Description
This detailed oncology presentation on prostate cancer covers the pathophysiology, risk factors, diagnostic parameters, and comprehensive treatment modalities for this common malignancy. The material outlines the molecular basis involving mutations in p53, BCL2, and Akt kinase signaling, alongside the role of androgens in disease progression. Key diagnostic tools such as Prostate-Specific Antigen (PSA) testing, digital rectal examination, biopsy with Gleason scoring, and imaging (MRI/CT) are explained for staging and metastasis evaluation. Treatment strategies range from surgery (prostatectomy) and radiotherapy to advanced hormonal therapies including Luteinizing Hormone blockers, anti-androgens, triple androgen blockade, and novel agents like enzalutamide and abiraterone. Chemotherapy options for castrate-resistant disease and bone-targeted therapies like radium-223 are also discussed. This resource is essential for medical students, oncology trainees, and practitioners in Zambia, providing structured, exam-focused content for understanding prostate cancer management within a tertiary medical education framework. Download these comprehensive notes for thorough preparation and clinical insights.
What's inside
PROSTATE CANCER PRESENTER: MWEWA MUSONDA MODERATOR; DR MWANZA Prostate Cancer Prostate cancer is the carcinoma of the carcinoma of prostate gland that may spread to other parts of the body, particularly bones and lymph Pathophysiology In prostate cancer, the cells of the prostate gland mutate into cancer cells. Mutation is majorly in p53 genes, BCL2 and ERK5 alternations in Akt kinase signaling contribute the development of prostate cancer The prostate gland requires hormones known as Androgens that are involved in cell survival apoptosis. Androgens include; testosterone, dehydroepiandrosterone and dihydrotestosterone. Initially, small clumps of cancer cells remain confined to the prostate gland, that’s carcinoma in situ or prostatic intraepithelial neoplasia. Overtime the cancer cells spread to surrounding tissue forming a tumor. Invades nearby lymph nodes or rectum or metastasize to bone. RISK FACTORS Obesity Age Family history Lower levels of vit.D Prostatitis Elevated blood levels of Testosterone SYMPTOMS Weak or interrupted urine flow Haematuria Nocturia Dysuria Pain in pelvis, spine and ribs Lymphedema Renal insufficiency DIAGNOSTIC PARAMETERS Prostate-Specific Antigen Blood Test PSA is a protein produced by the prostate gland, all men have a small amount in their blood and increases with age. In prostate, PSA production is increased which is a sign in early stages levels above 4.0 ng/ml is an indication for biopsy. 2. Digital Rectal Examination DRE is useful in ruling out prostate enlargement caused by benign prostatic hyperplasia. Diagnostic parameters 3. Biopsy Aids in the diagnosis and help to determine the Gleason score The lower the score the less likely the cancer will spread; A Gleason score of six or less means the cancer is unlikely to spread A Gleason score of seven means there is a moderate chance of the cancer spreading A Gleason score of eight means or above means there is a significant chance the cancer will spread Diagnostic parameters 4. MRI and CT Scan To access the extension into the bladder and lymph nodes for staging the cancer and to evaluate bone metastasis. TREATMENT Prostatectomy; Removal of prostate gland 2. Radiotherapy External beam radiotherapy and Brachytherapy[radioactive seeds] Hormone Therapy: The goal is to reduce levels of hormones, called androgens in the body or to prevent them from reaching prostate cancer cells There are different typesof drugs that lower testosterone levels Lteining Hormone (LH) Blockers: Luteinisin homorne blockers stop the pituitary gland maing the hormone. So the testicles don’t receive the message telling them to make testosterone Examples of LH blockers include - Leprorelin Gosereline Acetate Buserelin Triptorelin Histrelin LH blockers are given as injections or as implants under the skin Anti Androgens These stop androgens from woring by binding to he receptors and stop testosterone to bind with receptors so that cancer cant grow. Examples of anti adrogens include Bicalutamide Flutamide Enzaltamide Anti-androgen treatment may be combined with LH blockers as first line hormone therapy This is called combined androgen blockade (CAB) TRIPLE ANDROGEN BLOCKADE (TAB) Some doctors have suggested taking combined therapy one step further by adding a drug called 5-alpha Reductase Inhibitor (drugs that block the conversion of testosterone to the more active dihydrotestosterone (DHT) Either Finasteride or Dutasteride to the combined androgen blockade ENZALUMIDE This drug is a newer type of anti-androgen. When androgens bind t the androgen receptor, the receptor sends signal for the cells to grow and divide Enzalutamide blocks this signal from the androgen receptor to the cell ABIRATERONE (ZYTIGA) Recent advances have demonstrated that androgen-based pathways continue to have a clinically significant role in the progression of castrate-resistant prostate cancer (Relapse cases of cancer that are insensitive to androgens) In addition to androgen production b the adrenal gland and testis, several of the enzymes involved in the synthesis of testosterone and dihydrotestosterone including CYP 17 are highly expressed in tumor tissue especially in relapse cases ZYTIGA This is an oral androgen biosynthesis inhibitor that works by inhibiting the CYP 17 enzyme complex which is required for the production of androgens at these three sources (Adrenal gland, Testis and Prostate Tumor) Zytiga and prednisone combination is given in such cases Another new drug being studied known as Orteronel works in similar way to abiraterone. This drug may target CYP17 more precisel, which may do away with the …
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