{"id":1381,"date":"2024-03-08T20:50:15","date_gmt":"2024-03-09T01:50:15","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=1381"},"modified":"2026-01-03T16:16:38","modified_gmt":"2026-01-03T21:16:38","slug":"prostate-cancer","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/prostate-cancer\/","title":{"raw":"Prostate Cancer","rendered":"Prostate Cancer"},"content":{"raw":"

Prostate Cancer - What is it?<\/strong><\/h3>\r\nThe glandular epithelial cells normally produce prostatic fluid which is required for sperm function.\u00a0 After, skin cancer, prostate cancer is the most common form of cancer in biological males (XY).\u00a0 Prostate cancer most often occurs at the age of 50 and is generally slow growing, meaning that routine screening can result in earlier diagnosis.\u00a0 Despite this, prostate cancer remains the 2nd most common cause of cancer death in males.\u00a0 In 95% of all prostate cancers, the glandular epithelial cells within the prostate (typically on the periphery) become cancerous through DNA mutations, and the cancer is considered an adenocarcinoma.\u00a0 Mutations often involve proto-oncogenes and tumor suppressor genes (TSG) that are responsible for regulating the rates of cell cycling, cell differentiation, and apoptosis.\u00a0 Mutations in p53 TSG are common in prostate cancer and lead to an inappropriate increase in cell proliferation and cells accumulate uncontrollably.\r\n\r\n \r\n

Prostate Cancer - Risk Factors and Prevention Strategies\u00a0<\/strong><\/h3>\r\nAge and country of residence are risk factors, with males living in countries with the highest economic indexes being the most at risk.\u00a0 \u00a0The balance of hormones are thought to play a role as some prostate cancers are androgen dependent and higher testosterone, androgen receptor levels, insulin-like growth factor-1 (IGF-1), and tall adult height are known risk factors.\u00a0 However, given that testosterone levels decrease with age and the fact that prostate cancer is rare before the age of 40, other factors are thought to play pivotal roles.\u00a0\u00a0 Family history, particularly having first-degree relatives that have been diagnosed with prostate cancer is a pre-disposing factor.\u00a0 Genetic susceptibility may be part of the reason Black males (of African or Caribbean ancestry) are more at risk for prostate cancer and more aggressive metastatic forms of prostate cancer, however socioeconomics can also be factors and are considered significant contributors to all diseases.\u00a0 Mutations in several genes (including BRCA1 and BRCA2) are risk factors. \u00a0Other pre-disposing factors include: abdominal obesity (apple-shape), high BMI, metabolic syndrome, and smoking.\u00a0 Additionally, sedentary behaviour, consumption of red meat and a high-fat, low-vegetable diet also all increase the risk of prostate cancer.\r\n\r\nPrevention strategies include healthy diet, regular physical activity, maintaining healthy BMI, and cessation of smoking.\r\n\r\n \r\n

Prostate Cancer - Signs and Symptoms<\/strong><\/h3>\r\nAs with many cancers, frequently there are no signs and symptoms until the cancer has developed.\r\n\r\nAs the growth of the tumor begins to impinge on the urethra, the first signs and symptoms can be similar to benign prostatic hyperplasia (BPH), and include lower urinary tract symptoms (LUTS):\u00a0 urinary frequency, urinary urgency, decreased urine flow rates, dysuria, and hematuria. There can also be erectile dysfunction and back pain, pelvis pain, or pain when sitting or when ejaculating.\r\n\r\nMore advance stages of metastatic prostate cancer include signs and symptoms that are common with other metastatic cancers:\u00a0 unexplained weight loss and anorexia (loss of appetite), fatigue, cachexia, anemia, and bone pain, pain and edema, and signs of kidney failure (e.g., uremic symptoms = high blood urea nitrogen, BUN and serum creatinine levels, pruritis, nausea, vomiting, brain fog, fatigue).\u00a0 Metastasis to local lymph nodes and bones of the pelvic girdle, vertebrae, ribs may occur without treatment.\r\n\r\n \r\n

