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Global Cancer Conference & Medicare Summit September 15-17, 2014 Hyderabad International Convention Centre, India 207 th OMICS Group Conference Page 99 GCC-2014 Posters

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Page 1: Posters - OMICS Publishing Group · 2015-01-21 · apoptosis, stimulating cell proliferation and inhibiting DNA repair. Over production of ROS may cause ‘oxidative stress’ which

Global Cancer Conference & Medicare SummitSeptember 15-17, 2014 Hyderabad International Convention Centre, India

207th OMICS Group Conference

Page 99

GCC-2014

Posters

Page 2: Posters - OMICS Publishing Group · 2015-01-21 · apoptosis, stimulating cell proliferation and inhibiting DNA repair. Over production of ROS may cause ‘oxidative stress’ which

Page 100

Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitGPCR Mediator cancer signalingAnkita BoxiNIT Rourkela, India

The chemokine receptor CXCR4 belongs to the large superfamily of G-protein-coupled receptors, and is directly involved in a number of biological processes including organogenesis, hematopoiesis, and immunity. Recent evidence shows the role

of CXCR4 in a variety of diseases including cancer and WHIM syndrome. Expression of CXCR4 in cancer metastasis appears to be due to dysregulation of the receptor leading to enhanced signaling. CXCR4 was also found to be a prognostic marker in various types of cancer including leukemia and breast cancer. These observations reveal that CXCR4 is an important molecule involved in several aspects of cancer progression. The SDF-1-CXCR4 axis is also involved in normal stem cell homing. Cancer stem cells also express CXCR4 suggesting that the SDF-1-CXCR4 axis directs their trafficking/metastasis to organs that highly express SDF-1 such as the lymph nodes, lungs, liver, and bones and the regulation of CXCR4 and how dysregulation contributes to disease progression.

[email protected]

Ankita Boxi, J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

Page 3: Posters - OMICS Publishing Group · 2015-01-21 · apoptosis, stimulating cell proliferation and inhibiting DNA repair. Over production of ROS may cause ‘oxidative stress’ which

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Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitWingless (WNT) antagonist, sFRP4 sensitizes glioblastoma stem cells to chemotherapeutic drug, doxorubicin by the apoptotic and antioxidant pathwaysPrathyusha PavanramNational Center for Biological Sciences, India

The treatment of glioblastomamultiforme (GBM) is a challenge worldwide in the field of oncology. Despite the development of advanced surgical interventions, radiation therapies and the use of multiple anti-cancer drugs, a cure for GBM remains

unclear. The low efficacy of current treatments is explained by the cancer stem cell hypothesis that verifies, solid tumours are maintained by a small population of cancer cells with stem cell properties and chemo-resistant properties. Hence, the key lies in improving the effectiveness of chemotherapy by targeting cancer stem cells (CSCs). This study aims at targeting glioblastoma CSCs obtained from the U138MG glioblastoma cell line, using an inhibitor of WNT pathway namely secreted frizzled related protein 4 (sFRP4).

Materials and Methods: Our methodology included the establishment of a successful protocol for U138MG sphere enrichment and characterization. Also standardisation of optimal concentrations of sFRP4 and Doxorubicin when used in combination for treatment purpose was done. After combination treatment, JC1 Assay, Colony Forming Unit assay, Secondary sphere formation assay, Differentiation assay, were done along with checking the anti-oxidant gene expression levels.

Results: Efficient U138MG sphere enrichment was seen when cells were grown on low adherent dishes using serum free medium supplemented with B27. The enriched spheres being CSCs showed positivity for markers like CD133, Nestin and p-glycoprotein. 125pg/ml concentration of sFRP4 and 50ng/ml concentration of Doxorubicin were found most suitable for usage as combination treatment in this study. The combination treatments on CSCs showed an increase in cellular apoptosis and differentiation ability. It also showed decrease in anti-oxidant gene expression and self-renewal ability.

