The National Cancer Institute (2009d) estimates that approximately 11.1 million Americans alive today have a history of cancer. This has increased from 7.4 million Americans in 2003. Of the survivors, some may be completely cured, whereas others have some evidence of disease. Cancer accounts for 22.9% of all deaths. Between 1950 and 2001 death rates from cancer have remained stable. The 5-year relative survival rate for all cancers diagnosed between 1996 and 2004 is 66%, which is up from 50% in 1975 to 1977. The improvement in survival reflects progress in diagnosing certain cancers at an earlier stage and improvements in treatment. Nonetheless, in 2010, Americans are expected to die of cancer at the rate of more than 1500 people a day. In the United States, cancer accounts for nearly one of every four deaths (American Cancer Society, 2008).

Both incidence and death rates from all cancers combined showed a statistically significant (P < .05) decrease in men and women overall and in most racial and ethnic populations in the last 5 years. These decreases reflect declines in both incidence and death rates for the three most common cancers in men (lung, colorectum, and prostate) and for two of the three leading cancers in women (breast and colorectum). There has also been a leveling off of lung cancer death rates in women. Although the national trend in female lung cancer death rates has stabilized since 2003 after increasing for several decades, there are significant prominent state and regional variations. This decrease in overall cancer incidence and death rates is encouraging, but the rates among women increased in 18 states, 16 of them in the South or Midwest. California was the only state with decreasing lung cancer incidence and death rates in women (Horner et al, 2008).

Based on 2001 through 2003 data, the likelihood of developing cancer during one’s lifetime is approximately one in two for men and one in three for women. The 5-year relative survival rate for all cancers diagnosed between 1996 and 2004 is 66%, up from 50% in 1975 to 1977 (American Cancer Society Cancer, 2008). The 5-year relative survival rate for all types combined ranges from 16% for patients with lung cancer to 99% for patients with prostate cancer. Cancer survival varies by stage of disease and race; survival rates are lower in blacks compared with whites (National Cancer Institute, 2009c).

During the past 15-year period, the cancer death rate among men dropped by 19.2% while the cancer death rate for women fell by 11.4%. Cancer incidence rates also declined from 1.8% a year among men from 2001 to 2005 and 0.6% a year from 1998 to 2005 among women. A decrease of 1% or 2% per year equates to 650,000 cancer deaths avoided over 15 years (American Cancer Society, 2008).

Racial and Ethnic Patterns

Like the rest of the population in the United States, the aging population is becoming more diverse. In addition to whites of European descent, four other main racial and ethnic groups are present in the American population: African Americans, Hispanic Americans, Asian/Pacific Islanders, and Native Americans. Cancer affects Americans of all racial and ethnic groups; however, the incidence of cancer does demonstrate patterns according to racial and ethnic origins. African Americans have higher overall incidence rates than whites, whereas Hispanic Americans and Native Americans have lower incidence rates overall (Tables 19–1 and 19–2).

TABLE 19–1

CANCER INCIDENCE RATES (NUMBER OF NEW CASES EACH YEAR)^∗

GROUP	BOTH SEXES	MALES	FEMALES
African American	467.30	582.95	388.10
White	458.13	524.68	412.53
Asian/Pacific Islander	297.80	228.35	280.07
Hispanic/Latino	331.00	379.86	300.14
American Indian/Alaskan Native	307.37	303.31	312.78

^∗Statistics are for 2000 to 2006, age adjusted to the 2000 U.S. standard population, and represent the number of new cases of invasive cancer per year per 100,000 of both sexes, males and females, respectively.

From National Cancer Institute. (2009). Surveillance epidemiology and end results (SEER). Retrieved June 2009, from http://seer.cancer.gov/faststats/selections.php#Output.

