Living and Dying with Prostate Cancer
On the Sixth Anniversary of Dad's Passing
In early October 2006, just prior to my forty-ninth birthday, I met the love of my life. About six weeks later, Dan and I spent an idyllic Indian summer afternoon on the Sonoma coast. Perched atop a bluff overlooking the area where the Russian River empties into the Pacific Ocean, we watched the late afternoon sun lazily sink down to meet the horizon. We chatted about our hopes and dreams, as those who are in the early stages of a new relationship often do. During a momentary pause in the conversation, it became evident that Dan had something important that he wanted to discuss.
He quietly told me that ten months earlier he had undergone treatment for prostate cancer. He was particularly sensitive about my feelings because he knew that my dad had died from metastatic prostate cancer in late 2003.
Personal and Professional Experience
I’m very familiar with cancer from both personal and professional experience. On the personal level, my stepfather and a family friend had prostate cancer. More recently, Dan was affected by it and is now a two-year prostate cancer survivor. My brother was treated for lymphoma several years ago, and a year ago he was treated for colon cancer. A dear friend recently had a mastectomy. My mother is a four-year breast cancer survivor. Ironically, Mom had received the news of her breast cancer diagnosis during her vigil at my stepfather’s hospital bedside the afternoon before he died.
Professionally, from 1989 to 1993, during my career in public relations, I worked for a 450-bed regional hospital in the San Diego area. Grossmont Hospital had a respected oncology department that included an active patient education and outreach program. Many of the projects with which I was involved were in support of the oncology department and the new David and Donna Long Center for Cancer Treatment. I was part of the team that developed the cancer center’s promotional and educational materials for hospital employees, the public, and the media. I was involved with developing the center’s fund-raising materials and special events, including black tie dinners, golf tournaments, and 10-K fun runs.
Throughout my four years at Grossmont Hospital, I collaborated with oncologists, nurse educators, and hospital administrators to develop patient information brochures, newsletters, treatment information cards, and media awareness campaigns. I worked directly with patients who recounted their own stories to me. I spent a great deal of time with patient advocates, chaplains, licensed clinical social workers, and other allied health professionals who were involved in the hospital’s oncology department and the Cancer Treatment Center. I also spent a weekend with cancer survivors who celebrated their victories over the disease that had disrupted and changed their lives. The weekend was dubbed “We Can Weekend,” and the public awareness campaign I developed and implemented won recognition from my peers.
Healthy cells divide, fulfill their functions, and die. Cancer occurs when cells grow and divide abnormally (figure 1). Dixon (2004) wrote that cancer cells grow out of control and replace healthy tissue, creating tumors. These cellular abnormalities occur when a cell’s DNA (the cell’s information and control center) is damaged to such an extent that the DNA cannot repair itself (p. 66).
Fig. 1: When normal cells are damaged beyond repair, they are eliminated by apoptosis. Cancer cells avoid apoptosis and continue to multiply in an unregulated manner. (Wikipedia, from the National Cancer Institute, 2008).
Damage can occur to DNA as a result of heredity and/or environmental factors such as an unhealthful lifestyle or exposure to toxic substances. According to Dixon:
Most cancers result from genetic changes that occur over decades within the cells of a particular organ. These changes can usually be traced to an interaction of genetics and the environment, including behavior and lifestyle. Other factors that influence cancer risk are age, race, gender, preexisting disease, and nutritional impairment. (p. 66)
Apoptosis occurs during a cell’s normal life cycle and is a form of “programmed death.” When a cell doesn’t die because of genetic or biochemical interference with its normal process, it continues to divide and develops into a tumor (Genetech, 2008).
The abnormal cells replicate chaotically and rapidly. If the tumor remains in the originating organ without invading other organs, the cancer is localized. However, cancer cells can travel to other parts of the body through the circulatory and/or lymphatic systems in a process called “metastasis.” The cancer cells attach to their new locations, causing more tumors. In my stepfather’s case, prostate cancer cells metastasized to his lungs; this ultimately caused his death.