Conclusion: This study demonstrates that the drug refractory CSCs are made more responsive to drugs such as doxorubicin upon treatment with sFRP4. This treatment also showed decreased stemness property of CSCs. Thus, this study opens up novel routes for better combinatorial cancer treatment.

[email protected]

Prathyusha Pavanram, J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitCancer stem-cells in oral cancer and pre-cancerAntony GeorgeMES Dental College, India

The traditional stochastic clonal expansion model for cancer hypothesized that a single cell having acquired mutations for transformation into a cancer cell yielded bulk of the primary tumor which comprised of cells having heterogenic

potential. “Cancer stem cell hypothesis” postulates that cancer heterogeneity is theresult of mutations that renders a normal stem cell cancerous, or cause a cancerous cell to develop stem cell-like characteristics. Cancer stem cells (CSC), like the somatic progenitor counterpart are capable of self-renew, differentiation into heterogeneous population, have modified anti-apoptotic properties, and are resistant to chemotherapy and radiation. In 2003, Clarke et al. first identified CSC in solid tumors, namely breast cancer. In 2007, Prince et al. identified subpopulation of head and neck carcinoma (HNSCC) cells that had CSC-like phenotype. Liu et al. in 2011 proposed the horizontal hierarchal model of CSC consisting of precancerous CSC, primary CSC, migrating CSC, and chemo-radio-resistant CSC. Traditional cancer therapies do not target CSC, and being chemo-radio-resistant they could be playing a major role in post-surgical recurrence and metastasis. Researchers are unsure of the utility of CSC surface and intra-cellular markers they studied, as their expression varied with the type of cancer and as different researchers obtained different results with the same bio-marker. Understanding CSC shall enhance our knowledge with regards to cancer initiation, progression, response to therapy, metastasis, and recurrence.

[email protected]

Antony George, J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitProtein coated gold nanoparticle synthesis: A mathematical model approach for proteasome inhibitionDevarai Santhosh Kumar, Sura Venkata Suresh Kumar and Kadhurla SrilathaIndian Institute of Technology Hyderabad, India

Cancer is characterized by the uncontrolled cell division and proliferation. As compared to normal cells, the NF-kB signaling pathway is highly active in multiple myeloma as well as in many other cancers. Inhibition of this pathway has

been shown to undermine the survival of myeloma cells, making NF-kB an attractive therapeutic target. NF-kB is activated by ubiquitin proteasome complex which ubiquitinates and degrades its inhibitor, I-kB. Inhibiting I-kB degradation leaves NF-kB in an inactive state and hence proteasomal inhibitors have great potential in cancer therapy. The reduction in NF-kB activity by proteasome inhibition reduces the cell proliferation and induces the apoptosis of multiple myeloma cells. The only proteasome inhibitor, bortezomib had been approved by US – FDA and few drugs under clinical trials to treat multiple myeloma. Here we propose ubiquitin tagged monoclonal antibody to Gold nanoparticles (Ub-AuNPs) with core diameter of <2 nm has comparable dimensions of proteasome subunits, can evolve as potential novel proteasomal inhibitors (PIs). The gold acts as a theranostic agent and it is having excellent biocompatibility where it directly attached to the highly oxidative stress of cancerous cells. In this model as the monoclonal antibody is already ubiquitinated it easily finds its way to proteasome of myeloma cells. Further we use a mathematical model to analyze how these monoclonal antibody associated with gold nanoparticles enter to the target site for proteasome inhibition. And also gives an idea about proposed mechanism of inhibition by invading the proteasome and block the lumen of proteasomes, further inhibiting the degradation of I-kB. Thus, PIs has emerged as a powerful strategy for treatment of multiple myeloma (MM).