TABLE 19–2

CANCER DEATH RATES (NUMBER OF DEATHS EACH YEAR)^∗

GROUP	BOTH SEXES	MALES	FEMALES
African American	218.79	287.74	176.91
White	180.09	218.74	153.43
Asian/Pacific Islander	107.77	128.23	93.31
Hispanic/Latino	119.49	145.57	101.49
American Indian/Alaskan Native	150.40	171.27	136.40

From National Cancer Institute. (2009). Surveillance epidemiology and end results (SEER). Retrieved June 2009, from http://seer.cancer.gov/faststats/selections.php#Output.

Racial and ethnic group age cohorts demonstrate different patterns of cancer incidence. Older Japanese immigrant women demonstrate a lower incidence of breast cancer than second- and third-generation Japanese women born in America. Age is an important factor, especially when environmental influences are evaluated in cases in which persons of the same race and ethnicity had different exposures as children; any examination of patterns of cancer among racial or ethnic groups should include age and environmental considerations.

Because the incidence of cancer has demonstrated patterns by race and ethnicity, both these factors are important in determining which groups are at risk. When incidence is examined by race, several cautions are in order. First, race and ethnicity are both prone to misclassification. The U.S. Census Bureau has defined race and ethnicity (Box 19–1), but there is no accepted scientific definition for race. Persons with mixed-race parents lack a single classification. Second, as demonstrated by Freeman (1989) in his landmark investigation of genetics and cancer, there is no known genetic basis to explain the major racial differences in cancer incidence. Third, race and ethnicity may be viewed as a rough indicator for certain lifestyle and environmental factors. Race and ethnicity are highly correlated with socioeconomic status. Persons living in poverty tend to lack education, employment, adequate housing, good nutrition, preventive health practices, and access to health care. Within any one race or cultural group, economic status is the major determinant for cancer risk and outcome. Economic status as a risk factor for cancer is demonstrated globally. For most cancers, there are notable geographic variations in incidence rates that reflect socioeconomic differences, particularly differences between developing and developed countries (Hansen, 1998). Freeman (1989) concluded that correcting poverty among groups of people, regardless of their race or ethnic origin, would lead to decreased cancer incidence and increased survival rates.

BOX 19–1 U.S. CENSUS BUREAU DEFINITIONS OF RACE AND ETHNICITY

RACE/ETHNICITY	DEFINITION
African American	Persons having their origins in any of the black racial groups of Africa.
Asian/Pacific Islander	Persons having their origins in any of the original peoples of the Far East, Southeast Asia, the Indian subcontinent, or the Pacific Islands. This group is very diverse, including individuals from at least 24 ethnic populations who speak more than 30 major languages or dialects.
Native American	Persons who are American Indians and Alaskan Natives, having their origins in the original peoples of North America, and who maintain cultural identification through tribal affiliations or community recognition. American Indians and Alaskan Natives represent more than 500 tribes, each with unique cultural, genetic, and sociodemographic characteristics.
Caucasian (white)	Persons having their origins in any of the original peoples of Europe, North Africa, or the Middle East. Caucasians are the largest racial group in America.
Hispanic	Persons having their origins in Mexico, Puerto Rico, Cuba, Central or South America, or another Spanish culture, regardless of race. By this definition, Hispanics are present in every racial group.

From US Census Bureau: Profile of general demographic characteristics, Washington, DC, 2000, US Department of Commerce.

The leading cancers among white men are prostate, lung, colorectal, urinary bladder, melanoma, and non–Hodgkin’s lymphoma. White men have higher urinary bladder cancer incidence rates than men of any other racial or ethnic group: the rates are almost two times higher than those of Hispanic men, who have the second highest rates along with African American men. Breast cancer rates among white women are higher than those for women of any other racial or ethnic group. African American men have a higher overall cancer incidence rate than any other racial or ethnic group in America (666.4 vs. 558.3 for white men per 100,000). In contrast, white women have the highest cancer incidence rate among all ethnic groups (424.6 per 100,000) (Tables 19–3 and 19–4). In the United States the incidence rate for all cancers combined was 16% higher among African American men than white men (a decrease of 4% in the last 5 years), whereas the incidence rate for all cancers combined was 7% higher for white women than African American women (an increase of 2% over the last 5 years) (American Cancer Society Cancer Facts and Figures for African Americans, 2007 to 2008).