Prostate Cancer - Diagnosis<\/strong><\/h3>\r\nScreening that involves assessing for increases in blood levels of prostate-specific antigen (PSA) as well as digital rectal exams (DRE) has allowed for asymptomatic cases to be diagnosed and treated earlier.\u00a0 DRE can reveal hard nodules on the prostate gland as well as changes in size or contour that can occur with prostate cancer.\u00a0 Prostate cancer found early have a 100% survival rate, whereas metastatic prostate cancer is rarely curable.\r\n\r\nPSA is a glycoprotein protease normally produced by the epithelial cells of the prostate gland and is an important component of seminal fluid.\u00a0 Interestingly, PSA is not as specific as it sounds, in that other tissues also produce this protein and it is found at low levels in biological females as well.\u00a0 In all people, small amounts of PSA enter the blood stream and the amount of PSA in the blood is indicative of the size of the prostate gland.\u00a0 PSA tests are generally more sensitive than DRE and are highly recommended due to their value in early detection.\u00a0 That being said, increases in PSA do not necessarily indicate prostate cancer, confirmational testing is required.\u00a0 Histological (microscopic) examination of a biopsy can confirm whether prostatic masses are cysts, benign, or malignant based on cell morphology (i.e., cellular appearance may indicate metaplasia, dysplasia, or anaplasia) and stage of undifferentiation.\u00a0 Typically, biopsies are guided by imaging (e.g., MRI or transrectal ultrasonography)\r\n\r\nBiopsies of the prostate gland and nearby lymph nodes, if positive for prostatic cancer, are frequently followed up with imaging (e.g., CT scans, MRI, bone scans, transrectal ultrasonography) to determine the location and extent of any spread (metastasis).\r\n\r\n \r\n

Prostate Cancer - Treatment<\/strong><\/h3>\r\n \r\n\r\nTreatments options for prostate cancer depend on the extent of spread and include:\r\n
    \r\n \t
  • surgery (e.g., TURP, radical prostatectomy, orchiectomy),<\/li>\r\n \t
  • chemotherapy,<\/li>\r\n \t
  • radiation therapy (often using brachytherapy, temporary implant of radioactive seed in prostate),<\/li>\r\n \t
  • hormonal therapy (e.g., anti-androgens, androgen suppressants and orchiectomy) and<\/li>\r\n \t
  • targeted therapy (e.g., inhibitors that block PARP enzymes required by BRCA1\/2 mutated cancerous cells)<\/li>\r\n \t
  • supportive treatments (e.g., support, counselling, nutrition plans, support for urinary incontinence and bowel problems).<\/li>\r\n<\/ul>\r\nSide Note:\u00a0 In addition to BRCA1, BRCA2, other genes that carry a risk of developing prostate cancer include:\u00a0 Herditary Prostate Cancer 1 and 2 (HPC1 and\u00a0 HPC2), HOXB13, HPCX, CAPB, ATM, and FANCA.","rendered":"

    Prostate Cancer – What is it?<\/strong><\/h3>\n

    The glandular epithelial cells normally produce prostatic fluid which is required for sperm function.\u00a0 After, skin cancer, prostate cancer is the most common form of cancer in biological males (XY).\u00a0 Prostate cancer most often occurs at the age of 50 and is generally slow growing, meaning that routine screening can result in earlier diagnosis.\u00a0 Despite this, prostate cancer remains the 2nd most common cause of cancer death in males.\u00a0 In 95% of all prostate cancers, the glandular epithelial cells within the prostate (typically on the periphery) become cancerous through DNA mutations, and the cancer is considered an adenocarcinoma.\u00a0 Mutations often involve proto-oncogenes and tumor suppressor genes (TSG) that are responsible for regulating the rates of cell cycling, cell differentiation, and apoptosis.\u00a0 Mutations in p53 TSG are common in prostate cancer and lead to an inappropriate increase in cell proliferation and cells accumulate uncontrollably.<\/p>\n

     <\/p>\n

    Prostate Cancer – Risk Factors and Prevention Strategies\u00a0<\/strong><\/h3>\n

    Age and country of residence are risk factors, with males living in countries with the highest economic indexes being the most at risk.\u00a0 \u00a0The balance of hormones are thought to play a role as some prostate cancers are androgen dependent and higher testosterone, androgen receptor levels, insulin-like growth factor-1 (IGF-1), and tall adult height are known risk factors.\u00a0 However, given that testosterone levels decrease with age and the fact that prostate cancer is rare before the age of 40, other factors are thought to play pivotal roles.\u00a0\u00a0 Family history, particularly having first-degree relatives that have been diagnosed with prostate cancer is a pre-disposing factor.\u00a0 Genetic susceptibility may be part of the reason Black males (of African or Caribbean ancestry) are more at risk for prostate cancer and more aggressive metastatic forms of prostate cancer, however socioeconomics can also be factors and are considered significant contributors to all diseases.\u00a0 Mutations in several genes (including BRCA1 and BRCA2) are risk factors. \u00a0Other pre-disposing factors include: abdominal obesity (apple-shape), high BMI, metabolic syndrome, and smoking.\u00a0 Additionally, sedentary behaviour, consumption of red meat and a high-fat, low-vegetable diet also all increase the risk of prostate cancer.<\/p>\n