[email protected]

Devarai Santhosh Kumar et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

Page 6: Posters - OMICS Publishing Group · 2015-01-21 · apoptosis, stimulating cell proliferation and inhibiting DNA repair. Over production of ROS may cause ‘oxidative stress’ which

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Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitHPLC Screening of Clerodendrum viscosum leaf extract show possible photochemical responsible for antioxidant and anticancer activitiesDipankar Chaudhuri, Nikhil Baban Ghate, Sourav Panja, Tapasree Basu Mallik and Nripendranath MandalBose Institute, India

The use of herbal based medicine is gaining importance worldwide and medicinal plants are believed to be an important source of new lead chemicals with potential therapeutic effects. Free radicals play a key role in many degenerative diseases

such as cardiovascular disease, cataracts, weak immune system, brain dysfunction and cancer. Antioxidants modify the behavior of cancer cells by changing their redox surroundings as well as reduce their genetic instability and can be appraise as an innovative way for cancer therapy. Traditionally C. viscosum leaf was used in the folklore medicinal practices in anthelmintic, metic, mild laxative cholagogue, skin diseases and tumors. Initial screening for in vitro antioxidant and anticancer activity of 70% methanolic extract of C. viscosum leaf (CVLM) exhibited significantly promising results. The antioxidant property of hexane, chloroform, ethyl acetate and water fractions of CVLM was evaluated. The chloroform and ethyl acetate fractions displayed better antioxidant efficacy. So, the samefractions were tested on human breast cancer (MCF-7) as well as human lung adenocarcinoma epithelial cell line (A549) for their cytotoxicity and cell cycle distribution. The presence of phytochemicals in the fractions was assessed through high performance liquid chromatography (HPLC). Ethyl acetate fraction possessed highest cytotoxic activity on MCF-7 cells followed by chloroform fraction and it also further confirmed by cell cycle distribution. Since, the chloroform and ethyl acetate fractions exhibited potent antioxidant as well as anticancer activity, it was concluded that the phytochemicals in different fractions are responsible for antioxidant property could be useful in cancer treatment.

BiographyDipankar Chaudhuri is completing his PhD under the guidance of Prof. Nripendranath Mandal from Bose Institute and the University of Calcutta, India. He is a dynamic Researcher in the field of isolation of newer bioactive moleculesfrom Indian medicinal plants, along with assessing their antioxidant and anticancer capacities. In this respect, he has published 18 research articles in reputed international peer-reviewed journals.

[email protected]

Dipankar Chaudhuri et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitAntioxidants from indegenous medicinal plants inhibit proliferation of ascitic cancer cellsSourav Panja, Nikhil Baban Ghate, Dipankar Chaudhuri and Nripendranath MandalDivision of Molecular Medicine, Bose Institute, P-1/12 C.I.T. Scheme VII M, Kolkata-700054, India

A number of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are essential parts of aerobic life and metabolism. ROS and RNS are normally generated by tightly regulated enzymes, such as NAD(P)H oxidase isoforms

and NO synthase (NOS), respectively. Free radicals increase tumorigenesis by causing DNA damage and mutation, inhibiting apoptosis, stimulating cell proliferation and inhibiting DNA repair. Over production of ROS may cause ‘oxidative stress’ which leads to the development of many diseases such as cancer, diabetes, neurodegenerative disorders, liver injury, and cardiovascular disease. Reduction of unstable and reactive free radicals, induction of apoptosis, and inhibition of cell proliferation can be achieved via antioxidants that protect cells from free radical attack. We hope to identify natural antioxidants from herbal medicine as sources for replacing synthetic antioxidants, which are limited by their adverse side effect. Previously, it is reported that 70% methanol extract of Terminalia chebula, Terminalia belerica, Emblica officinalis and Spondias pinnata showed excellent efficacy in their antioxidant and radical scavenging abilities, compared to the standards. Cytotoxic effect of various doses of all four extracts were also observed in vitro on Ehrlich’s Ascites Carcinoma (EAC) cells and normal splenocyte cells. These extracts showed significant cytotoxicity against EAC cells and found non-toxic to splenocytes. This study suggests that 70% methanol extract of the same four plants might be useful as potent sources of natural antioxidant and could be useful in cancer treatment.

