Prostate cancer forms when the rate of cell death and cell division are not equal, which leads to uncontrolled tumor growth. After the beginning of the transformational event, further mutation of a large number of genes, such as genes for p53 and retinoblastoma, that lead to tumor progression and proliferation of cancer. Around 95% of the prostate cancer are adenocarcinomas.
About 4% of the cases of prostate cancer have transitional cell morphology and believed to arise from the urothelial lining of the prostatic urethra. The few cases that have neuroendocrine morphology are believed to arise from the neuroendocrine stem cells normally present in the prostate or from aberrant differentiation programs during cell transformation.
Squamous cell carcinomas constitute less than 1% of all prostate carcinomas. In many cases, prostate carcinomas with squamous differentiation arise after radiation or hormone treatment.
Of prostate cancer cases, 70% arise in the peripheral zone, 15-20% arise in the central zone, and 10-15% arise in the transitional zone. Most prostate cancers are multifocal, with the synchronous involvement of multiple zones of the prostate, which may be due to clonal and nonclonal tumors.
When these cancers are locally invasive, the transitional-zone tumors spread to the bladder neck, while the peripheral-zone tumors extend into the ejaculatory ducts and seminal vesicles. Penetration through the prostatic capsule and along the perineural or vascular spaces occurs relatively late.
The mechanism for distant metastasis is poorly understood. Cancer spreads to bone early, often without significant lymphadenopathy. Currently, 2 predominant theories have been proposed for spread: the mechanical theory and the seed-and-soil theory.
The mechanical theory attributes metastasis to direct spread through the lymphatics and venous spaces into the lower lumbar spine. Advocates of the seed-and-soil theory, however, believe that tissue factors that allow for preferential growth in certain tissues, such as bone, must be present. Lung, liver, and adrenal metastases have also been documented. Specific tissue growth factors and extracellular matrices are possible examples.
The doubling time in early stage disease is variable. In the majority of cases, doubling time is longer than 4 years. Only a small percentage of prostate cancers double in less than 2 years. Doubling time tends to accelerate as the tumor grows and becomes more aggressive. Larger tumors usually have a higher Gleason grade and a faster doubling time.
The standard approach for grading prostate cancer depends on a Gleason score, which is based on pathologic evaluation of a prostatectomy specimen and is commonly estimated from prostate biopsy tissue. Prostate cancer patterns are assigned a number from 1-5; the score is created by adding the most common pattern and the highest-grade patterns.
This picture shows about how prostate cancer looks like under the microscope. Immunohistochemical stains showing normal basal cells(brown) in a benign gland with no basal cells in malignant glands (on the right side with no brown staining). Malignant glands show increased expression of racemase (red cytoplasmic stain).
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