You wouldn’t see Robert Daly (chairman of Warner Bros

14th Saturday, 2012  |   Uncategorized  |  no comments

Bueno ahora solo leo mi correo electronico y me voy a acostar despues de un agotador dia vida. Chaus. Tambien la Aleska me llevo un regalo. “At Columbia, the young executives who are in charge like Mark Canton, Peter Guber and Barry Josephson are interested in fashion and guys study them,” says one production executive at another company. “But that’s not true at Warner Bros. You wouldn’t see Robert Daly (chairman of Warner Bros.) in a Romeo Gigli suit.

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Then, after lots of feedback from Bon Appetit Digital Editor Dawn Perry, Watson began learning how to develop recipes. Think of the app as a sous chef in the kitchen. Type in a protein, a cuisine which can range from Indian to Mexican to British or French, and the computer creates something you’d never imagine..

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Rhein inhibits angiogenesis and the viability of hormone-dependent and -independent cancer cells under normoxic or hypoxic conditions in vitro.

11th Wednesday, 2012  |   Others  |  no comments

Hypoxia is a hallmark of solid tumors, including breast cancer, and the extent of tumor hypoxia is associated with treatment resistance and poor prognosis. Considering the limited treatment of hypoxic tumor cells and hence a poor prognosis of breast cancer, the investigation of natural products as potential chemopreventive anti-angiogenic agents is of paramount interest. Rhein (4,5-dihydroxyanthraquinone-2-carboxylic acid), the primary anthraquinone in the roots of Cassia alata L., is a naturally occurring quinone cialis for sale nz which exhibits a variety of biologic activities including anti-cancer activity. However, the effect of rhein on endothelial or cancer cells under hypoxic conditions has never been delineated. Therefore, the aim of this study was to investigate whether rhein inhibits angiogenesis and the viability of hormone-dependent (MCF-7) or -independent (MDA-MB-435s) breast cancer cells in vitro under normoxic or hypoxic conditions. Rhein inhibited vascular endothelial growth factor (VEGF(165))-stimulated human umbilical vein endothelial cell (HUVEC) tube formation, proliferation and migration under normoxic and hypoxic conditions. In addition, rhein inhibited in vitro angiogenesis by suppressing the activation of phosphatidylinositol 3-kinase (PI3K), phosphorylated-AKT (p-AKT) and phosphorylated cialis dose maximum extracellular signal-regulated kinase (p-ERK) but showed no inhibitory effects on total AKT or ERK. Rhein dose-dependently inhibited the viability of MCF-7 and MDA-MB-435s breast cancer cells under normoxic or hypoxic conditions, and inhibited cell cycle in both cell lines. Furthermore, Western blotting demonstrated that rhein inhibited heat shock protein 90alpha (Hsp90?) activity to induce degradation of Hsp90 client proteins including nuclear factor-kappa B (NF-?B), COX-2, and HER-2. Rhein also inhibited the expression of hypoxia-inducible factor-1 alpha (HIF-1?), vascular endothelial growth factor (VEGF(165)), epidermal growth factor (EGF), and the phosphorylation of inhibitor of NF-?B (I-?B) under normoxic or hypoxic conditions. Taken together, these data indicate that rhein is a promising anti-angiogenic compound for breast cancer cell viability and growth. Therefore, further studies including in vivo and pre-clinical need to be performed. Source: Fernand VE, Losso JN, Truax RE, Villar EE, Bwambok DK, Fakayode SO, Lowry M, Warner IM. Chem Biol Interact. 200mg cialis 2011 Jul 15;192(3):220-32. Epub 2011 Mar 30.