BiographySourav Panja is pursuing his Ph.D. under the guidance of Prof. Nripendranath Mandal from Bose Institute, Kolkata, India. He is a dynamic researcher in the field of antioxidant activity of Indian medicinal plants, along with their anticancer and anti-inflammatory capacities. In this respect, he has published 3 papers in reputed international peer-reviewed journals.

Sourav Panja et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitRole of CD151 in the induction of EMT in cancer stem cellsGayatri Devi V, Anil Kumar Badana, Nagaseshu Pudi and Rama Rao MallaGITAM University, India

Solid tumor contains highly malignant subpopulation of cells with stem cell properties like self-renewal, tumorigenecity and differentiation. Recent reports have suggested that epithelial mesenchymal transition (EMT) induction enhances self-

rejuvenation and acquires stem cell properties. EMT is an orchestrated event characterized by switching of marker from non-motile epithelial to invasive mesenchymal cells. The major changes during EMT include loss of E-cadherin, Rho dependent changes in cell shape and secretion of proteases. The transcriptional reprogramming of epithelial tumor cells leads to loss of cell polarity and down regulation of cell-junction proteins. Recent study of targeting the 3' UTRs of EMT related mesenchymal genes by miRNA showed the suppression of snai2, VIM and CD151 expression. The multimeric complex of tetraspanin, CD151 with E-cadherins, integrins recruits proteinkinase C-β-II, transmembrane proteinkinase phosphatise (PTPµ) and promotes the association of cytoskeletal elements and supports cadherin mediated cell-cell adhesions. CD151 is a key mediator of cell-cell adhesion, EMT induction and tumor progression. CD151 play an important role in filopodia based adhesion zipper formation on one hand and cancer metastasis on other hand. The design and development of innovative shRNA therapeutic targeting CD151 may helpful in reducing EMT mediated CSC population in solid tumors.

BiographyGayatri Devi V has completed her Post graduation in Biochemistry from GITAM University. She is currently working as a Junior Research Fellow in Department of Science & Technology (DST) funded project in the Dept. of Biochemistry, GITAM University, and Visakhapatnam under the guidance of Dr. Rama Rao Malla.

[email protected]

Gayatri Devi V et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

Page 9: Posters - OMICS Publishing Group · 2015-01-21 · apoptosis, stimulating cell proliferation and inhibiting DNA repair. Over production of ROS may cause ‘oxidative stress’ which

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Volume 6, Issue 9J Cancer Sci Ther 2014

ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitExpression of notch signaling pathway genes in human astrocytic gliomas of different WHO gradesNarayanappa Rajeswari and Madhuri G S Aithal Dayananda Sagar College of Engineering, India

Astrocytic gliomas are the most common type of brain malignancies accounting for more than half of all brain tumors. Though these tumors have been classified into four grades based on their malignancy, it is more appropriate to differentiate

by discovering dysregulated pathways which can be used as biomarkers for diagnosis. Notch signaling is one such pathway which plays an important role in determining cell fates and is involved in cell proliferation, differentiation, and apoptosis. Since it is found to play a critical role in oncogenesis, we investigated the role of Notch signaling in astrocytic gliomas, with an aim to identify biomarkers. Using Real time PCR, we assessed the expression of Notch pathway genes including receptors (Notch-1, Notch-2, Notch-3 and Notch-4), ligands (Delta-Like ligand 3, Jagged-1 and Jagged-2), downstream targets (HEY2 and HES1) as well as activators and inhibitors (Deltex-1 and NUMB) along with other genes involved in the pathway in 18 formalin fixed paraffin embedded (FFPE) patient samples of different WHO grades and compared it with normal FFPE brain samples. We show that Notch-1 is overexpressed in 14 out of 18 tumor samples and Notch-3 is overexpressed in 7 out of 18 tumor samples. However the ligands showed low expression compared to non-neoplastic tissue. mRNA of Hes1 but not Hey2, both of which are major downstream molecules of the Notch pathway, was also down regulated. Our results clearly show that Notch pathway genes particularly Notch-1 is dysregulated and can be used as a biomarker for a more precise diagnosis of astrocytic gliomas. Further, studies are required to understand specific molecular events to discover more functional markers characteristic of each stage.

