A mature cell continues to
function until it degenerates and dies.
United States are diagnosed each year with cancer. This number All the body’s cells are controlled by an intracellular mech-
excludes basal and squamous cell skin cancers and carcinoma in anism that determines when cell proliferation is necessary. A
situ of any site except the bladder.1 state of dynamic equilibrium is present under normal condi-
Overall, both the incidence and mortality rates of cancer tions. This means cell proliferation equals cell degeneration
have been declining.2 The incidence of many cancers, such as or death. Normally, the process of cell division and prolifer-
colorectal, lung, and laryngeal cancers, have declined largely ation is activated only in the presence of cell degeneration or
because of preventive efforts. The incidence of other cancers, death (apoptosis). Cell proliferation also occurs if the body
such as kidney, pancreas, liver, uterus, melanoma, multiple has a physiologic need for more cells. For example, a nor-
myeloma, and oropharyngeal, is increasing.3 mal increase in white blood cell (WBC) count occurs with
Overall cancer incidence is higher in men than women. infection.
Differences in incidence and death rates for specific cancers are Another means of proliferation control in normal cells is
shown in Box 16.1 and Tables 16.1 and 16.2. contact inhibition. Normal cells respect the boundaries and ter-
Although mortality rates from all cancers combined are on ritory of the cells around them. They will not invade a territory
the decline, it is still the second most common cause of death in that is not their own. We think the neighboring cells inhibit cell
the United States. Cancer is the leading cause of death of people growth through the physical contact of their cell membranes.
40 to 79 years of age. Each year about 606,520 Americans die Cancer cells grown in tissue culture have a loss of contact inhi-
from cancer. This is more than 1600 people per day.1,2 bition. They have no regard for cell boundaries. They grow on
We have made great progress in controlling cancer for long top of one another and on top of or between normal cells.
periods. More than 16.9 million Americans with a history of The rate of cell proliferation from the time of cell birth to the
cancer are alive today. This includes those who have cancer and time of cell death differs in each body tissue. In some tissues,
are undergoing treatment, are disease free, or are in remission.2 such as bone marrow, hair follicles, and epithelial lining of the
, CHAPTER 16 Cancer 267
Continuously cycling labile cells
(e.g., epidermis, GI tract epithelium)
Some RNA
synthesized
S G2
DNA is synthesized. RNA and
protein synthesis continue
CELL
CYCLE
Relatively dormant with some
RNA and protein synthesized
M Mitosis (cellular
division)
G1
Resting phase: Cells are not
in the process of cellular division
Cell
G0 division
Permanent cells
(e.g., neurons,
cardiac myocytes)
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). (Adapted from Kumar V, Abbas AK, Fausto
N, et al.: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)
gastrointestinal (GI) tract, the rate of cell proliferation is rapid. Think of the protooncogene as the genetic lock that keeps the
In other tissues, such as myocardium and cartilage, cell prolifer- cell in its mature functioning state. When this lock is “unlocked,”
ation does not occur or is slow. which can occur through exposure to carcinogens (agents that
Cancer cells proliferate at the same rate as the normal cells of cause cancer) or oncogenic viruses, genetic alterations and
the tissue from which they arise. However, cancer cells respond mutations occur. Thus oncogenes can change a normal cell to a
differently to the intracellular signals that regulate cell prolif- malignant one. This cell regains a fetal appearance and function.
eration and death. The result is that cancer cell proliferation is For example, some cancer cells make new proteins character-
indiscriminate and continuous. Sometimes they produce more istic of the embryonic and fetal periods of life. These proteins,
than 2 cells at the time of mitosis. In this way, there is continu- found on the cell membrane, include carcinoembryonic antigen
ous growth of a tumor mass: 1 × 2 × 4 × 8 × 16 and so on. We (CEA) and α-fetoprotein (AFP). They can be found in the blood
call this the pyramid effect. The time needed for a tumor mass to by laboratory studies. Other cancer cells, such as small cell lung
double in size is known as its doubling time. cancer, make hormones that are usually made by cells arising
from the same embryonic cells as the tumor cells.
Defect in Cell Differentiation Tumor suppressor genes suppress growth. They prevent cells
Cell differentiation is normally an orderly process that pro- from going through the cell cycle. Mutations can change tumor
gresses from a state of immaturity to a state of maturity. Because suppressor genes and make them inactive. This results in a loss
all body cells are derived from the fertilized ova, all cells have of their tumor-suppressing action. Examples of tumor suppres-
the potential to perform all body functions. As cells differen- sor genes are BRCA1 and BRCA2. Alterations in these genes
tiate, this potential is repressed. The mature cell can perform increase a person’s risk for breast and ovarian cancer. Another
only specific functions. With cell differentiation, there is a stable tumor suppressor gene is the APC gene. APC mutations increase
and orderly phasing out of cell potential. Normally, the differ- a person’s risk for familial adenomatous polyposis, a precursor
entiated cell is stable and will not dedifferentiate or return to its for colorectal cancer (see Chapter 47). Mutations in the p53
previous undifferentiated state. tumor suppressor gene have been found in many cancers. These
include bladder, breast, colorectal, esophageal, liver, lung, and
Genetic Link ovarian cancers.
