OVERVIEW

INTRODUCTION

Cervical cancer develops in the cells of the cervix—the lower part of the uterus that connects to the vagina. It is primarily caused by persistent infection with high-risk human papillomavirus (HPV) strains. Cervical cancer is one of the most common cancers affecting women worldwide, though it is highly preventable through vaccination and early screening. Symptoms often include abnormal vaginal bleeding, pelvic pain, and discomfort during intercourse. Standard treatments include surgery, chemotherapy, radiation therapy, and emerging integrative oncology approaches. Personalized genomic medicine is paving the way for more effective and targeted treatments.

TRADITIONAL THERAPIES FOR CERVICAL CANCER

CHEMOTHERAPY

Chemotherapy is commonly used for cervical cancer, especially in advanced stages or when the cancer has metastasized. It is often combined with radiation therapy (chemoradiation) to enhance effectiveness. Chemotherapy may also be used before surgery to shrink tumors (neoadjuvant) or after surgery to eliminate remaining cancer cells (adjuvant).

CISPLATIN AND PACLITAXEL

Mechanism: Cisplatin forms DNA cross-links, preventing replication, while paclitaxel stabilizes microtubules, hindering cell division.

Clinical Applications: Standard first-line treatment for advanced cervical cancer and part of concurrent chemoradiation protocols.

Study Reference: Rose PG, Bundy BN, Watkins EB, et al. ‘Concurrent cisplatin-based radiotherapy and chemotherapy for locally advanced cervical cancer.’ *New England Journal of Medicine*, 1999, 340(15):1144–1153.

IMMUNOTHERAPY AND CHECKPOINT INHIBITORS

PEMBROLIZUMAB (KEYTRUDA)

Mechanism: Pembrolizumab is a PD-1 inhibitor that enhances the immune system’s ability to detect and destroy cancer cells.

Clinical Applications: Approved for recurrent or metastatic cervical cancer with PD-L1 expression, especially after chemotherapy failure.

Study Reference: Chung HC, Ros W, Delord JP, et al. ‘Efficacy and safety of pembrolizumab in previously treated advanced cervical cancer: results from the phase II KEYNOTE-158 study.’ *Journal of Clinical Oncology*, 2019, 37(17):1470–1478.

RADIATION THERAPY

Radiation therapy is a cornerstone in the treatment of cervical cancer, especially in advanced stages. It is often used in combination with chemotherapy (chemoradiation) to enhance its effectiveness. Two main types are used: External Beam Radiation Therapy (EBRT) and Brachytherapy.

EXTERNAL BEAM RADIATION THERAPY (EBRT)

Mechanism: Delivers high-energy rays to the tumor site from outside the body, shrinking tumors and killing cancer cells.

Clinical Applications: Often used for locally advanced cervical cancer and to prevent recurrence after surgery.

Study Reference: Morris M, Eifel PJ, Lu J, et al. ‘Pelvic radiation with concurrent chemotherapy compared with pelvic and para-aortic radiation for high-risk cervical cancer.’ *New England Journal of Medicine*, 1999, 340(15):1137–1143.

BRACHYTHERAPY

Mechanism: Involves placing radioactive material directly into or near the tumor site, delivering high doses of radiation while sparing healthy tissue.

Clinical Applications: Essential for treating locally advanced cervical cancer, often combined with EBRT.

Study Reference: Haie-Meder C, Potter R, Van Limbergen E, et al. ‘Recommendations from Gynaecological (GYN) GEC-ESTRO Working Group (I): Concepts and terms in 3D image-based treatment planning in cervix cancer brachytherapy.’ *Radiotherapy and Oncology*, 2005, 74(3):235–245.

TARGETED THERAPY

Targeted therapy for cervical cancer focuses on specific molecular pathways that contribute to cancer cell growth and survival. These therapies aim to inhibit cancer progression with minimal impact on healthy cells.

BEVACIZUMAB (AVASTIN)

Mechanism: Inhibits vascular endothelial growth factor (VEGF), reducing blood supply to tumors and slowing their growth.

Clinical Applications: Approved for persistent, recurrent, or metastatic cervical cancer in combination with chemotherapy.

Study Reference: Tewari KS, Sill MW, Long HJ, et al. ‘Improved survival with bevacizumab in advanced cervical cancer.’ *New England Journal of Medicine*, 2014, 370(8):734–743.

INTEGRATIVE ONCOLOGY THERAPIES FOR CERVICAL 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.

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.

HYDROGEN THERAPY

Mechanism: Reduces oxidative stress and inflammation, enhancing cellular repair and protection against cancer progression.

Study Reference: Ohsawa I, Ishikawa M, Takahashi K, et al. ‘Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals.’ *Nature Medicine*, 2007, 13(6):688–694.

EVALUATION OF CIRCULATING CANCER STEM CELLS

Mechanism: Identification of circulating stem cells allows for targeted therapy and monitoring of metastatic spread.

Study Reference: Alix-Panabières C, Pantel K. ‘Challenges in circulating tumour cell research.’ *Nature Reviews Cancer*, 2014, 14(9):623–631.

CHEMO-SENSITIVITY TESTING

Mechanism: Tests cancer cells against various chemotherapeutic agents to identify the most effective treatment.

Study Reference: Matsuo K, Eno ML, Im DD, et al. ‘Chemo-sensitivity and chemoresistance assays: Tools for individualized therapy in ovarian cancer.’ *Future Oncology*, 2010, 6(9):1411–1427.

METRONOMIC LOW-DOSE TARGETED CHEMOTHERAPY

Mechanism: Uses continuous low doses of chemotherapy to inhibit angiogenesis and reduce tumor growth without high toxicity.

Study Reference: Bertolini F, Paul S, Mancuso P, et al. ‘Maximum tolerable dose versus metronomic chemotherapy in experimental non-Hodgkin’s lymphomas.’ *Journal of Clinical Oncology*, 2003, 21(5):815–820.

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 cervical 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 cervical cancer cells.

Clinical Applications: Inhibits cervical cancer growth and prevents metastasis.

Study Reference: Shan X, Zhou J, Ma T, et al. ‘Quercetin inhibits 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 cervical 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 cervical 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 cervical 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 cervical cancer cell growth and enhancing sensitivity to chemotherapy.

Study Reference: Jiang H, Shen Z, Luo H, et al. ‘Rapamycin inhibits cervical 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 cervical 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 cervical cancer cell growth and preventing metastasis.

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

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