Frey (2002) described how cancer cells break down protein barriers to allow movement of the cells to other parts of the body (figure 2):
Once a cancer develops, the first stage in the development of metastasis is the tumor's penetration of the basement membrane, which separates epithelial tissue from underlying connective tissue. The basement membrane is a specialized layer of extracellular matrix, which is a mass of connective tissue fibers and proteins that support and nourish the body's connective tissues. Under normal circumstances, the extracellular matrix is a barrier that keeps cells from moving away from their sites of origin. Cancer cells, however, secrete several different types of enzymes that digest the proteins in the basement membrane. When the membrane has been sufficiently weakened, the tumor can push through it.
She indicated that metastatic lung cancer occurs in six of 100,000 people and that twenty to fifty-four percent of “…patients dying of cancer are found to have metastases in the lungs” (p. 697).
Fig 2: (1) A cell is transformed. (2) Cancerous cell proliferates and cells pile up to form a malignant tumor. (3) Angiogenesis: the tumor acquires a blood supply, which also allows (4) the cancer cells access into the circulatory system. (5) Cancer cells travel through the blood stream. (6) The cells stop in a capillary bed, and (7) adhere to the layer of cells that line the blood vessel. (8) The cells invade the essential, functional tissue of the organ surrounding the blood vessel. (9) In this new organ, cancer cells pile up to form secondary tumors, which (10) induce angiogenesis. (11) Metastases (secondary tumors) are now evident. (Illustration by Argosy Publishing in Frey, p. 698).
Prostate cancer, as its name suggests, occurs in the prostate gland, which is part of the male reproductive system. It is located at the base of the bladder and surrounds the upper part of the urethra (figure 3). The gland produces and stores semen, which combines with sperm during ejaculation. In prostate cancer, the gland’s healthy cells are replaced by cancerous cells (figure 4).
Fig. 3: Diagram of male pelvic area, including prostate (National Cancer Institute, 2008).
Prostate cancer is one of the most common forms of cancer in the United States. The National Cancer Institute (2000) indicated that, other than skin cancer, prostate cancer is the most common cancer diagnosed in American men. In 2007, Hsiao, Loescher, and Moore wrote that in this country, one in six men will be affected by prostate cancer, and it is the second leading cause of death in men. The American Cancer Society (2007) stated that prostate cancer is most prevalent among African-American men and is least prevalent among Asian-American and Latino-Hispanic men. The National Prostate Cancer Coalition (2008) reported that nearly 29,000 men will die from prostate cancer in 2008, compared with approximately 27,000 deaths in 2007.
While the specific cause of prostate cancer is not known, the National Prostate Cancer Coalition described several risk factors that are common among men who have the disease. They include:
· Age. Prostate cancer occurs most frequently in older men. It typically begins to appear in men who are fifty years old and older. Risk rises with age, increasing from one in thirty-nine between the ages of forty and fifty-nine, to one in seven between the ages of sixty and seventy-nine.
· Diet. Diets that include high amounts of sugar, animal protein, and saturated fat, and that are low in fruits and vegetables often are indicated in men with prostate cancer. Men who are obese also tend to have a higher incidence of prostate cancer, although there is no clear link between obesity and the disease. Since prostate cancer is linked to testosterone, some researchers believe that obesity may affect hormone function and therefore may play a role in the development of prostate cancer.
· Race and ethnicity. Race does appear to be a strong factor in the development of prostate cancer. Disease incidence and morbidity are highest among African-American men, with the lowest rates occurring in Asian-American and Hispanic men.
· Family history. Men who have a close relative who has or has had the disease are at double the risk for developing prostate cancer than those who have no family history of it. The risk increases almost exponentially in families that have two or more members affected by the disease.
Despite its high rate of occurrence, prostate cancer is one of the most easily diagnosed and most treatable cancers, with a high rate of long-term survival if the disease is detected and treated early in its progression.
In its early stages, there are no discernable symptoms, according to research conducted by Miller, Hafez, Stewart, et al (2003). They found that if the tumor is localized within the prostate, symptoms might not be present (Cancer 98: 1169).
In more advanced disease, symptoms listed by the National Cancer Institute (2000) include:
· Urination problems, including the inability to urinate, weak or interrupted flow, painful urination, the inability to start or stop urination, and frequent urination, especially at night;
· Difficulty or inability to have and/or maintain an erection;
· Pain with ejaculation;
· Blood in the semen or in the urine; and
· Chronic pain or stiffness in the pelvis, lower back, and/or legs.