Cordyceps militaris Grown on Germinated Soybean Induces G2/M Cell Cycle Arrest through Downregulation of Cyclin B1 and Cdc25c in Human Colon Cancer HT-29 Cells

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Cordyceps militaris (CM) is an insect-borne fungus that has been used in traditional Chinese medicine because of its wide range of pharmacological activities. In this paper, we studied CM grown on germinated soybean (GSC) and investigated the possible mechanisms underlying antiproliferative effect of GSC on HT-29 human colon cancer cells. In comparison with CM extracts and germinated soybean (GS) BuOH extracts, BuOH extracts of GSC showed remarkable inhibitory and antiproliferative effects on HT-29 colon cancer cells. After GSC treatment, HT-29 cells became smaller and irregular in shape. High G2/M phase cell populations were observed in the GSC-treated group. The levels of cyclin B1 and Cdc25 in the GSC-treated group were lower than those in the control group. These findings suggest that GSC BuOH extracts might act as an effective anti-proliferative agent by inducing G2/M cell cycle arrest in colon cancer cells.
Due to the increasing incidences and relatively low remission rates of colon cancers, there is a need to establish more effective treatment regimens by adopting novel and innovative approaches [16]. The use of active medicinal compounds or extracts from traditional medicines or natural sources is considered as one such alternative treatment approach. Many naturally derived compounds/extracts are considered safe as they are obtained from commonly consumed foodstuffs. CM is a well-known medicinal mushroom that has been used in oriental medicine for treating various diseases, including cancers. Previous studies have demonstrated that CM has a wide range of pharmacological activities, including immunomodulatory and anti-inflammatory activities [7–11].Cancer cells generally exhibit few characteristics such as high proliferation, migration, and matrix-invasion potentials [17, 18]. Inhibition of tumor growth is one of the therapeutic targets in the development of anticancer agents. The regulation of tumor cell growth and the induction of cell death are the 2 major ways to inhibit tumor growth [19]. The present study evaluated whether GSC BuOH extracts had anti-proliferative activities against HT-29 cells. Although GSC BuOH, GS, and CM BuOH extracts exhibited anti-proliferative activity against HT-29 cells, GSC BuOH extracts showed anti-proliferative activity with the lowest IC50 (100??g/mL) value. Severely distorted HT-29 cells and loss of colony formation ability were observed after GSC BuOH treatment. We analyzed the changes in HT-29 cell cycle progression after GSC BuOH treatment by flow cytometry. Cellular proliferation is controlled by various genetically defined checkpoints, which ensure the progression of cells through the various stages of the cell cycle [20]. In cancer cells, cell cycle checkpoint control systems are known to be disrupted through the accumulation of mutations [21]. In the G2/M phase, damaged cells have the opportunity to repair DNA or permanently arrest cell growth if the degree of damage is severe [22]. Several anticancer agents arrest the cell cycle in G2/M phase, and then induce apoptosis and necrosis, resulting in cell death [23, 24]. In general, the G2/M transition is regulated by a complex of cell-division cyclins, namely, Cdc2 and a B-type cyclin [22]. The protein tyrosine phosphatase, Cdc25c, plays the role of a mitotic activator by dephosphorylating Cdc2/p34, which forms the Cdc2/cyclin B1 complexes that permit cells to enter into mitosis [25]. Many studies showed that Cdc2/p34 kinase activity was enhanced in some human cancer cells because of their genetic and epigenetic alterations [22]. Therefore, we investigated whether the expressions of the molecules involved in G2/M transition in HT-29 cells were altered after GSC BuOH extract treatment. We found that GSC treatment resulted in downregulation of Cdc25c and cyclin B1 expression in HT-29 colon cancer cells. The results of the present study indicated that GSC caused G2/M-phase cell cycle arrest along with a decrease in the levels of cyclin B1 and Cdc25c, which are involved in cell cycle progression from the G2/M phase. In addition, the identification of such compounds will improve our understanding of the anti-proliferative activities of GSC. Further experiments need to be done to clarify the anti-proliferative mechanisms of these identified compounds.