TABLE 19–3

CANCER INCIDENCE RATES OF AFRICAN AMERICAN AND WHITE MALES

TYPE	AFRICAN AMERICAN	WHITE	ABSOLUTE DIFFERENCE	RATE RATIO
All Types	666.4	558.3	108.1	1.2
Prostate	258.3	163.4	94.9	1.6
Lung/Bronchus	112.2	81.7	30.5	1.4
Urinary/Bladder	19.8	30.2	-20.4	0.5
Skin Melanoma	1.1	-26.5	-25.5	<0.1

TABLE 19–4

CANCER INCIDENCE RATES OF AFRICAN AMERICAN AND WHITE FEMALES

TYPE	AFRICAN AMERICAN	WHITE	ABSOLUTE DIFFERENCE	RATE RATIO
All Types	395.5	424.6	–29.1	0.9
Colon/Rectum	56.1	44.7	11.4	1.3
Breast	118.0	134.0	–16.0	0.9
Lung/Bronchus	53.1	54.7	–1.4	1.0

Cancer incidence rates vary considerably among the subgroups of Asian/Pacific Islanders. Although Asian/Pacific Islanders experience lower rates overall compared with other groups, they do experience higher death and incidence rates for certain cancers, especially liver and stomach cancer for both sexes. For men, the top three sites among Chinese, Filipinos, Hawaiians, and Japanese are prostate, lung, and colorectal; among Koreans the top sites are lung, stomach, and colorectal; among Vietnamese the top sites are lung, liver, and prostate. Stomach cancer rates among Korean men and liver cancer rates among Vietnamese men are higher than those among men of any other racial or ethnic group. The top three cancer sites among Asian/Pacific Islander women are breast, lung, and colorectal with the following exceptions: The stomach is the leading site among Japanese and Korean women, and the cervix is the leading site among Vietnamese women. Cervical cancer incidence rates among Vietnamese women are more than 2½ times higher than for any other racial or ethnic group. Asian Americans have the highest overall incidence of liver, bile duct, and stomach cancer for both men and women (American Cancer Society, 2008).

Information on cancer incidence among Native Americans is based on 54% of the U.S. Indian/Native American population in 624 counties. Alaskan Natives have the highest cancer incidence rates among any racial group for the kidney and pelvis. Alaskan Natives have a relatively high incidence of cancers of the esophagus, stomach, liver, gallbladder, and pancreas. According to the National Cancer Institute: Surveillance epidemiology and end-results program (1975-2006), American Indians who live in New Mexico and Arizona have excessive incidence rates for stomach, cervix, uterine, liver, and gallbladder cancer. American Indians have the highest gallbladder cancer incidence rate of any racial group, including blacks, whites, or Hispanics (National Cancer Institute, 2009c).

The leading cancer sites for Hispanic men and women are the same as those for whites—prostate, breast, lung, and colorectal. Other cancers commonly diagnosed among Hispanics include cancers of the urinary bladder and stomach in men. Hispanic women have the highest overall incidence of cervical cancer (American Cancer Society SEER Results, 2008). (See Cultural Awareness Box.)

Aging and Its Relationship to Cancer

Age is consistently considered the most important determinant of cancer risk. However, what is it about the aging process that predisposes a person to cancer?