Screening and Diagnosis
Symptoms of prostate cancer are similar to symptoms of other urological problems and aren’t always indicative of cancer. However, because symptoms generally don’t occur until prostate cancer is more advanced, the National Prostate Cancer Coalition (2008) suggested that regular screenings should commence for Caucasian men when they reach the age of fifty. For African-American men or for men who have other risk factors, regular screening is recommended to start as early as age thirty-five or forty.
The most common screening test is known as a “PSA test.” According to the Prostate Centre (2008), prostate specific antigen (PSA) is an enzyme that is produced in the prostate and is absorbed into the bloodstream. A simple blood test measures the amount of enzyme that is present. A normal PSA range is from zero to four nanograms per milliliter (ng/ml).
A number of factors can cause variations in PSA levels, including infection or inflammation, increased testosterone, and increased sexual activity. PSA levels also may be significantly lower in men who take medications for baldness and blood pressure.
Increased PSA levels aren’t necessarily indicative of the presence of prostate cancer. If a test indicates elevated PSA, additional tests may be done to determine whether it is a unique occurrence or whether additional diagnostic procedures are needed.
If the prostate is removed, PSA levels normally will decrease. If PSA levels continue to increase after the prostate is removed, it is an indication that the cancer cells have metastasized to other parts of the body, and further testing, diagnosis, and treatment are required (Malecare, 2008).
Digital rectal exam (DRE) is another technique that is used to detect the presence of a tumor or mass in the prostate. A physician inserts a gloved finger into the rectum to palpate the back of the prostate to feel whether it is lumpy or has areas of swelling (figure 5). If a mass is detected, additional tests are needed.
The combination of the PSA test and DRE is considered to be the most accurate form of prostate cancer detection (Prostate Centre, 2008).
Organizations such as the American Cancer Society, National Cancer Institute, and others recommend regular screenings to detect prostate cancer because early detection is considered to be the best chance of a cure. However, such screenings are controversial, according to Cherath and Johnson (2002). They wrote that the side effects of treatment could have a greater impact on quality of life than the disease itself:
The availability of an early detection system for prostatecancer with the development of the PSA serum test has complicated the treatment of this disease. Early detection of an often slow-growing cancer, where treatment can significantly impact the quality of life of the patient, can be complicated. Long-term studies are currently in progress that should provide the first real quantitative information about the relative efficacy of the different treatment options, the actual occurrence of side effects, and the comparative benefits of watchful waiting treatment compared with more aggressive action.
Even with concerns about whether regular screening is necessary, PSA testing is on the rise in the United States.
If prostate cancer is suspected as a result of the tests, a biopsy of the prostate is necessary to confirm whether cancer cells are present. Several core samples are taken with special needles that are inserted into the prostate through the rectum (figure 6). The tissue samples are viewed under a microscope to determine whether cancer cells are present.
Fig. 6: Biopsy of prostate. (Prostate Centre, 2008)
If cancer cells are found, a pathologist will analyze the cells to determine what stage the cancer is in. A “Gleason score” is used to determine the cancer’s stage. The higher the score, the more advanced the cancer (figures 7 and 8). The Gleason score aids in deciding upon an appropriate treatment and in ascertaining possible treatment outcomes.
Fig. 7: Gleason scale. (Wikipedia, 2008)
Low Grade (slow growth)
2 | 3 | 4
This is the least
dangerous type of cancer.
The cells look most like normal prostate cells and are described as being "well-differentiated".
This type of cancer tends to be slow growing.
Medium-grade (unpredictable growth)
5 | 6 | 7
may behave like low-grade or high-grade cancers.
The cells' behaviour may depend on the volume of the cancer and the PSA level.
This is the most common grade of prostate cancer.
8 | 9 | 10
High-grade cancers are
usually very aggressive and quick to spread to the tissue surrounding the
These cancer cells look least like normal prostate cells and are usually described as "poorly-differentiated".
