Is there a link between BPH and prostate cancer?
of prostate-specific antigen (PSA) testing has dramatically influenced the detec - The relation between benign prostatic hyperplasia and prostate cancer was. Interestingly, the average PSA levels at baseline biopsy in both groups were very similar . The link between benign prostatic hyperplasia and prostate cancer. When the prostate increases in size, whether due to BPH, cancer, or other texture of the prostate; and the prostate-specific antigen (PSA) test.
PCa is an adenocarcinoma, which classically arises from epithelial cells located in the peripheral zone of the prostate gland alongside a small percentage arising from those cells that are located in the transition zone.
BPH and prostate cancer risk
Advances in healthcare quality and provisions globally and the resultant increase in worldwide life-expectancy will ultimately lead to a significant percentage of men that will face either BPH or PCa individually or in combination. Furthermore, with the advent of more screening and disease detection strategies that have been adopted in national healthcare commitments throughout the world, the incidence and pick-up rates of these diseases will naturally increase in the younger population of men.
Despite both these diseases being well established histologically, a definitive link between them has proven to be one that leads to a healthy debate and controversy within the urological community. Both diseases have striking similarities with regards to androgen-dependence driving their pathophysiology, inflammatory components which contribute to the development of the diseases, and shared genetic and epigenetic alterations.
However, a causal relationship between these diseases has not been established. This study did demonstrate a mixed outcome of incidence and mortality of BPH patients in relation to PCa, and the authors correctly highlighted that the differences in statistics may be from underlying health factors creating bias for surgical treatment choice.
Furthermore, all patients evaluated in this study were assessed in the pre-PSA era where two issues arise. First, the risk of prostate cancer-specific mortality associated with a finding of BPH will have been significantly higher. Second, the identification of PCa is made at an earlier stage during the current PSA-era in comparison to the pre-PSA era; therefore, the rate of discovering a new incidence of PCa from the surgical treatment of BPH has substantially decreased.
This figure increased to 3. Limitations of this study included that the diagnosis of BPH was not a histological one but clinical, the relatively homogenous nature of this population group, and the issue that the study included use of patients in the pre-PSA era. Despite large-scale studies demonstrating the epidemiological link between PCa and BPH, [ Table 1 ], studies contradicting this finding have concluded that there is no association between these diseases.
It has been over a decade since genetic overlapping between these two diseases was identified. However, the genetic and epigenetic insight into BPH has somewhat lagged behind relatively in comparison to the progress that has been made with PCa. With the utilization of technology, such as next-generation sequencing, it has provided us the ability to uncover disease-related variants by processing large genomic intervals in a rapid and thorough manner. Mutations in the HBOX13 gene have been established to be associated with the development of prostate cancer.
As expected, a mutation in HBOX13 was strongly associated with the prostate cancer specimens. However, BPH patients carrying this mutation had a 4. This is the first study to report genetic predisposition to developing PCa in BPH patients and gives a future potential of predicting those men with BPH who will later go on develop PCa.
Similarly, variants of numerous other genes have been shown to confer an increased risk of the development of both BPH and prostate cancer. In PCa, there are numerous genes that have been shown to be hypermethylated and hence inactivated, ultimately leading to the progression of prostate cancer.
Its loss of expression has been established in numerous cancers including PCa. Despite the progress made in the genetic and epigenetic insight in to prostatic disease, to-date, there are no genetic markers that are currently utilized in routine general clinical practice for either BPH or prostate cancer. Chronic inflammation is thought to be one of the numerous driving factors for the development of PCa.
Genes associated with inflammation have also demonstrated to be aberrantly expressed resulting in a pro-tumorigenic outcome in PCa. GSTpi are thought to have an important role in cancer prevention by providing cellular protection and subsequent inflammatory reaction.