BiographyNarayanappa Rajeswari is an associate professor and member of Indian Association for Cancer Research (IACR). She has 18 International and 7 National publications. In 1994, she got Young Scientist Award by Indian Society of Human Genetics. Presently, she is engaged (i) to identify and characterize genes involved in the development and progression of human cancers; (ii) to understand mechanisms of the alterations in carcinogenesis; (iii) to translate the basic research outcomes into clinical research that will eventually improve detection, diagnosis, prognosis, prevention and treatment of human cancers.

[email protected]

Narayanappa Rajeswari et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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ISSN: 1948-5956, JCST an open access journalGCC-2014

September 15-17, 2014

September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitA novel cinnamyl sulfonamide hydroxamate derivative, NMJ-1 as a small molecule HDAC inhibitor with anti-cancer potentialNeetinkumar D Reddy, Shoja M H, B S Jayashree, Karthik Gourishetti, Subhankar Biswas, K S R Pai and C Mallikarjuna RaoManipal University, India

Cancer is caused by abnormal epigenetic modifications in addition to multiple genetic mutations. Histone deacetylase (HDAC) enzyme over expression has been found in many types of cancer, which is responsible for silencing of tumor

suppressor genes and activation of proto oncogenes to oncogenes. Cinnamic acid derivatives were recently, found to have great anti-cancer potential through HDAC enzyme inhibition. Hence, the present study was based on modification of Cinnamic acid to cinnamyl sulfonamide hydroxamate derivative. The compound NMJ-1 was synthesized, purified and structurally confirmed by IR, GC-MS, and NMR and CHN-S elemental analysis. The HDAC enzyme inhibition activity for NMJ-1 was observed through whole cell HDAC assay and showed HDAC enzyme inhibition IC50 (3.89±0.17 µM). The cytotoxicity was studied by MTT assay using HCT-116 cancer cell-line in vitro and showed cell-growth inhibition IC50 (4.07±0.9 µM). The pro-apoptotic potential of NMJ-1 was observed throughG2/M arrest by cell-cycle analysis, increase in Annexing V binding and activation of cleaved caspase 3/7by flow cytometry. The acute oral toxicity study for NMJ-1 was performed according to OECD-425 guideline and was safe up to 2000 mg/kg dose in rats. DMH, a chemical carcinogen was administered weekly once i.p. at a dose of 20 mg/kg for 35 weeks to induce colon adenocarcinoma in rats. NMJ-1 and 5 FU were administered at dose of 50 mg/kg p.o. and 10 mg/kg i.p. respectively for 21 days in DMH induced colon cancer in rats. NMJ-1 and 5 FU administrations significantly reduced ACFs and tumor size. The histopathological study also showed reduction in number of tumors, tumor size and neutrophil infiltration with NMJ-1 and FU treatments. Our findings indicate that NMJ-1 has potential against colon cancer through HDAC enzyme inhibition and activation of intrinsic mitochondrial apoptotic pathway. Further detailed mechanistic studies are needed to confirm its anti-cancer efficacy.

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Neetinkumar D Reddy et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitTo enhance the knowledge, awareness about the risk factor and screening practices of breast cancer among women in holy city VaranasiPrem Prakash Solanki, S Paul, A Pandey, H Sabia, U P Shahi and S SrikrishnaBanaras Hindu University, India

Breast cancer is second most cause of death worldwide after lung cancer. The global burden of breast cancer is 1.38 million, 10.9% of all cancers. The annual age-adjusted rate (AAR) varies between urban and rural areas in India. In the urban areas,