Fig. 7: This chart describes the type of cancer usually associated with each grade of cancer. A lower Gleason grade indicates a well differentiated cancer, or a lower potential to spread. A higher Gleason grade indicates a poorly differentiated cancer, or more likely to spread. The Gleason grade is an important factor in the doctor’s decision to recommend a treatement plan to a patient. (Prostate Centre, 2008)
Additional testing may be called for to determine whether the cancer is confined to the prostate or whether it has spread to other organs and bones. These additional tests include computed tomography (CT), magnetic resonance imaging (MRI), and bone scans (Harvard Health Publications Group, 2006).
When prostate cancer is confirmed, many different treatment options are available depending on what stage the cancer is in and whether it is localized or has invaded other organs. Harvard Health (2006) suggested that several things need to be taken into account before deciding on a treatment plan:
· The extent of the cancer,
· Chance of cancer growth or spread,
· Age and life expectancy,
· General health, and
· Willingness to risk or deal with treatment side effects.
“Treatment in younger men is more aggressive, in part because it is thought that the nature of the disease may be biologically different from that found in older patients” (Stony Brook, 2006). According to all of the literature I have reviewed, the following are the most common treatments for prostate cancer:
· Watchful waiting. This involves monitoring the cancer on a regular basis.
· Radiation therapy. Radiation therapy kills cells, whether they are diseased or healthy. Two forms of radiation therapy are used most frequently in the United States:
1. External beam radiation provides a sequence of targeted doses of radiation to the prostate. There are intervals between doses, which allow the cancer cells to die while the healthy cells recover. Side effects include fatigue, incontinence, and impotency. Newer techniques minimize damage to surrounding tissues and nerves, however.
2. Brachytherapy. Approximately 100 small radioactive seeds or pellets are injected into the prostate. The seeds release a constant, localized dose of radiation in to the prostate for about six months, eventually killing the prostate. The seeds remain in place. There are fewer long-term side effects from this type of therapy. However, impotence, urinary and bowel problems can occur. Seeds can also migrate to other parts of the body, although this is rare.
· Surgery. A radical prostatectomy removes the prostate, seminal vesicles, and nearby pelvic lymph nodes. Many physicians believe this therapy provides the best chance of eliminating the disease. Side effects can include incontinence and impotency. Newer surgical techniques strive to preserve the nerves that control erections, sparing the patient from impotency.
· Hormone therapy. Prostate cancer is affected by testosterone levels. Hormone therapy restricts the growth of cancer cells by restricting testosterone. This can be accomplished by removing the testes, by taking an injection that blocks signals to the testes to produce testosterone, or by taking a pill to block testosterone from reaching the prostate. According to the Prostate Centre (2004), hormone therapy doesn’t cure the cancer, but it does slow the growth of cancer cells.
· The Prostate Centre (2004) indicated that alternative treatments are still being developed, including:
1. Trans Perineal Microwave Ablation of the Prostate (TAP). Microwave energy is delivered to the prostate by the use of needles. The prostate is heated to a point at which the cancer cells are killed.
2. Cryosurgery or, cryotherapy. This is the use of extreme cold to destroy the cancer cells.
3. Green Tea. Some studies suggest that green tea has an anti-tumor effect.
4. Chemotherapy. Anticancer drugs help to treat prostate cancer that has spread to other areas of the body.
5. Gene Therapy. This could cause the body to kill cancer cells that have metastasized to other parts of the body.
6. Nutrition Therapy. Reducing the intake of animal or saturated fats could help to prevent or slow the growth of cancer cells in the prostate.
Prostate cancer is one of the slowest cancers to grow and progress. It is rarely found in men younger than fifty, and it is most often discovered in men older than sixty, with the median age at diagnosis being seventy years (State University of New York School of Medicine Department of Urology, 2007).
The National Cancer Institute (2007) reported:
Almost 100% of men diagnosed with prostate cancer are still alive in 5 years*. Over 90% of prostate cancer cases are found while the cancer is still eitherlocal or regional, and nearly 100% of these men are still alive 5 years after being diagnosed. In cases where the cancer has spread to distant parts of the body, 34% survive 5 years. After 10 years, about97.9% of men diagnosed with early stage prostate cancer are still alive*, but only 17.6% of those diagnosed with advanced stage prostate cancer survive 10 years*.
*not including those who died from other causes.
