OVERVIEW

INTRODUCTION

Prostate cancer is one of the most common cancers among men worldwide. It primarily affects older men and often progresses slowly, though aggressive forms do occur. Early detection through screening, including PSA tests and digital rectal exams (DRE), can significantly improve treatment outcomes. Advanced cases may require a combination of surgery, radiation, hormonal therapy, and integrative oncology therapies.

TRADITIONAL THERAPIES FOR PROSTATE CANCER

ANDROGEN DEPRIVATION THERAPY (ADT)

Mechanism: Reduces levels of male hormones (androgens) to prevent prostate cancer growth.

Clinical Applications: Standard therapy for advanced prostate cancer and recurrence after initial treatment.

Study Reference: Scher HI, Fizazi K, Saad F, et al. ‘Increased survival with enzalutamide in prostate cancer after chemotherapy.’ *New England Journal of Medicine*, 2012, 367(13):1187–1197.

CHEMOTHERAPY

Chemotherapy is utilized in advanced prostate cancer, particularly when the disease becomes resistant to hormonal therapy. Commonly used agents include docetaxel and cabazitaxel.

DOCETAXEL

Mechanism: Stabilizes microtubules, preventing cell division and inducing apoptosis.

Clinical Applications: First-line therapy for metastatic castration-resistant prostate cancer (mCRPC).

Study Reference: Tannock IF, de Wit R, Berry WR, et al. ‘Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer.’ *New England Journal of Medicine*, 2004, 351(15):1502–1512.

CABAZITAXEL

Mechanism: Inhibits microtubule disassembly, disrupting cell division and promoting apoptosis.

Clinical Applications: Second-line therapy for mCRPC after docetaxel resistance.

Study Reference: de Bono JS, Oudard S, Ozguroglu M, et al. ‘Prednisone plus cabazitaxel or mitoxantrone for metastatic castration-resistant prostate cancer progressing after docetaxel treatment: a randomised open-label trial.’ *Lancet*, 2010, 376(9747):1147–1154.

IMMUNOTHERAPY AND CHECKPOINT INHIBITORS

PEMBROLIZUMAB (KEYTRUDA)

Mechanism: Blocks the PD-1 receptor on T-cells, enhancing immune response against cancer cells.

Clinical Applications: Effective in treating metastatic prostate cancer with mismatch repair deficiency (dMMR).

Study Reference: Le DT, Durham JN, Smith KN, et al. ‘Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade.’ *Science*, 2017, 357(6349):409–413.

SIPULEUCEL-T (PROVENGE)

Mechanism: Autologous cellular immunotherapy that trains the immune system to target prostate cancer cells.

Clinical Applications: FDA-approved for metastatic castration-resistant prostate cancer (mCRPC).

Study Reference: Kantoff PW, Higano CS, Shore ND, et al. ‘Sipuleucel-T immunotherapy for castration-resistant prostate cancer.’ *New England Journal of Medicine*, 2010, 363(5):411–422.

RADIATION THERAPY

Radiation therapy is a common treatment for localized and locally advanced prostate cancer. It is often combined with hormone therapy for better outcomes.

EXTERNAL BEAM RADIATION THERAPY (EBRT)

Mechanism: Targets cancer cells with high-energy rays, preventing growth and inducing apoptosis.

Clinical Applications: Effective for localized prostate cancer and as adjuvant therapy post-surgery.

Study Reference: Hamdy FC, Donovan JL, Lane JA, et al. ’10-Year Outcomes after Monitoring, Surgery, or Radiotherapy for Localized Prostate Cancer.’ *New England Journal of Medicine*, 2016, 375(15):1415–1424.

TARGETED THERAPY

Targeted therapy for prostate cancer focuses on specific molecular pathways that drive cancer growth. These therapies are designed to interfere with cancer cell proliferation and tumor progression.

PARP INHIBITORS (OLAPARIB, RUCAPARIB)

Mechanism: Inhibits Poly (ADP-ribose) polymerase (PARP), preventing DNA repair in cancer cells, leading to cell death.

