Pathology > Study Images > Male Genitals > Prostate > Neoplasms
Objectives Anat & Hist Benign Neoplasms

III. Neoplasms


After completing this section you will know:

  • the clinical and histologic features of prostatic carcinoma
  • the serum markers for prostatic carcinoma
  • the importance of histologic grade and clinical stage in assessing treatment and prognosis of prostatic cancer
  • the typical radiographic appearance of prostatic carcinoma metastatic to bone
  • the management of occult carcinoma of the prostate

Carcinoma is the only common tumor of the prostate. Benign tumors are uncommon and rarely of clinical significance.


Prostatic adenocarcinoma is the most frequently diagnosed carcinoma in males. It occurs at an increasing rate with advancing age. It is rare before the age of 50 years and most patients are over 60 years at the time of diagnosis. The incidence of detected carcinoma of the prostate has increased dramatically due to new screening and biopsy techniques.

There are remarkable racial differences in incidence. The disease is rare in Asians and most common in blacks, who also have the highest death rates from prostatic cancer.

About 10% of cases are familial, with a significantly increased risk in men whose first-degree relatives have had the disease. No specific chromosomal abnormalities have been detected. The vast majority of cases are sporadic.

The cause of prostatic carcinoma is unknown. There is some suggestion but no proof yet that dietary fat may increase the risk of developing prostatic adenocarcinoma by influencing levels of testosterone, which in turn affects the growth of the prostate. There is no evidence of a relationship between nodular hyperplasia and carcinoma. The role of sex hormones in prostatic carcinoma is poorly understood. While it is clear that inhibition of prostatic carcinoma can be achieved with exogenous estrogens and orchiectomy, higher levels of serum androgens or significant alteration in their metabolism have not been shown consistently in patients with the disease. The role of androgens in prostatic carcinoma may be permissive, being required for maintenance of the neoplastic prostatic epithelium, which like their normal counterparts, have androgen receptors.

In most cases of prostatic carcinoma, foci of glands lined by dysplastic epithelium, referred to as prostatic intraepithelial neoplasia (PIN) are seen. PIN and carcinoma both occur in the peripheral zone and high grade PIN and invasive carcinoma have similar cytologic features. PIN is presumed to be the precursor lesion for invasive carcinoma.

Both early and advanced carcinoma of the prostate may be asymptomatic at the time of diagnosis and in the past more than 80% of patients had advanced or metastatic disease at the time of diagnosis. With screening programs, which employ digital rectal examination and serum PSA (see below) measurement, many prostatic carcinomas are diagnosed at an early stage. Symptoms when present include dysuria, difficulty of micturition, or increasing urinary frequency, and others referable to metastatic tumor. Clinically detectable disease usually manifests as firm to hard, nodular and irregular areas palpated transrectally. The cut surface of resected specimens shows hard, ill defined, gray to grayish-yellow nodules.

Histologically, the disease produces well-defined, readily discernable glandular patterns. The glands are usually small and lined by a single layer of cuboidal cells and may show papillary or cribriform patterns. Less often the glands are large and without papillary tufting while in poorly differentiated forms gland formation is rudimentary or absent. Mixed patterns are common.

Prostatic adenocarcinoma

Prostatic adenocarcinoma. Note single layer epithelium with moderate nuclear pleomorphism.

Prostatic adenocarcinoma, cribriform pattern.

In others there is no gland formation.

Prostatic adenocarcinoma. Note lack of gland formation.

Several histologic grading systems of prostatic carcinomas have been suggested because there is fairly good correlation with prognosis independent of the clinical stage. The combination of pathologic grade and clinical stage allows even better prediction of prognosis. Although stage and grade are often related in that high grade tumors tend to present at an advanced stage, this is not invariably so. Prognosis correlates with stage approximately as follows:



A (occult)


B (confined to gland)


C (extraglandular spread)


D (metastatic disease)



Perineural invasion, although common, has no prognostic significance.

Carcinoma of the prostate spreads by both hematogenous and lymphatic routes. The tumor spreads through the pelvic lymphatics to the lymph nodes around the internal and common iliac arteries and the aorta. Hematogenous spread via the pelvic veins and thence the inferior vena cava occurs late in the disease and produces systemic metastases. Generally, prostatic carcinoma shows a tendency to cause bony metastases, particularly to the vertebral column and pelvic bones, which are osteoblastic (increasing bone density) rather than osteoclastic (bone destruction).

Pale, osteoblastic metastases in several vertebral bodies.

X-ray of pelvic bones showing osteoblastic metastases.

Question: What is the possible anatomic explanation for the frequent occurrence of skeletal metastases in the lower vertebral column and pelvic bones in patients with carcinoma of the prostate?

Answer: There are many connections between the prostatic venous plexus and the vertebral veins. The veins forming the prostatic plexus do not contain valves and it is thought that straining to urinate causes prostatic venous blood to flow in a reverse direction and enter the vertebral veins carrying malignant cells to the vertebral column.

Biochemical markers for prostatic cancer include prostatic acid phosphatase and prostatic specific antigen (PSA). Prostatic acid phosphatase is typically elevated in patients with extraglandular disease and may be followed as a serum marker of disease progression. It cannot be used to reliably detect intraglandular (curable) disease at this time. Serum PSA is elevated in most patients with prostatic carcinoma, including many with disease confined to the gland. However, PSA is an imperfect marker because of reduced sensitivity (does not detect all cases of prostatic carcinoma due to false negative results) and lack of specificity (many false positive cases) as PSA may also be increased in some benign prostatic conditions such as nodular hyperplasia. Nonetheless, screening programs are increasingly employing serum PSA estimations, along with digital rectal examinations, as "first line" measures to identify patients for further study.

Treatment of prostatic adenocarcinoma is dependent on carcinoma. Surgical resection of lesions confined to the prostate is often curative. There is no good therapy for this tumor once it escapes the prostate gland and treatment for this stage of the disease is usually palliative. This includes a combination of radiation therapy, androgen deprivation (via use of estrogens or castration), and, less commonly, other chemotherapeutic agents or limited surgical resections of recurrent disease. Although the incidence of detected prostatic carcinoma has increased the mortality from the disease has not increased at all. Also the true frequency of prostatic cancer is considerably higher than its clinical incidence. The difference is due largely to higher frequency of occult carcinomas found at autopsy and specimens resected for nodular hyperplasia or in patients with marginally elevated PSA levels. These findings suggest that these small tumors have limited biologic potential and their treatment is therefore highly controversial. Depending on clinical circumstances (age, co-morbidities, patient’s wishes, etc), patients may be treated wit follow-up only, interstitial radiation (radioactive seeds), external beam radiation, or surgical resection (radical prostatectomy).

Objectives Anat & Hist Benign Neoplasms