According to Harvard Health (2006), after the cancer has spread, it’s very difficult to cure. However, many men in that situation live for many years. “In fact,” according to Harvard Health (2006), “many more men die from other causes while they have prostate cancer than die as the result of the cancer.”
The National Cancer Institute (2008) estimated that 186,320 new cases of prostate cancer will be diagnosed in the United States in 2008. The NCI also predicted that 28,660 men will die of the disease in 2008.
Even though prostate cancer is one of the most prevalent cancers in the United States, its cause is not known. In general, however, certain lifestyle behaviors are accepted as having the effect of reducing the chances of getting cancer. Carson-De Witt (2002) suggested the following actions as a means to prevent cancer and/or to reduce its risks:
· Eat plenty of fruits and vegetables and limit intake of animal fats and red meats,
· Get plenty of exercise and avoid weight gain,
· Avoid exposure to tobacco (including second hand smoke) and limit alcohol consumption,
· Limit sun exposure,
· Use “safe” sexual practices, and
· Avoid toxic chemicals and stay away from “known carcinogens in the environment or workplace.”
The Human Experience
My experience knowing men who have or have had prostate cancer supports the statistics. My stepfather was sixty-three years old when he was diagnosed and treated for prostate cancer in 1998. My mother recalled that prior to his diagnosis he had never had a PSA test or a digital rectal exam. He was a “typical man of his era” according to Mom. He was tested after he started to experience symptoms that included impotency and problems with urination. She encouraged him to see the family doctor, but he resisted. He assumed that these symptoms were related to aging, and that he “wasn’t an old man.”
After six months of symptoms, he finally agreed to see his doctor. Cancer was confirmed, and it appeared to be localized. He opted for surgical removal of the prostate. He had an artificial heart valve that required him to take blood thinners. To minimize the risk of serious bleeding, he was required to stop taking the medication several days before his prostate surgery. On the morning of the surgery, while he was being prepped for the procedure, he had a small stroke. His doctor was concerned about blood clots dislodging from the area around his valve and restarted the blood thinning medication. Surgery was no longer a possibility. Dad was sent home and scheduled to begin radiation therapy.
In the months following the radiation therapy, his doctors believed that the cancer had been arrested and that he would live to a ripe old age. For the first few months following the therapy he experienced fatigue and some discomfort when urinating. These symptoms mitigated over time. My mother reported that Dad had a very positive outlook and was optimistic about having beaten the cancer.
However, about two years later, he developed a chronic cough and began to experience symptoms that resembled bronchitis. His old habit of refusing to see his doctor prevailed until my mother took him to the doctor’s office herself. Testing revealed lung cancer, and additional tests indicated that the cancer cells had metastasized from the prostate.
He was treated for lung cancer with radiation, and it was believed that the lung cancer had been stopped. Unfortunately, some small tumors toward the back of his lungs were undetected, and his symptoms returned. Several months after his radiation therapy, he began chemotherapy. Shortly after his first round of chemotherapy, my stepdad went into shock. He died in the hospital shortly thereafter, in October 2003. My mother believes that had he had regular screenings earlier in his life, he would be a thriving seventy-year-old today.
In contrast, Dan (the love of my life) began regular PSA screening tests when he was in his early forties. His physician believed that it was important to establish a baseline against which to measure future test results.
An increase in his PSA level was noted in late 2003. A digital rectal exam didn’t reveal any masses or swelling, and Dan didn’t experience any symptoms related to prostate or urinary problems. He and his physician decided to adopt the “watchful waiting” strategy. A year later, Dan’s PSA level continued to rise. A biopsy revealed a very small tumor that was localized in the prostate.
Because his father had become ill, Dan decided to wait a little longer before undergoing treatment. Shortly after his dad died in late 2005, Dan had another PSA test. His PSA level had increased dramatically, and it became evident that treatment was imperative.
After becoming educated about the disease and reviewing his treatment options and their potential side effects, Dan chose to undergo brachytherapy in early 2006. He felt that, at forty-seven, he still wanted to be sexually active, and brachytherapy gave him the best chance of arresting the cancer while preserving his ability to achieve and maintain an erection.
The therapy’s side effects included painful urination, slow and weak stream, frequent urination at night, and fatigue. He worked a part-time schedule during the first six months after the therapy. About eight months following therapy, he began to feel better and started to date again. We met ten months after the seed implantation.