Mohammad Lalmoddin Mollah, Dong Ki Park, and Hye-Jin Park. Evidence-Based Complementary and Alternative Medicine Volume 2012. doi:10.1155/2012/249217
7. C. Park, S. H. Hong, J. Y. Lee et al., “Growth inhibition of U937 leukemia cells by aqueous extract of Cordyceps militaris through induction of apoptosis,” Oncology Reports, vol. 13, no. 6, pp. 1211–1216, 2005.
8. H. Lee, Y. J. Kim, H. W. Kim, D. H. Lee, M. K. Sung, and T. Park, “Induction of apoptosis by Cordyceps militaris through activation of caspase-3 in leukemia HL-60 cells,” Biological and Pharmaceutical Bulletin, vol. 29, no. 4, pp. 670–674, 2006. View at Publisher · View at Google Scholar
9. C. S. Kim, S. Y. Lee, S. H. Cho et al., “Cordyceps militaris induces the IL-18 expression via its promoter activation for IFN-? production,” Journal of Ethnopharmacology, vol. 120, no. 3, pp. 366–371, 2008. View at Publisher · View at Google Scholar · View at PubMed
10. J. Y. Han, J. Im, J. N. Choi et al., “Induction of IL-8 expression by Cordyceps militaris grown on germinated soybeans through lipid rafts formation and signaling pathways via ERK and JNK in A549 cells,” Journal of Ethnopharmacology, vol. 127, no. 1, pp. 55–61, 2010. View at Publisher · View at Google Scholar · View at PubMed
11. G. Y. Kim, W. S. Ko, J. Y. Lee et al., “Water extract of Cordyceps militaris enhances maturation of murine bone marrow-derived dendritic cells in vitro,” Biological and Pharmaceutical Bulletin, vol. 29, no. 2, pp. 354–360, 2006. View at Publisher · View at Google Scholar
16. D. M. Parkin, F. Bray, J. Ferlay, and P. Pisani, “Global cancer statistics, 2002,” Ca-A Cancer Journal for Clinicians, vol. 55, no. 2, pp. 74–108, 2005.
17. C. J. Sherr, “Principles of tumor suppression,” Cell, vol. 116, no. 2, pp. 235–246, 2004. View at Publisher · View at Google Scholar
18. M. Z. Fang, Y. Wang, N. Ai et al., “Tea polyphenol (?)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines,” Cancer Research, vol. 63, no. 22, pp. 7563–7570, 2003.
19. S. T. Huang, R. C. Yang, L. J. Yang, P. N. Lee, and J. H. S. Pang, “Phyllanthus urinaria triggers the apoptosis and Bcl-2 down-regulation in Lewis lung carcinoma cells,” Life Sciences, vol. 72, no. 15, pp. 1705–1716, 2003. View at Publisher · View at Google Scholar
20. M. A. Hoyt, “A new checkpoint takes shape,” Nature Cell Biology, vol. 6, no. 9, pp. 801–803, 2004. View at Publisher · View at Google Scholar · View at PubMed
21. B. C. Dash and W. S. El-Deiry, “Cell cycle checkpoint control mechanisms that can be disrupted in cancer,” Methods in Molecular Biology, vol. 280, pp. 99–161, 2004.
22. W. R. Taylor and G. R. Stark, “Regulation of the G2/M transition by p53,” Oncogene, vol. 20, no. 15, pp. 1803–1815, 2001. View at Publisher · View at Google Scholar · View at PubMed
23. W. T. Hsieh, K. Y. Huang, H. Y. Lin, and J. G. Chung, “Physalis angulata induced G2/M phase arrest in human breast cancer cells,” Food and Chemical Toxicology, vol. 44, no. 7, pp. 974–983, 2006. View at Publisher · View at Google Scholar · View at PubMed
24. J. Li, H. Y. Cheung, Z. Zhang, G. K. L. Chan, and W. F. Fong, “Andrographolide induces cell cycle arrest at G2/M phase and cell death in HepG2 cells via alteration of reactive oxygen species,” European Journal of Pharmacology, vol. 568, no. 1–3, pp. 31–44, 2007. View at Publisher · View at Google Scholar · View at PubMed
25. J. Gautier, M. J. Solomon, R. N. Booher, J. F. Bazan, and M. W. Kirschner, “cdc25 is a specific tyrosine phosphatase that directly activates p34cdc2,” Cell, vol. 67, no. 1, pp. 197–211, 1991.

