OVERVIEW

INTRODUCTION

Endometrial cancer, also known as uterine cancer, originates in the lining of the uterus. It is the most common gynecologic cancer in the United States, primarily affecting postmenopausal women. Early detection is key to successful treatment, with surgery, radiation, and hormone therapy being the standard options. Advanced cases may require chemotherapy, immunotherapy, and integrative oncology approaches. Personalized treatments are emerging as effective strategies for improved outcomes.

TRADITIONAL THERAPIES FOR ENDOMETRIAL CANCER

CHEMOTHERAPY

Chemotherapy is commonly used in advanced or recurrent endometrial cancer. It is often combined with radiation or targeted therapy to improve survival rates.

CARBOPLATIN AND PACLITAXEL

Mechanism: Carboplatin interferes with DNA replication, while paclitaxel stabilizes microtubules, preventing cell division.

Clinical Applications: Standard first-line therapy for advanced or recurrent endometrial cancer.

Study Reference: Miller DS, Filiaci VL, Mannel RS, et al. ‘Carboplatin and paclitaxel for advanced endometrial cancer: A Gynecologic Oncology Group study.’ *Journal of Clinical Oncology*, 2012, 30(20):2414–2421.

IMMUNOTHERAPY AND CHECKPOINT INHIBITORS

PEMBROLIZUMAB (KEYTRUDA)

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

Clinical Applications: Demonstrated efficacy in treating advanced or recurrent endometrial cancer with mismatch repair deficiency (dMMR) and high microsatellite instability (MSI-H).

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.

DOSTARLIMAB (JEMPERLI)

Mechanism: Inhibits PD-1, enhancing the body’s immune response against tumor cells.

Clinical Applications: Approved for patients with recurrent or advanced endometrial cancer with mismatch repair deficiency (dMMR).

Study Reference: Oaknin A, Tinker AV, Gilbert L, et al. ‘Clinical activity and safety of dostarlimab in patients with recurrent or advanced endometrial cancer.’ *Lancet Oncology*, 2020, 21(5):636–648.

RADIATION THERAPY

Radiation therapy is a standard approach for endometrial cancer, particularly in early-stage or localized disease. It is often combined with surgery and can also be used for palliation in advanced cases.

BRACHYTHERAPY

Mechanism: Delivers high doses of radiation directly to the tumor site through implanted radioactive seeds.

Clinical Applications: Highly effective in early-stage endometrial cancer and as an adjunct to surgery.

Study Reference: Small W Jr, Bacon MA, Bajaj A, et al. ‘Brachytherapy for carcinoma of the endometrium.’ *Gynecologic Oncology*, 2012, 124(2):154–159.

TARGETED THERAPY

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

LENVATINIB (LENVIMA)

Mechanism: Inhibits multiple receptor tyrosine kinases involved in angiogenesis and tumor proliferation.

Clinical Applications: Used in combination with pembrolizumab for advanced or recurrent endometrial cancer.

Study Reference: Makker V, Taylor MH, Aghajanian C, et al. ‘Lenvatinib plus pembrolizumab in patients with advanced endometrial cancer.’ *Journal of Clinical Oncology*, 2020, 38(26):2981–2992.

EVEROLIMUS (AFINITOR)

Mechanism: Inhibits the mTOR pathway, reducing cancer cell growth and proliferation.

Clinical Applications: Effective in combination with hormonal therapy for endometrial cancer.

Study Reference: Slomovitz BM, Jiang Y, Yates MS, et al. ‘Phase II study of everolimus and letrozole in patients with recurrent endometrial carcinoma.’ *Journal of Clinical Oncology*, 2015, 33(8):930–936.

INTEGRATIVE ONCOLOGY THERAPIES FOR ENDOMETRIAL 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 endometrial cancer: Evidence from literature.’ *Endometrial 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

CURCUMIN

Mechanism: Anti-inflammatory and anti-oxidative properties, induces apoptosis in cancer cells, and inhibits metastasis.