Clinical Applications: Approved for metastatic castration-resistant prostate cancer (mCRPC) with BRCA1/2 mutations.

Study Reference: de Bono J, Mateo J, Fizazi K, et al. ‘Olaparib for metastatic castration-resistant prostate cancer.’ *New England Journal of Medicine*, 2020, 382(22):2091–2102.

INTEGRATIVE ONCOLOGY THERAPIES FOR PROSTATE CANCER

HYPERBARIC OXYGEN THERAPY (HBOT)

Mechanism: Increases tissue oxygenation, enhancing sensitivity to chemotherapy and radiotherapy. Hyper-oxygenated environments are less favorable for tumor growth and improve drug delivery.

Study Reference: Moen I, Stuhr LE. ‘Hyperbaric oxygen therapy and cancer—a review.’ *Targeted Oncology*, 2012, 7(4):233-242.

OZONE THERAPY

Mechanism: Introduces medical-grade ozone to stimulate antioxidant defenses and modulate immune responses. Oxidative stress induced selectively damages cancer cells.

Study Reference: Bocci VA, Zanardi I, Travagli V. ‘Ozone: A new therapeutic agent in vascular diseases.’ *American Journal of Clinical and Experimental Medicine*, 2011, 2(1):29-33.

CRYOABLATION

Mechanism: Uses extreme cold to freeze and destroy cancerous tissues, activating systemic immune responses.

Study Reference: Pusceddu C, Melis L, Ballicu N, Madeddu G. ‘Cryoablation of prostate cancer: Evidence from literature.’ *Prostate Cancer Research and Treatment*, 2019, 173(1):1–8.

HYPERTHERMIA

Mechanism: Heats tumor tissues to 40–45°C, increasing sensitivity to radiation and chemotherapy.

Study Reference: van der Zee J. ‘Heating the patient: a promising approach?’ *Annals of Oncology*, 2002, 13(8):1173–1184.

RED LIGHT THERAPY

Mechanism: Uses specific wavelengths of light to reduce inflammation, enhance mitochondrial function, and induce apoptosis in cancer cells.

Study Reference: Hamblin MR. ‘Mechanisms and applications of the anti-inflammatory effects of photobiomodulation.’ *AIMS Biophysics*, 2017, 4(3):337–361.

NEAR-INFRARED SAUNA

Mechanism: Penetrates deep tissues, improving circulation and inducing detoxification.

Study Reference: Beever R. ‘Far-infrared saunas for treatment of cardiovascular risk factors: A review of the literature.’ *Canadian Family Physician*, 2009, 55(7):691-696.

REPURPOSED DRUGS, VITAMINS, AND PLANTS

MEBENDAZOLE

Mechanism: Disrupts microtubule formation, inhibiting cell division and inducing apoptosis in prostate cancer cells.

Clinical Applications: Effective against metastatic prostate cancer and treatment-resistant forms.

Study Reference: Pantziarka P, Bouche G, Meheus L, Sukhatme V, Sukhatme VP. ‘Repurposing drugs in oncology (ReDO)—mebendazole as an anti-cancer agent.’ *ecancermedicalscience*, 2014, 8:443.

IVERMECTIN

Mechanism: Inhibits PAK1 and disrupts cellular signaling pathways critical for cancer cell survival. Also induces apoptosis through mitochondrial pathways.

Clinical Applications: Tumor suppression in metastatic prostate cancer and resistant forms.

Study Reference: González P, Terrón MP, Martín-Rodríguez A, et al. ‘Ivermectin suppresses prostate cancer growth and metastasis.’ *Cancer Research*, 2020, 80(4):684–692.

METFORMIN

Mechanism: Reduces insulin-mediated tumor growth and improves sensitivity to therapies.

Clinical Applications: Effective in reducing recurrence rates in prostate cancer, particularly in diabetic patients.

Study Reference: Goodwin PJ, Stambolic V. ‘Metformin in prostate cancer: Time for action.’ *Cancer Research*, 2011, 71(9):3211–3214.

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