Ellagic Acid – Chemopreventive Role in Oral Cancer

11th Wednesday, 2012  |   Others  |  no comments

Ellagic acid is an antioxidant and an anti-proliferative compound present in fruits, nuts and vegetables. In spite of evidences for anticancer activity in various cancer cell-lines, human cancer cells, the mechanistic role of ellagic acid is not conclusive enough to be recommended for a clinical use. The present review provides information about the chemopreventive role of ellagic acid in oral cancer and proposes molecular basis for ellagic acid’s inhibitory activity against oral cancer. We show that ellagic acid modulates growth of tumor cells through regulation of multiple cell signaling pathways including cell proliferation pathway (cyclin dependent kinase 2, cyclin A2, cyclin B1, cyclin D1, c-myc, PKC?), cell survival/apoptosis pathway (Bcl-XL, Bax, Caspase 9/3, Akt), tumor suppressor pathway (p53, p21), inflaming Metastasis pathways (IL-1 beta, TNF-?, matrix metalloproteinases 9/3, COX-2), angiogenesis pathways (VEGF), cell immortalization (TERT), NF-??.
Oral cancer is the 10th most common form of cancer worldwide. Developing countries share major global burden of deaths due to oral cancer; countries like India contributes ~ 26% of global oral cancer incidence. Oral cancer is 2nd most common form of cancer among Indian males [1]. Oral cancer is a multi-factorial disease which has implicating attributes like genetics, environmental, life-style and behavioral [2]. Around half of the patients detected for oral cancer will die within 5 years of initial diagnosis. Five year survival rate has not improved in spite of better understanding of cancer at a molecular level and with the advent of rationally targeted drugs [3].
Oral cancer develops by complex interplay between intrinsic and extrinsic factors playing important role in tumor development from primary lesion. The process of expression of tumorigenesis is based on a tightly controlled sequence of events which are dependent on the proper levels of transcription and translation of certain genes. There is a small subset that seems to be particularly important in the prevention, development, and progression of cancer. These genes have been found to be either malfunctioning or non-functioning in oral cancer. It is, therefore, logical to believe that success of any therapy will depend on its effectiveness to modulate these genes controlling different pathways to restore homeostasis. Molecular targets of ellagic acid are the key regulators, spread across all cancer hallmarks, which should make it an effective agent for prevention of oral cancer. Ellagic acid
is known to modulate key regulators like NF-??, p53 and CK2. The versatility of EA to inhibit oral carcinogenesis through multiple pathways makes ellagic acid a potent chemopreventive agent [4,5].
Bisen PS, Bundela SS, Sharma A (2012) Ellagic Acid – Chemopreventive Role in Oral Cancer. J Cancer Sci Ther 4: 023-030. doi:10.4172/1948-5956.1000106
1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C et al. (2008) Cancer Incidence and Mortality Worldwide: IARC Cancer Base No. 10.
2. Wake M (1993) The urban/rural divide in head and neck cancer–the effect of atmospheric pollution. Clin Otolaryngol Allied Sci 18: 298-302.
3. Massano J, Regateiro FS, Januario G, Ferreira A (2006) Oral squamous cell carcinoma: Review of prognostic and predictive factors. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 102: 67-76.
4. Hanahan D, Weinberg RA (2000) The hallmarks of cancer. Cell 100: 57-70.
5. Mantovani A (2009) Cancer: Inflaming metastasis. Nature 457: 36-37.

Cancer Chemoprevention: Prevention is Better than Cure

11th Wednesday, 2012  |   Others  |  2 comments

Rajendra Sharma

Cancer is one of the major causes of morbidity and mortality throughout the world. Carcinogenesis is a multistep molecular process induced by genetic and epigenetic changes that disrupt pathways controlling cell proliferation, apoptosis, differentiation, and senescence [1,2]. Therefore, several diverse approaches are required for the treatment and management of cancer which include radiation, chemotherapy, and surgical removal of malignant tissues.