Biologic aging is a process that occurs naturally in adult life and results in changes in both structure and function. Although it occurs at a variable pace, the aging process creates a pattern of changes that predictably unfolds over a course of time—a biologically programmed life span. Each species has a uniquely programmed life span. For humans that life span is around 100 years, which is to say that it is biologically improbable that a human will live much beyond 100 years. On the other hand, life expectancy is the number of years an individual can be expected to live, based on averages within a population group born during a particular period and traced through time or cohort. Life expectancy is influenced primarily by external, environmental factors. For example, a cohort of persons living their childhood in conditions of famine and malnutrition might have a different life expectancy from a cohort that did not experience childhood malnutrition. Both biologically programmed life span and environmentally influenced life expectancy are important concepts when the relationship between aging and cancer is considered.

The relationship between aging and cancer begins at the cellular level, where two types of cells should be considered: replicating cells and postreplicating cells. Cells show a limited replicating potential, that is, cells divide only a limited number of times before entering a phase in which they can no longer reproduce. At that point, cells survive in a senescent postreplicating state; they continue to metabolize and synthesize nutrients necessary for survival except that deoxyribonucleic acid (DNA) synthesis ceases and replication does not occur. Human cells are estimated to undergo approximately 50 population replications before entering the senescent postreplicating phase. Although the cell-replicating capacity generally decreases with age, several age-related processes involve accelerated replication, or hyperproliferation. Prostatic hypertrophy, atherosclerosis, and cancer are examples of disease states among older adults thought to be influenced by accelerated cellular replication.

The aging cell has a tendency toward aberration or abnormalcy as it replicates. Aberrant cell growth is related to failure of growth control mechanisms, which leads to less cell regulation during replication. Cancer occurs more commonly in replicating than in nonreplicating cell groups, which suggests that changes in internal cellular control mechanisms give rise to cancer.

External or environmental factors are believed to contribute to decreased regulation of cell growth by causing cell damage and then promoting the replication of damaged cells (Cohen, 1994).

The process of cancer growth is believed to occur in three stages: initiation, promotion, and progression (Fig. 19–1). Initiation results from intense or prolonged exposure to an external agent that causes mutation of genetic material. The mutations are nonlethal, but they are passed on to future cell generations during replication. An initiated cell will continue to produce the mutations with each cell replication; however, the mutations alone are not enough to lead to cancer. Cancerous cell growth begins when an initiated cell encounters a promoting agent; thus the second stage of cancer development is called promotion. Promoting agents are external or environmental agents. A number of substances may be considered promoters of cancer in humans; they may come from a variety of sources, including air, water, or soil, and they may be naturally occurring or chemically produced. Promoting agents share the common property of inducing replication of an initiated mutant cell, thus transforming the initiated cell into a cancer cell. The promoting agent cannot cause cellular transformation unless the cell has been initiated, regardless of the intensity of exposure to the promoting agent. Promotion is dose dependent in its effect, and although promotion can transform a cell immediately after initiation, promotion is thought to be most successful when it involves repeated exposure to an initiated cell. Prevailing thought is that initiation is irreversible, whereas promotion is reversible. This belief has been demonstrated clinically in tobacco smokers: once the exposure to the promoter (tobacco) is withdrawn, the incidence of cancer is reduced.

Progression is the third stage of cancer growth. This stage may be subdivided into transformation, clonal progression, and metastasis. Transformation involves conversion of initiated cells to cancer cells. Clonal progression involves further growth of the small cluster of transformed cancer cells. The transformed cells contain mutated genetic material. As the transformed cells replicate, the progeny cells show more and more genetic abnormalities. Unless detected and treated, the cluster of cancer cells will continue to replicate in a somewhat unregulated fashion, ultimately metastasizing. Metastasis involves a change in location of the cancer cells from one organ or part of the body to another that is not directly connected.

Within normal human DNA material are genes that code cell growth–regulating substances. Oncogenes, thought to be part of normal human DNA material, are genes that produce abnormal codes for growth-regulating substances. Oncogenes are believed to play a role in the development of cancers because, once activated, oncogenes interfere with normal physiologic regulation of cell growth. Oncogene activation is believed to result in excessive production of cell growth–regulating substances. Because oncogenes can cause improper regulation of cell growth, they are capable of causing cancerous transformation in normal cells. The mechanism controlling oncogene activation is unclear; however, activation appears to be tightly controlled. The immune system is believed to play an important role in controlling oncogenes.