I am happy to report that a little more than two years after treatment, he experiences no residual effects from the therapy. He participates in a spiritual men’s group that provides him with an excellent support network. He has regular PSA tests, and his levels are well under the threshold for concern.
The concern about a recurrence always remains at the back of his mind. Naturally, I am also concerned, particularly after watching my stepdad’s five-year struggle with metastatic prostate cancer. But I know that Dan is well-educated about the disease and is very proactive about his health. He belongs to a different generation of men than Dad did.
I am looking forward to many more Indian summer evenings atop that bluff, watching the sunset at River’s End along the Sonoma coast. I am not afraid of a little cancer. I, too, am educated and proactive, and I am optimistic about Dan’s future and about our future together.
I hope my son never experiences prostate cancer, but the statistics are overwhelmingly against him. Screening methods, treatments, and education constantly evolve. If and when my son Andy has to meet that challenge, I am confident that he will be among the group of statistics in favor of a long, productive, and happy life.
American Cancer Society. (2007). Overview: Prostate Cancer. What Causes Prostate Cancer? Retrieved April 24, 2008:
Carson-DeWitt, R..(2002). Cancer. In Jacqueline
L. Longe (Ed.), Gale Encyclopedia of Medicine, Vol. 2(2nd ed., pp. 631-638). Detroit: Gale. Retrieved April
27, 2008, from Gale Virtual Reference
Library via Gale:
Cherath, L P & Johnson, M
M (2002). Prostate Cancer. In Ellen
Thackery (Ed.), Gale Encyclopedia of Cancer, Vol. 2(pp. 904-909). Detroit: Gale. Retrieved April
27, 2008, from Gale Virtual Reference
Library via Gale:
Dixon, B K. (2004)
"Cancer." Pollution A to Z. Ed. Richard M. Stapleton. Vol. 1. New York: Macmillan Reference USA, 2004. 6 pp. 2 vols. Gale
Virtual Reference Library. Gale. University of San Francisco. 28
R. J. (2002). Metastasis. In Ellen Thackery (Ed.), Gale
Encyclopedia of Cancer, Vol. 2(pp. 694-701). Detroit: Gale. Retrieved April
27, 2008, from Gale Virtual Reference
Library via Gale:
Genetech. (2008). Retrieved April 27, 2008: http://www.gene.com/gene/research/focusareas/oncology/apoptosis.html
Hsiao, C.P., Loescher, L. J., & Moore, I. M. (2007). Symptoms and Symptom Distress in Localized Prostate Cancer. Cancer Nursing: An International Journal for Cancer Care. 30(6), E19-E32. Retrieved April 23, 2008: <http://ovidsp.tx.ovid.com/spb/ovidweb.cgi>
MaleCare. (2007). PSA. Retrieved April 24, 2008: < http://malecare.com/prostate-cancer_77.htm>
Miller, DC; Hafez, K.S., Stewart, A., et al (2003). Prostate carcinoma presentation, diagnosis, and staging: an update from the National Cancer Data Base. Cancer 98: 1169. Retrieved April 24, 2008: < http://www3.interscience.wiley.com/cgi-in/abstract/104550881/ABSTRACT?CRETRY=1&SRETRY=0>
National Cancer Institute. (2008). Prostate cancer. Retrieved April 26, 2008: <http://www.cancer.gov/cancertopics/types/prostate>
National Prostate Cancer Coalition. (2007) Prostate cancer facts and statistics. Retrieved April 23, 2008: <http://18.104.22.168/~pcacoal/about_stats.htm>
“Prostate Cancer. (Disease/Disorder overview).” Health A-to-Z. Harvard Health Publications Group, 2006. NA. Academic OneFile. Gale. University of San Francisco. 25 Apr. 2008.
State University of New YorkSchool of Medicine Department of Urology. (2007). Prostate cancer FAQs. Retrieved April 25, 2008.
The Prostate Centre. (2007). Retrieved April 25, 2008: <http://www.prostatecentre.ca/>
Wikipedia. (2008). Prostate cancer. Retrieved April 23, 2008: <http://en.wikipedia.org/wiki/Prostate_cancer>