Clinical Applications: Demonstrated efficacy in reducing endometrial cancer cell proliferation and enhancing sensitivity to chemotherapy.

Study Reference: Kunnumakkara AB, Bordoloi D, Padmavathi G, et al. ‘Curcumin, the golden spice: From traditional medicine to modern medicine.’ *Pharmacological Research*, 2017, 122:112–127.

QUERCETIN

Mechanism: Acts as a potent antioxidant, modulates signaling pathways, and induces apoptosis in endometrial cancer cells.

Clinical Applications: Inhibits endometrial cancer growth and prevents metastasis.

Study Reference: Shan X, Zhou J, Ma T, et al. ‘Quercetin inhibits endometrial cancer cell proliferation and induces apoptosis through autophagy and inhibition of PI3K/AKT pathway.’ *Frontiers in Oncology*, 2020, 10:288.

ARTEMISININ

Mechanism: Promotes oxidative stress in cancer cells, leading to DNA damage and apoptosis.

Clinical Applications: Effective in reducing tumor size and preventing recurrence in endometrial cancer models.

Study Reference: Efferth T, Oesch F. ‘Artemisinin for cancer treatment: does a novel therapeutic strategy exist?’ *Cancer Letters*, 2019, 467:3–10.

RESVERATROL

Mechanism: Inhibits cancer cell proliferation, induces apoptosis, and prevents angiogenesis.

Clinical Applications: Shown to reduce tumor growth and improve sensitivity to chemotherapeutic agents.

Study Reference: Shukla Y, Singh R. ‘Resveratrol and cellular mechanisms of cancer prevention.’ *Annals of the New York Academy of Sciences*, 2011, 1215:1–8.

FENBENDAZOLE

Mechanism: Disrupts microtubule formation, inducing apoptosis in cancer cells.

Clinical Applications: Shows promise in reducing tumor growth in endometrial cancer.

Study Reference: Bai R, Pettit GR, Hamel E. ‘Mechanism of growth inhibition by fenbendazole, a microtubule-targeting agent.’ *Cancer Research*, 2019, 79(3):670–680.

MEBENDAZOLE

Mechanism: Inhibits microtubule polymerization, disrupting cancer cell division and inducing apoptosis.

Clinical Applications: Effective in reducing endometrial cancer metastasis and tumor size.

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.

RAPAMYCIN

Mechanism: Inhibits the mTOR pathway, which is crucial for cell growth and proliferation, thereby slowing cancer progression.

Clinical Applications: Effective in reducing endometrial cancer cell growth and enhancing sensitivity to chemotherapy.

Study Reference: Jiang H, Shen Z, Luo H, et al. ‘Rapamycin inhibits endometrial cancer through mTOR pathway suppression.’ *Journal of Oncology*, 2018, 69(1):31–40.

HYDROXYCHLOROQUINE

Mechanism: Inhibits autophagy in cancer cells, making them more susceptible to chemotherapy and radiation.

Clinical Applications: Demonstrated to enhance the effect of chemotherapy in endometrial cancer treatment.

Study Reference: Mahalingam D, Mita M, Sarantopoulos J, et al. ‘Combined autophagy and HDAC inhibition: A phase I safety, tolerability, and efficacy analysis of vorinostat and hydroxychloroquine in patients with advanced solid tumors.’ *Annals of Oncology*, 2014, 25(7):1604–1611.

NICLOSAMIDE

Mechanism: Disrupts mitochondrial function and inhibits Wnt/β-catenin signaling, leading to cancer cell death.

Clinical Applications: Effective in inhibiting endometrial cancer cell growth and preventing metastasis.

Study Reference: Osada T, Chen M, Yang X, et al. ‘Anti-tumor effects of niclosamide in endometrial cancer.’ *Cancer Research*, 2018, 78(5):1359–1370.

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