In 2003, researchers identified the sequence of the genome in the human body as part of the Human Genome Project. Each cell in the human body contains about 20,500 genes. Genes are the blueprints that direct growth and development. They are arranged in pairs and are made of genetic material called DNA. The totality of one’s genes is known as a genome. Genomics is the study of what genes do and their interaction with each other.

A growing area of cancer research, cancer genome research, studies the differences in genes found in tumors to understand which ones are important in the development and proliferation of a tumor. Researchers collect thousands of samples from different types of tumors to find a tumor’s genetic “fingerprint.” Different genes are involved in different tumor types, and understanding what genes are important to the development of cancer may lead to improvements in detecting, diagnosing, and treating cancer.

Studying or “mapping” the cancer genome helps researchers understand the mutated genes that lead to cancer. By identifying mutated genes that cause cancer to develop or spread, researchers hope to develop drugs that target those specific genes to stop the cancer’s growth. Also, identifying the genes responsible for cancer helps researchers and doctors develop tests to detect cancer earlier. The identification of many mutated genes in breast cancer, colon cancer, melanoma, and other cancers has led to the development of tests that can determine which treatment will be the most effective as well as to the development of several new treatments that target mutated genes. For example, the drug imatinib (Gleevec) treats chronic myeloid leukemia, gastrointestinal stromal tumors (GISTs), and several other types of cancer. Trastuzumab (Herceptin) is another example of a drug that works in treating breast cancers with a specific genetic mutation that causes tumors to have too much of a protein called HER2.

One of the biggest efforts underway to map the cancer genome is The Cancer Genome Atlas (TCGA) project. This project was started several years ago by the National Cancer Institute and the National Human Genome Research Institute. As part of TCGA, researchers are collecting tissue samples from patients treated at cancer centers across the United States. By studying these tissue samples and comparing them to tissue samples from people who do not have cancer, researchers will map the genomes of glioblastoma, lung cancer, and ovarian cancer. Depending on the results of this research, TCGA may map the genomes of other types of cancer.

Although some results of cancer genome mapping may not be ready for use in cancer treatment today, discoveries from this research may lead to better tests for diagnosing cancer, as well as more effective treatments (American Society of Clinical Oncology, 2007).

Immune function declines with age. Although immunogenic tumors can be more aggressive in older adults, solid tumors influenced by hormones are usually less aggressive. Environmental influences over the course of time are likely to have an effect on older adults in relation to prolonged exposure to carcinogens. Heredity may also contribute to cancer etiology. In addition to exposure to environmental carcinogens, the older adult may be at increased risk of developing cancer because of mutations in DNA repair or metabolic detoxification. Aging may also predispose older adults to increased cancer risks if they have inherited mutated genes. It remains unknown whether cancer in older adults is caused by any one of these factors or a combination of them (Coleman, Hutchins, & Goodwin, 2004).

Several mechanisms have been proposed to explain the way in which the aging process directly influences the cancerous transformation of cells (Box 19–2):

BOX 19–2 STAGES OF CANCER GROWTH AND INFLUENCE OF AGING ON CANCER DEVELOPMENT

STAGE OF CANCER GROWTH	INFLUENCE OF AGING ON CANCER DEVELOPMENT
Initiation	Longer time for exposure to agents that may cause cell mutations
	Aged cells more vulnerable to damage
Promotion	Longer time for exposure to dose-dependent cancer-promoting agents
	Aged cells less able to repair damage
Progression	Longer time for transformed cells to grow into cancer clusters
	Aged immune system resulting in decreased surveillance
	Increased oncogene activation, resulting in greater misregulation of cell growth
	Continued cluster growth for a time sufficient for development of clinical signs and symptoms

• Aging increases the duration of exposure to substances that may act as promoting agents. Because the effects of promoters are dose dependent, older adults can accumulate a significant dose over decades. Also, cellular transformations and progression of cancer cells occur over time. Cancer cells grow at various rates, and in some cases significant time is needed for the small cluster of cancer cells to grow large enough to cause signs and symptoms.

