Cancer Types


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Prostate Cancer
is the most common cancer in men and accounts for 25% of all male cancers, and is second to lung cancer as the leading cancer killer in men. The lifetime risk of a man getting prostate cancer is almost 16% or one in six (in African American men the risk is 20% or one in five). So in 2009 there were 192,000 new cases and over 27,000 deaths.

For basic information about prostate cancer start with anatomy then the NIH Booklet, the NCI patient page, the NCCN Site, the ACS site more patient information here and then read the other web sources
See nursing instruction sheets here.

For the role of diet go here. The seriousness, survival or prognosis of prostate cancer is related to the following key factors in the pull-down menu below (e.g. Gleason score or PSA)

New blood tests may replace PSA in the future (go here). Some of the things that increase the risk are noted below. There is increasing evidence of the role of genes in increasing the risk of this cancer (go here). There may be new molecular analyses that help that help predict prognosis more accurately than just Gleason score (e.g.genetic tests).




(note that prostate cancer is almost always adenocarcinoma, though there are unusual histological types , like transitional cell carcinoma which are treated differently.) The cancer usually involves both lobes of the gland (go here).

Prostate cancer is a malignant tumor that begins in the prostate gland of men. More than 95% of prostate cancers are adenocarcinomas, cancers that develop in glandular tissue.

The prostate is a walnut-sized gland located behind the base of the penis, in front of the rectum and below the bladder. It surrounds the urethra, the tube-like channel that carries urine and semen through the penis. The prostate's main function is to produce seminal fluid, the liquid in semen that protects, supports, and helps transport sperm.

Cancer develops when changes occur in DNA, the genetic material containing "instructions for growth and development" for all types of cells. When DNA is altered, normal cells may grow unregulated by the processes that normally control cell birth and death, and tumors can form.

Some prostate cancers grow very slowly and might not cause problems for years. Many men with slow-growing prostate cancer do not die from prostate cancer, but rather live with their disease. In this situation, the cause of death is usually not from prostate cancer, but other causes. However, if cancer does spread quickly to other parts of the body, treatment can help eliminate the cancer, and also control pain, fatigue, and other symptoms, and prolong life. Prostate cancer is somewhat unusual in that many patients with very advanced, metastatic cancer will respond to treatment and survive in excellent health for many years.

Prostate cancer is the most common cancer among men. In 2005, approximately 232,090 new cases of prostate cancer are expected to be diagnosed in the United States.
Prostate cancer is the second leading cause of cancer death in men, and an estimated 30,350 deaths are expected to occur in 2005. Although the number of deaths from prostate cancer is declining among all men, the death rate remains more than twice as high in blacks than in whites.

Ninety percent of all prostate cancer cases are discovered when the disease is limited to the prostate and surrounding organs. In these cases, nearly 100% of patients are expected to live at least five years after diagnosis. The overall relative five-year survival rate (the percentage of patients who survive after the cancer is detected, excluding those who die from other diseases) for all stages of prostate cancer is 99%. The 10-year and 15-year relative survival rates are 92% and 61%, respectively.
Risk Factors for Prostate Cancer Development (There is more evidence about the importance of genes in prostate cancer, go here.)


It is well-established that prostate cancer incidence increases dramatically with increasing age. While a very unusual disease in men younger than 50 years, rates increase exponentially thereafter. The registration rate by age cohort in England and Wales increased from 8 per thousand population in men aged 50 to 56 years to 68 per thousand in men aged 60 to 64 years, 260 per thousand in men aged 70 to 74 years, and peaked at 406 per thousand in men aged 75 to 79 years.

Family History

Approximately 15% of men with a diagnosis of prostate cancer will be found to have a first-degree male relative (brother, father) with prostate cancer, compared with approximately 8% of the US population. It has been estimated that approximately 9% of all prostate cancers may result from heritable susceptibility genes.


The development of the prostate is dependent upon the secretion of dihydrotestosterone (DHT) by the fetal testis. Other evidence suggesting that the degree of cumulative exposure of the prostate to androgens is related to an increased risk of prostate cancer includes the following:

  1. Neither BPH nor prostate cancer have been reported in men castrated prior to puberty.
  2. Androgen levels generally parallel prostate cancer risk in various populations of men. Although data are conflicting, a number of studies have demonstrated that levels of testosterone, and especially DHT, are highest in black males, of intermediate levels in white males, and lowest in native Japanese males.The risks for prostate cancer in these ethnic groups directly parallel these androgen levels.
  3. Androgen deprivation in almost all forms leads to involution of the prostate, a fall in PSA levels, apoptosis of prostate cancer and epithelial cells, as well as a clinical response in prostate cancer patients.


The risk of prostate cancer is dramatically higher among blacks, is of intermediate levels among whites, and is lowest among native Japanese. Survival is also related to ethnicity with 5-year survival with localized, regional, or metastatic prostate cancer being 94.7%, 86.6%, and 29.6%, respectively, for whites, compared with rates of 87.8%, 69.3%, and 22.7%, respectively, for blacks.

Dietary Fat

An interesting observation is that although the incidence of latent (occult, histologically evident) prostate cancer is similar throughout the world, clinical prostate cancer varies from country to country by as much as 20-fold. Previous ecologic studies have demonstrated a direct relationship between a country’s prostate cancer-specific mortality rate and average total calories from fat consumed by the country’s population. Studies of immigrants from Japan have demonstrated that native Japanese have the lowest risk of clinical prostate cancer, first generation Japanese-Americans have an intermediate risk, and subsequent generations have a risk comparable to the US population. Evidence from many case-control studies has generally found an association between dietary fat and prostate cancer risk, although studies have not uniformly reached this conclusion. In a review of published studies of the relationship between dietary fat and prostate cancer risk, among descriptive studies, approximately half found an increased risk with increased dietary fat and half found no association. Among case-control studies, again, about half of the studies found an increased risk with increasing dietary fat, animal fat, and saturated and monounsaturated fat intake while approximately half found no association. Only in studies of polyunsaturated fat intake were 3 studies reported of a significant negative association between prostate cancer and fat intake. In general, fat of animal origin seems to be associated with the highest risk. In a series of 384 patients with prostate cancer, the risk of cancer progression to an advanced stage was greater in men with a high fat intake. The announcement in 1996 that cancer mortality rates had fallen in the United States prompted the suggestion that this may be due to decreases in dietary fat over the same time period.