Consistent with the old English proverb “Prevention is better than cure”, one of the multifactorial approaches to our fight against this dreaded disease is based on prevention of the disease through use of non-toxic dietary supplements, micronutrients and natural compounds. This approach is generally referred to as “chemoprevention” that is defined as the use of natural or synthetic agents that reverse, inhibit, or prevent the development of cancer. Thus the major goal of chemoprevention is to delay the onset of cancer as well as decrease its incidence. An effective chemoprevention requires the use of non-toxic agents that inhibit specific molecular steps in the carcinogenic pathway. It has been advocated that vegetarian diet may be an important source of cancer-inhibiting bioactive phytochemicals [3]. Although these compounds are generally viewed as non-essential for normal body functioning, an increasing number of them have been shown to possess biological activity relevant to disease-fighting and prevention of cancer. Interestingly, a number of population based studies indicate that people in South East Asian countries have much lower risk of developing colon, prostate, breast, lung and other cancers as compared to their Western counterparts. It has been suggested that constituents of their diet such as garlic, ginger, soy, turmeric, onion, tomatoes, cruciferous vegetables and green tea play a significant role in cancer prevention. Recognition of such an importance of diet in cancer prevention has finally lead to an accelerated pace of research in the area of chemoprevention. A number of bioactive compounds have been isolated from garlic, turmeric and cruciferous vegetables which showed significant potential to inhibit carcinogenesis. For example, diallyl disulfides present in garlic [4], isothiocyanates (such as sulforaphane) [5] from cruciferous vegetables, and curcumin [6] isolated from the turmeric have been shown to inhibit growth of various cancer cells types including prostate, breast, lung, colon and leukemia and skin [7]. During late 70s Wattenberg’s research group demonstrated that dietary chemicals including phenolic antioxidants can significantly inhibit chemical induced carcinogenesis in laboratory animals [8]. Studies conducted during last four decades have shown that both natural and synthetic chemopreventive agents essentially inhibit carcinogenesis by two major mechanisms 1) inhibition of carcinogen activation and 2) induction of xenobiotic metabolizing enzymes that protect from the toxic effects of environmental chemicals [9]. Besides these, other molecular targets shown to be inhibited by chemopreventive agents in cancer cells are: a) the proteins involved cell cycle progression and proliferation b) anti-apoptotic proteins c) drug transport, MDR, MRP d) growth factor pathway e) NF-kB activation pathway f) Angiogenesis g) inflammatory proteins such as COX-2 [3-9].

In this Special issue of the Journal of Cancer Science and Therapy on the Chemoprevention of Cancer we have included authoritative Reviews on the chemoprevention of prostate and colorectal cancer as well as original articles describing the efficacies of natural and synthetic chemopreventive agents in inhibition of prostate, lung and acute promyelocytic leukemia. These articles will not only benefit the researchers and clinicians working in this field but also to other scientists interested in exploring the significance of dietary supplements in the prevention of cancer. It is high time to appreciate the fact that economic burden associated with the treatment and management of cancer is huge and prevention of this disease by diet and dietary supplements is important to offset this burden. Basic and clinical research studies have already demonstrated the efficacy of chemopreventive agents in protection against cancer and other chronic diseases. Therefore, it is high time to channelize resources in this direction.
Sharma R (2012) Cancer Chemoprevention: Prevention is Better than Cure. J Cancer Sci Ther S3:e001. doi:10.4172/1948-5956.S3-e001
1. López-Lázaro M (2010) A new view of carcinogenesis and an alternative approach to cancer therapy. Mol Med 16: 144-153.
2. Jaffe LF (2003) Epigenetic theories of cancer initiation. Adv Cancer Res 90: 209-230.
3. Huber MH, Lee JS, Hong WK (1993) Chemoprevention of lung cancer. Semin Oncol 20: 128-141.
4. Conaway CC, Yang YM, Chung FL (2002) Isothiocyanates as cancer chemopreventive agents: their biological activities and metabolism in rodents and humans. Curr Drug Metab 3: 233-255.
5. Singh AV, Xiao D, Lew KL, Dhir R, Singh SV (2004) Sulforaphane induces caspase-mediated apoptosis in cultured PC-3 human prostate cancer cells and retards growth of PC-3 xenografts in vivo. Carcinogenesis 25: 83-90.
6. Fahey JW, Zhang Y, Talalay P (1997) Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proc Natl Acad Sci U S A 94: 10367-10372.
7. Fleischauer AT, Arab L (2001) Garlic and cancer: a critical review of the epidemiologic literature. J Nutr 131: 1032S-1040S.
8. Aggarwal BB, Kumar A, Bharti AC (2003) Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res 23: 363-398.
9. Surh YJ (2003) Cancer chemoprevention with dietary phytochemicals. Nat Rev Cancer 3: 768-780.