• Aging cells demonstrate a tendency toward abnormal growth. Aged cells are more vulnerable to damage; thus aging likely increases the susceptibility of cells to substances that cause genetic mutations.

• Once an aged cell is damaged by an initiating substance, it is more difficult to repair.

• Oncogene activation might be increased in older persons, resulting in increased loss of regulation of cell growth and the development of cancer cells.

• Decreased immune surveillance, or immunosenescence, may contribute to increased development of cancers and their progression, although the evidence on the role of the immune system in the development of cancer is inconclusive (Crawford & Cohen, 1987; Pfeifer, 1997a).

Aging and Cancer Prevention

The risk of cancer, either increased or decreased, frequently reflects changes in the habits of a particular birth cohort. Because most cancers are the result of a lifelong exposure, the risk of developing malignant disease after age 65 is probably already determined by the time one reaches that age. Frequently, cancer risk is similar for a given birth cohort within specific environmental boundaries. Although it appears difficult to undo or reverse the cellular damage sustained in younger years, prolonged exposure to promoting agents is nonetheless needed for the initiated cells to be transformed. If exposure to promoters can be avoided or reduced and antipromoters can be used, then cancerous transformation may not take place or may be delayed.

Interference with the promotion stage of cancer would seem to offer the best prospects for cancer prevention. Only recently has research included the search for interventions that halt the promotion phase. It is currently believed that fresh fruits and vegetables may contain antipromoters. Behaviors earlier in life that promote a predisposition to certain types of cancer can also be decreased; for example, limiting the number of severe sunburns in youth or reducing exposure by applying sunscreen may both be ways to interfere with the promotion stage of cancer. Secondary to this, various vitamins and minerals contained in foods are being examined for their effects on the promotion phase. Older adults should be encouraged to consume the recommended daily requirements of fruits and vegetables because dietary habits may be beneficial in halting the cancer process. In addition, evaluation of environmental risk factors can lead to specifically targeted education and screening programs among selected high-risk cohorts.

Common Malignancies in Older Adults

Breast Cancer

Breast cancer is the most common neoplasm in women, increasing in incidence with advancing age. The incidence of breast cancer is rising, although the death rate has been declining since the early 1990s. The disease will develop in 1 in 8 women who live to be 85, which is an approximate doubling of the incidence since 1970. Based on rates from 2004 to 2006, 12.08% of women born today will be diagnosed with cancer of the breast at some time during their life. Of all breast cancer cases, 80% occur in women older than age 50. From 2002 to 2006, the median age at diagnosis for cancer of the breast was 61 years.

Approximately 0.0% were diagnosed younger than age 20; 1.9% between 20 and 34; 10.5% between 35 and 44; 22.5% between 45 and 54; 23.7% between 55 and 64; 19.6% between 65 and 74; 16.2% between 75 and 84; and 5.5% at 85 years of age or older. The age-adjusted incidence rate was 123.8 per 100,000 women per year. These rates are based on cases diagnosed in 2002 to 2006 from 17 SEER geographic areas.

Breast cancer is the leading cause of death in women ages 55 to 74. Late-stage diagnosis is a serious concern for older adults. The primary presenting symptom is a lump in the breast; however, approximately 10% of women show symptoms of metastasis as the first indication of disease. The lung, liver, bones, and adrenal glands are predominant metastatic sites for breast cancer. Specific symptoms are related to the metastatic site and extent of disease (American Geriatric Society [AGS], 2000).