This is achieved by preventing cellular damage from free radicals and other carcinogenic compounds. A recently reported study investigated the use of NSAIDs in the form of aspirin and ibuprofen in nearly men. There is limited evidence that the use NSAIDs may provide a protective effect in the development of prostate cancer.
Not only are androgens explicitly required for pathological growth of the prostate, they are vital for normal growth and development of this gland. This disrupted androgen cycle overcomes apoptosis within the prostate, therefore, disrupting the homeostatic regulation of prostate cell proliferation and cell death. The suppression of androgen activity on the prostate forms the basis of pharmacological treatment of both BPH and PCa. The hypothesis that higher circulating androgens may confer increased risk of prostate cancer has been assessed by large trials investigating the action anti-androgen agents have on the development of PCa.
However, on a cellular and molecular level, no study has shown that the development of BPH tissue has later converted into an oncological disease. Furthermore, the exact pathways of these prostatic diseases have yet to be fully understood. This is essential for us to optimize future treatment strategies for both diseases and an issue that future basic science studies should target.
Epidemiological data suggests that the presence of BPH increases the risk for a man to develop PCa in his lifetime. However, a causal link cannot be established from the current data. To determine the risk of the development of PCa of men presenting with BPH, we require further detailed epidemiological studies, which would ideally include a large cohort of men from a global platform.
Footnotes Conflict of Interest: Am J Manag Care. Normal histology of the prostate. The association of benign prostatic hyperplasia and cancer of the prostate. Prostate carcinoma risk subsequent to diagnosis of benign prostatic hyperplasia: A population-based cohort study in Sweden.
Is there evidence of a relationship between benign prostatic hyperplasia and prostate cancer? Findings of a literature review. Association of clinical benign prostate hyperplasia with prostate cancer incidence and mortality revisited: A urinary flow test measures the speed of your urine flow.
A post-void residual volume test measures how much urine is left in your bladder after you urinate.
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Tests to diagnose prostate cancer These tests can confirm a prostate cancer diagnosis: Ultrasound uses sound waves to make pictures of your prostate gland. A biopsy removes a sample of prostate tissue and checks it under a microscope for cancer. Which treatments you get for BPH depend on the size of your prostate and how severe your symptoms are. For mild to moderate symptoms, your doctor might prescribe one of these medicines: Alpha-blockers relax muscles in your bladder and prostate to help you urinate more easily.
They include alfuzosin Uroxatraldoxazosin Carduraand tamsulosin Flomax. They include dutasteride Avodart and finasteride Proscar. Doctors use surgery to treat severe BPH symptoms: Transurethral resection of the prostate removes only the inner part of the prostate. Transurethral incision of the prostate makes small cuts in the prostate to allow urine to pass through it.
Transurethral needle ablation uses radio waves to burn off extra prostate tissue. Laser therapy uses laser energy to remove excess prostate tissue.
Open prostatectomy is only done if your prostate is very large. The surgeon makes a cut in your lower belly and removes prostate tissue through the opening. Active surveillance or watchful waiting: A procedure called a radical prostatectomy removes the prostate gland and some of the tissue around it. Radiation uses high-energy X-rays to destroy prostate cancer.
Is there a link between BPH and prostate cancer?
Or you can get it through small radioactive pellets or seeds placed inside your prostate. This treatment uses intense cold to destroy prostate tissue. You take medicine to block the male hormones that fuel the growth of prostate cancer. Treatments should improve BPH symptoms.
You might have to keep taking the same medicine or go on a new treatment to prevent your symptoms from coming back. Surgery and other BPH treatments can have side effects such as trouble getting an erection or urinating. The outlook for prostate cancer depends on the stage of your cancer, or whether it has spread, and how far.
BPH vs. Prostate Cancer: What’s the Difference?
When treated, the five-year survival rate for all stages of prostate cancer is almost percent compared to men without this cancer. That means that when you eliminate other factors not related to prostate cancer, close to percent of men who are diagnosed and treated for prostate cancer are still living five years after treatment.
How often should you be screened?