Biodegradable multiblock poly(N-2-hydroxypropyl)methacrylamide gemcitabine and paclitaxel conjugates for ovarian cancer cell combination treatment

Preface.-1. Global Overview of the Role of Nutraceuticals in Cancer.-2. Cancer Stem Cells: Novel Target Using Dietary Components for Prevention and Treatment.-3. Polyphenols as Receptor Tyrosine Kinase Inhibitors and Anti-Cancer Agents.-4. Role of Nutraceuticals on Nrf2 and Its Implication in Cancer Prevention.-5. Current Status and Future Prospects of Nutraceuticals in Prostate Cancer.-6. Cellular, Molecular and Biological Insight Into Chemopreventive and Therapeutic Potential Of 3, 3'-Diindolylmethane (Dim).-7. Mechanism of Action of the Anti-Cancer Agent, Triptolide.-8. Nutraceuticals in Human Urinary Bladder Cancer Prevention andTreatment.-9. Exploiting resveratrol for the treatment of cancer.-10. Role of novel nutraceuticals garcinol, plumbagin and mangiferin in the prevention and therapy of human malignancies: mechanisms of anticancer activity.-11. Anthocyanins and Cancer Prevention.-12. Slow but Steady Progress in Cancer Chemoprevention with Phenethyl isothiocyanate: Fulfilled Promises and Translational Challenges.-13. Skin cancer chemoprevention: Current status and future potential.-14. Dietary Phytochemicals and Chemoprevention of Solar Ultraviolet Radiation-Induced Skin Cancer.-15. The Role of Vitamin E Forms in Cancer Prevention and Therapy - Studies in Human Intervention Trials and Animal Models.-16. Augmenting the efficacy of chemo- and radio-therapy by nutraceuticals: Evidence from pre-clinical and clinical trials. Index.

Nutraceuticals and cancer

The aim of the present study was to determine the expression of p-Akt in ovarian serous carcinoma (OSC) and its association with proliferation and apoptosis. Paraffin-embedded tissues of patients aged between 35 and 64 years old without history of radiotherapy, chemotherapy and hormone therapy prior to surgery were collected. In total, samples included 12 ovarian serous cystadenomas (OSAs), 18 ovarian serous borderline tumors (OS-BTs) and 46 OSCs. Of the 46 OSC samples, 16 were well-differentiated, 20 were moderately differentiated and 10 were poorly differentiated, while 22 developed lymphatic metastases and 24 were metastasis-free. An additional 10 paraffin-embedded normal ovarian tissues (NOTs) were used as controls. Streptavidin-peroxidase immunohistochemistry assays were used to investigate the expression of p-Akt and cyclin D1 in the collected samples. Compared with NOT, p-Akt expression in the OS-BT and OSC groups, as well as cyclin D1 expression in the OSA and OSC groups, was significantly elevated (P 0.05). The expression of p-Akt, caspase-3 and cyclin D1 was positively associated with lymphatic metastasis (r=0.334; P=0.023). The expression of p-Akt gradually increased with carcinoma development and was associated with differentiation and metastasis of OSC, revealing that the activation of the PI3K/Akt signaling pathway is involved in the development of OSC. Furthermore, the expression of cyclin D1 gradually increased in the NOT, OSA, OS-BT and OSC groups and was associated with tumor metastasis.

/pdf/expression-of-p-akt-in-ovarian-serous-carcinoma-and-its-2oh93w35hl.pdf

Expression of p-Akt in ovarian serous carcinoma and its association with proliferation and apoptosis.

/pdf/growth-inhibition-and-apoptosis-induction-in-ovarian-cancer-2kb66o5rhi.pdf

Growth inhibition and apoptosis induction in ovarian cancer cells : molecular mechanisms

Ovarian cancer is the fifth most common cancer among women and approximately 200,000 women are diagnosed as ovarian cancer every year in the world (Parkin et al., 2005). Platinum-containing chemotherapeutic agents such as cisplatin (cisdiamminedichloroplatinum II) and carboplatin have been most frequently used for the treatment of ovarian cancer. These platinum compounds specifically react with guanine residues in DNA to form interstrand and intrastrand cross-links in DNA, known as DNAadducts. This interferes with mitosis of cancer cells and causes cell death. However, ovarian cancer cells can become resistant to cisplatin and the majority of patients develop cisplatinresistant disease (Giaccone 2000; Hennessy et al., 2009; Kartalou & Essigmann 2001), and as a result, most ovarian cancers relapse. Paclitaxel (taxol) and two analogues of camptothecin, irinotecan and topotecan, are the drugs most commonly administered to platinum-resistant ovarian cancer patients. Paclitaxel (taxol) binds to -tubulin and stabilizes microtubule structure, which causes a G2/M block in the cancer cell cycle. Irinotecan, also known as CPT-11 (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxy camptothecin) and topotecan (10-hydroxy-9-dimethylaminomethyl-(S)-camptothecin) inhibit topoisomerase I by resealing DNA breaks, which results in the inhibition of cancer cell growth (Bookman et al., 1998; Swisher et al., 1997). However, the survival rate for relapsed patients is low; Thus, there is an urgent need for more effective chemotherapeutic approaches for ovarian cancer treatment. We have previously reported that some ovarian cancer cell lines are remarkably sensitive to vitamin K2 (Shibayama-Imazu et al, 2003, 2006, 2008). In this review, strategies for developing chemotherapeutic agents for ovarian cancer are described and vitamin K2 is proposed as a promising chemotherapeutic agent for ovarian cancer.

/pdf/vitamin-k2-as-a-chemotherapeutic-agent-for-treating-ovarian-593z04gwmf.pdf

Vitamin K2 as a Chemotherapeutic Agent for Treating Ovarian Cancer

Standard therapy for the treatment of ovarian cancer is radical surgery followed by radiation and/or chemotherapy using cisplatin and paclitaxel. Unfortunately, some patients relapse after this first line chemotherapy and some patients become platinum-refractory. Therefore, we analyzed two different ovarian carcinoma cell lines for their sensitivity for gamma-irradiation and treatment with cisplatin, irinotecan, paclitaxel and gemcitabine. We found that both cell lines were rather resistant against gamma-irradiation and treatment with cisplatin and irinotecan whereas paclitaxel and gemcitabine resulted in a considerable reduction of the viability of the cancer cells. Both paclitaxel and gemcitabine treatment resulted in the induction of apoptosis. This sensitivity profile might be due to a particular subset of p53, which reacted with monoclonal antibodies DO-1 and PAb1801 but not with PAb1620 and PAb421. Gemcitabine and paclitaxel are highly efficient in the induction of apoptosis in ovarian cancer cells, which express a particular subset of the growth suppressor protein p53. Thus, a sensitivity profile for each ovarian carcinoma seems to be highly recommended before starting treatment.

/pdf/growth-inhibition-and-apoptosis-induction-in-ovarian-cancer-3qscx2ayy5.pdf

Growth inhibition and apoptosis induction in ovarian cancer cells

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Growth inhibition and apoptosis induction in ovarian cancer cells