Although all women are at risk for developing breast cancer, the older a women is, the greater her chances of developing breast cancer. Breast cancer is more common in white women than in other racial or ethnic groups, but according to the most recent data, death rates are continuing to decline in white women. According to the SEER program of the National Cancer Institute (2009a), white Hawaiian and African American women have the highest incidence of invasive breast cancer in the United States. Korean, American Indian, and Vietnamese have the lowest incidence of invasive breast cancer in the United States. African American women have the highest death rate from breast cancer and are more likely to be diagnosed with a later stage of breast cancer in the age group 55 to 69. However, in the age group that is 70 years or older the death rate is higher for white women than for African American women (American Cancer Society, 2004a) (see Cultural Awareness Box).

Risk Factors

The risk of breast cancer increases with age. Dominant risk factors appear to be related to duration and intensity of exposure to hormonal influences, especially estrogen, and include early menarche (before age 12), late

CULTURAL AWARENESS

Cultural Considerations in Cancer

Patterns of cancer distribution among U.S. population groups vary according to racial and ethnic background. These patterns challenge nurses and other health care providers to discover explanations for the large differences in cancer incidence, mortality, and survival among the federally defined minority groups when compared with the white population.

African Americans have the highest overall rates of cancer incidence and cancer mortality of any U.S. population group. In 2005, the death rate for all cancers combined continued to be 33% higher in African American men and 16% higher in African American women than in white men and women. The overall 5-year relative survival rate among African Americans has improved from approximately 27% during 1960 to 1963 to 58% during 1996 to 2004. However, African Americans continue to be less likely than whites to survive 5 years at each stage of diagnosis for most cancer sites. The overall 5-year relative survival rate for cancer in African Americans is 11% below that of whites: 53% versus 64%. Of the 25 primary cancer sites for which survival data are available, all but three cancer sites (i.e., ovary, brain, and multiple myeloma) are associated with lower survival rates for African Americans (American Cancer Society, 2008).

Previously widely accepted reasons for this disparity centered around differences in survival status based on socioeconomic status and the overrepresentation of an ethnic group in the lower categories of socioeconomic status. Experts believed that socioeconomic status affected access to health services; nutritional status; immune status and function; educational level; employment; cancer prevention attitudes, awareness, and practices; and acceptance of cancer as a real and potential threat. All of these affect survival and, ultimately, mortality. However, a recent study (Albain, Unger, Crowley, et al 2009) was the first to find that the disparities remain even when African American patients receive identical medical treatment and other socioeconomic factors are controlled. Because patients of all races had the same doctors and received the same state-of-the-art treatments, it was a level playing field for everyone. These findings cast doubt on a widely accepted theory that African Americans’ lower survival rates for certain cancers are solely due to such factors as poverty and poor access to quality health care.

Higher Incidence Rates According to Location of Cancer

AFRICAN AMERICANS	HISPANICS	ASIAN/PACIFIC ISLANDERS (VARIES BY GROUP)
Prostate	Prostate	Prostate
Breast	Breast	Breast
Lungs and bronchus	Colon and rectum	Lungs and bronchus
Colon and rectum	Lung and bronchus	Colon and rectum
NATIVE AMERICANS (HIGHLY VARIABLE AMONG THE GREATER THAN 500 TRIBES)
Lung (Oklahoma Indians)
Gallbladder (Southwest Indians)
Liver (Alaskan Natives)

CULTURAL AWARENESS

Cultural Considerations in Breast Cancer Screening

Mammographic screening for early detection of breast cancer has been shown to be an effective method for reducing mortality in older women. Some women from ethnic minority groups have a high prevalence rate, whereas individuals from other groups such as middle-class whites have low prevalence rates. A study of women ages 75 and older by Caplan, Wells, and Haynes (1992) using national data found that 83.5% of African American women, 93.2% of Hispanic women, and 75% of white women have never had a mammogram.