Cancer involves the malfunction of genes that control differen-
tiation and proliferation. Two types of normal genes that can be Development of Cancer
affected by mutation are protooncogenes and tumor suppressor The following is a theoretical model of cancer development.
genes. Protooncogenes are normal cell genes that are important The cause and development of each type of cancer are likely to
regulators of normal cell processes. Protooncogenes promote be multifactorial. A common misbelief is that cancer develop-
growth. Mutations that change the expression of protoonco- ment is a rapid, haphazard event. However, cancer is usually an
genes can cause them to function as oncogenes (tumor-induc- orderly process that occurs over time. There are 3 stages: initia-
ing genes). tion, promotion, and progression (Fig. 16.2).
, 268 SECTION 3 Problems Related to Homeostasis and Protection
alter deoxyribonucleic acid (DNA). Carcinogens may be
Initiation Viruses
Target chemical, radiation, or viral.
Hormones cell Chemical carcinogens. Many chemicals are carcinogens
Radiation (e.g., benzene, arsenic, formaldehyde). People exposed to
Chemicals these chemicals over time have a greater incidence of certain
cancers. The long latency period from the time of exposure to
Genetic factors cancer development makes it hard to identify cancer-causing
Altered
Unknown factors cell chemicals.
Radiation. Radiation can cause cancer in almost any body
Dysfunction in tissue. When cells are exposed to a source of radiation, damage
differentiation occurs to DNA. A higher incidence of cancer may occur in
and proliferation
people exposed to radiation in certain occupations, such as
radiologists, radiation chemists, aircrews, and uranium miners.
Ultraviolet (UV) radiation has long been associated with
Cancer melanoma and squamous and basal cell skin cancers. Skin can-
cell cer is the most common type of cancer among whites in the
United States. Sunlight exposure is the main source of UV expo-
Promotion sure, giving off UVA and UVB rays. UV radiation from tanning
beds also causes skin cancer.4
Viral carcinogens. Certain DNA and ribonucleic acid
(RNA) viruses, termed oncogenic, can alter the cells they infect
and induce malignant transformation. These viruses have been
Proliferation identified as causative agents of cancer in animals and humans.
Burkitt lymphoma is associated with Epstein-Barr virus (EBV).5
People with acquired immunodeficiency syndrome (AIDS),
Progression caused by human immunodeficiency virus (HIV), have a high
Evidence of incidence of Kaposi sarcoma (see Chapter 15). Other viruses
clinical disease
linked to cancer include hepatitis B virus, which is associated
with primary liver cancer (hepatocellular cancer), and human
Evidence of papillomavirus (HPV). HPV can cause lesions that progress to
regional spread squamous cell cancers, such as cervical, anal, and head and neck
and metastasis
cancers.
Fig. 16.2 Process of cancer development.
Promotion
Initiation A single alteration of the cell’s genetic structure is not enough to
Cancer cells arise from normal cells because of changes in genes. cause cancer. However, the odds of cancer development increase
The first stage, initiation, involves a mutation in the cell’s genetic with the presence of promoting agents. Promotion, the second
structure. A mutation is any change in the usual DNA sequence. stage in cancer development, is characterized by the reversible
proliferation of the altered cells. An increase in the altered cell
Genetic Link population increases the likelihood of more mutations.
Gene mutations can occur in 2 ways: inherited from a parent An important distinction between initiation and promotion
(passed from one generation to the next) or acquired during a is that the activity of promoters is reversible. This is a key con-
person’s lifetime. See more about mutations in Chapter 13. cept in cancer prevention. Promoting factors include agents
We think the genetic predisposition to cancer plays a role in such as obesity, cigarette smoking, and alcohol use. Changing
about 5% to 10% of cancers. These genetic alterations lead to a a person’s lifestyle to modify these risk factors can reduce the
high risk for developing a specific type of cancer. However, most chance of cancer development. Around 40% of newly diagnosed
cancers do not result from inherited genes. They are acquired cancers in the United States are potentially avoidable. These
from damage to genes occurring during one’s lifetime. An include cancers caused by obesity, alcohol use, unhealthy diet,
acquired mutation is passed on to all cells that develop from that smoking, and physical inactivity.1
single cell. The damaged cell may die or repair itself. However, Several promoting agents have activity against specific body
if cell death or repair does not occur before cell division, the tissues. These agents tend to promote specific kinds of cancer.
cell will replicate into daughter cells, each with the same genetic For example, cigarette smoke is a promoting agent in lung can-
alteration. cer. In conjunction with alcohol use, it promotes esophageal and
Carcinogens. Carcinogens are cancer-causing agents bladder cancers.
capable of producing cell alterations. Many are detoxified by Some carcinogens, termed complete carcinogens, are capable
protective enzymes and harmlessly excreted. If this protective of both initiating and promoting cancer development. Cigarette
mechanism fails, carcinogens can enter the cell’s nucleus and smoke is an example of a complete carcinogen.