    Prevention strategies include healthy diet, regular physical activity, maintaining healthy BMI, and cessation of smoking.<\/p>\n

     <\/p>\n

    Prostate Cancer – Signs and Symptoms<\/strong><\/h3>\n

    As with many cancers, frequently there are no signs and symptoms until the cancer has developed.<\/p>\n

    As the growth of the tumor begins to impinge on the urethra, the first signs and symptoms can be similar to benign prostatic hyperplasia (BPH), and include lower urinary tract symptoms (LUTS):\u00a0 urinary frequency, urinary urgency, decreased urine flow rates, dysuria, and hematuria. There can also be erectile dysfunction and back pain, pelvis pain, or pain when sitting or when ejaculating.<\/p>\n

    More advance stages of metastatic prostate cancer include signs and symptoms that are common with other metastatic cancers:\u00a0 unexplained weight loss and anorexia (loss of appetite), fatigue, cachexia, anemia, and bone pain, pain and edema, and signs of kidney failure (e.g., uremic symptoms = high blood urea nitrogen, BUN and serum creatinine levels, pruritis, nausea, vomiting, brain fog, fatigue).\u00a0 Metastasis to local lymph nodes and bones of the pelvic girdle, vertebrae, ribs may occur without treatment.<\/p>\n

     <\/p>\n

    Prostate Cancer – Diagnosis<\/strong><\/h3>\n

    Screening that involves assessing for increases in blood levels of prostate-specific antigen (PSA) as well as digital rectal exams (DRE) has allowed for asymptomatic cases to be diagnosed and treated earlier.\u00a0 DRE can reveal hard nodules on the prostate gland as well as changes in size or contour that can occur with prostate cancer.\u00a0 Prostate cancer found early have a 100% survival rate, whereas metastatic prostate cancer is rarely curable.<\/p>\n

    PSA is a glycoprotein protease normally produced by the epithelial cells of the prostate gland and is an important component of seminal fluid.\u00a0 Interestingly, PSA is not as specific as it sounds, in that other tissues also produce this protein and it is found at low levels in biological females as well.\u00a0 In all people, small amounts of PSA enter the blood stream and the amount of PSA in the blood is indicative of the size of the prostate gland.\u00a0 PSA tests are generally more sensitive than DRE and are highly recommended due to their value in early detection.\u00a0 That being said, increases in PSA do not necessarily indicate prostate cancer, confirmational testing is required.\u00a0 Histological (microscopic) examination of a biopsy can confirm whether prostatic masses are cysts, benign, or malignant based on cell morphology (i.e., cellular appearance may indicate metaplasia, dysplasia, or anaplasia) and stage of undifferentiation.\u00a0 Typically, biopsies are guided by imaging (e.g., MRI or transrectal ultrasonography)<\/p>\n

    Biopsies of the prostate gland and nearby lymph nodes, if positive for prostatic cancer, are frequently followed up with imaging (e.g., CT scans, MRI, bone scans, transrectal ultrasonography) to determine the location and extent of any spread (metastasis).<\/p>\n

     <\/p>\n

    Prostate Cancer – Treatment<\/strong><\/h3>\n

     <\/p>\n

    Treatments options for prostate cancer depend on the extent of spread and include:<\/p>\n

      \n
    • surgery (e.g., TURP, radical prostatectomy, orchiectomy),<\/li>\n
    • chemotherapy,<\/li>\n
    • radiation therapy (often using brachytherapy, temporary implant of radioactive seed in prostate),<\/li>\n
    • hormonal therapy (e.g., anti-androgens, androgen suppressants and orchiectomy) and<\/li>\n
    • targeted therapy (e.g., inhibitors that block PARP enzymes required by BRCA1\/2 mutated cancerous cells)<\/li>\n
    • supportive treatments (e.g., support, counselling, nutrition plans, support for urinary incontinence and bowel problems).<\/li>\n<\/ul>\n

      Side Note:\u00a0 In addition to BRCA1, BRCA2, other genes that carry a risk of developing prostate cancer include:\u00a0 Herditary Prostate Cancer 1 and 2 (HPC1 and\u00a0 HPC2), HOXB13, HPCX, CAPB, ATM, and FANCA.<\/p>\n","protected":false},"author":1370,"menu_order":26,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"Pictures coming soon!","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-1381","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":35,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1381","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":23,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1381\/revisions"}],"predecessor-version":[{"id":1506,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1381\/revisions\/1506"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/35"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1381\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=1381"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=1381"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=1381"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=1381"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}