Among women age 75 or older, African American and Hispanic women had markedly lower rates of clinical breast examination in the past year (23.4% and 20.5%, respectively) than white women (35.2%). The most common reasons for not having a mammogram among African American women age 65 or older was that the physician or nurse practitioner did not recommend one. For Hispanic and white women in this age group, the most common reason was that a mammogram was not perceived as necessary.

Barriers to early detection of breast cancer among women from ethnic minority groups were identified as the following: inaccurate knowledge of breast cancer and early screening, low awareness of the necessity for early detection, lack of health insurance to cover screening mammograms, and lack of reimbursement to health care providers for clinical breast examinations and health teaching for early detection. Virtually no data were available on the knowledge and attitudes of older adult Asian American and Native American women.

The researchers identified the following strategies to reduce barriers to early detection of breast cancer among older African American and Hispanic women:

• Educate health care providers about the necessity of early breast cancer detection and their role in recommending it to clients.

• Conduct research to identify culturally appropriate messages and intervention strategies for each of the at-risk groups to influence their early detection behaviors.

• Use the media to increase knowledge and promote positive early detection practices among older women from culturally diverse backgrounds.

menopause (after age 55), lengthy exposure to postmenopausal estrogen, recent use of oral contraceptives, and never having given birth or having first given live birth at a late age (after age 35) (Reigle, 2000). The highest incidence of breast cancer is in women ages 50 to 59. A first peak of incidence occurs between ages 45 and 49, when women are either premenopausal or menopausal. The high incidence in this age group is thought to be related to ovarian estrogen. A second peak of incidence occurs in women between ages 65 and 69, most of whom are postmenopausal. The second peak appears to be related to an imbalance of adrenal estrogen. Given these findings, breast cancer appears to be two separate diseases differentiated by menopausal status. Although hormones are not inherently mutagenic, they may act as initiators or promoters by altering cell reproduction and growth (Pfeifer, 1997a).

A major advance in understanding breast cancer is that the disease has a genetic basis. Approximately 5% to 10% of breast cancers are hereditary. The genes involved in most inherited breast cancers are BRCA1 and BRCA2. These are tumor-suppressor genes that also serve to protect and preserve DNA. Mutation of these genes has been linked to hereditary breast and ovarian cancer. A woman’s risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious BRCA1 or BRCA2 mutation. Men with these mutations also have an increased risk of breast cancer. Up to 40% of inherited breast cancers are due to mutations in BRCA1, and mutations in BRCA2 are responsible for up to 30% of inherited cancer (Cummings & Olopade, 1998; American Cancer Society, 2008).

Genetic tests are available to check for BRCA1 and BRCA2 mutations. Federal and state laws help ensure the privacy of a person’s genetic information and provide protection against discrimination in health insurance and employment practices.Currently many research studies are being conducted to discover newer and better ways of detecting, treating, and preventing cancer in carriers of BRCA1 and BRCA2 mutations (American Cancer Society, 2008).

High-fat diets and obesity have been suggested as risk factors, although the evidence is inconclusive. In animal studies the proliferation of breast tissue may be altered by changes in estrogen levels and pituitary and thyroid function, which are all sensitive to dietary intake (London & Willett, 1989). The risk associated with obesity may differ according to menopausal status and is thought to be associated with the metabolism of estrogen. Additional risk factors associated with breast cancer include pesticide and other chemical exposure, alcohol consumption, and physical inactivity (Knobf, 1996).

Radiotherapy is indicated postlumpectomy. Postoperative breast irradiation is well tolerated by older women; therefore age is not a contraindication to breast preservation treatment (Wyckoff et al, 1994). In general, older women treated for breast cancer do not experience greater complications or treatment toxicities when compared with younger women (Masetti et al, 1996). Although mastectomy is not the treatment of choice, if mastectomy is done, breast reconstruction is an option, depending on personal preference and the extent of the disease. As with all women, older women should be given information and support to help make treatment decisions. Breast cancer should be treated promptly but is not an emergency. Nurses should provide a supportive atmosphere and encourage family members to participate in treatment decisions.