the AAR is 21.9 to 28.3 per 100,000, whereas in rural areas, it is 8.6 per 100,000. In study, we present level of awareness of risk factors and screening practices especially Breast Self Examination (BSE) among women of holy city Varanasi. The investigation tool is self-administrated questionnaire format which consist of seven different parts and approached to 560 women, in the age group of 18-65 years. Result showed that out of 560 women, 500 (89%) responded of them, 50% were married and 80% were educated. The knowledge about BSE was very low, 20.6% among them 0.2% had practised BSE only once. In Himachal Pradesh, Mumbai and Delhi the level of awareness and mainly practised of BSE were 97 % & 54%, 42% & 15% and 36% & 13.7% respectively. The awareness of risk factors of breast cancer were as follows: Heredity: 19.6%, age factor: 25%, early menarche: 22.2%, late menopause: 8%, nulliparity: 14%, late marriage: 13%, hormone therapy: 13% obesity: 34% and modern life-style: 4.6% respectively. The study revealed that the awareness of risk factors and practised of BSE among women in Varanasi was extremely low in compare to other cities.

BiographyPrem Prakash Solanki has completed his B.Sc., M.Sc. and PhD from Jai Narain Vyas University, Jodhpur, Rajasthan. He is working as an Assistant Professor in Department of Chemistry, Faculty of Science, BHU and he is a Principal Investigator of DST sponsored project (Project No. : M-21-124)

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Prem Prakash Solanki et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitAnticancer effect of green synthesized gold nanoparticles using leaf extract of Abutilon indicum on human colon cancer cell line HT-29M Rani and S Sudha Rani Pondicherry University, India

The bio-inspired gold nanoparticles are extensively used as novel therapeutic and diagnostic modalities in nano-medicine especially to treat cancer. This study reports the biosynthesis of gold nanoparticles using Abutilon indicum leaf extract (AILE)

and their anticancer effect. Gold nanoparticles were synthesized using 1 mM HAuCl4 and 1% Abutilon indicum leaf extract and the synthesized gold nanoparticles were characterized by various techniques including UV-visible spectroscopy, DLS particle size analyzer, Fourier transform infrared spectroscopy (FTIR), scanning electron microscope (SEM), X-ray diffraction (XRD), thermal gravimetric analysis (TGA)/differential scanning calorimeter (DSC). The spherical gold nanoparticles were found to have an average size of 32 nm and the major phytoconstituents in AILE like N-H of amino acids or proteins were involved in the bio-reduction of gold nanoparticles. Further, the green synthesized gold nanoparticles exhibited dose dependent cytotoxicity against human colon cancer cell line HT-29 by MTT assay. Apoptotic cell death in nanoparticles treated HT-29 cells was observed by acridine orange/ethidium bromide (AO/EB), propidium iodide (PI), 4', 6-diamidino-2-phenylindole (DAPI), AnnexineV-Cy3 staining techniques. The loss of mitochondrial membrane potential as indicated by Rhodamine123, high levels of ROS intermediates as observed with DCF-DA and DNA damage as indicated by TUNNEL assay could have played a major role in apoptotic cell death in HT-29 cells following treatment with gold nanoparticles. Also caspase-3 was found to be activated in treated HT-29 cells confirming apoptotic cell death. These results provided an evidence for the anticancer activity of gold nanoparticles synthesized from Abutilon indicum which may prove to be a valuable tool in cancer nano-therapy.

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M Rani et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitDocking studies of antiviral drugs with thyroid TF2BRoneet Choudhary, Arvind Agarwal and Amarnath ManipatraSRM University, India

Cancer can be described as the uncontrolled growth of abnormal cells. Thyroid cancer is a cancer originating from follicular or parafollicular thyroid cells. Some of the most commonly used thyroid cancer drugs are Cabozantinib-S-Malate,

Vandetanib, and Nexavar etc. These drugs mainly work by blocking (inhibiting) signals within the cancer cells that make them grow and divide. The Protein- Ligand interaction plays a significant role in structural based drug designing. This study is an attempt to develop a drug with minimal side effects, the problem which previous studies have not been able to address. In our research work we have taken the TFIIB or TF2B [pdb id: 2PHG] protein and the commercially available drugs against Thyroid cancer. Using Bioinformatics tool Autodock, we have predicted and analysed the interaction of this protein with several ligands. In future this could leads to the application of existing sources of anti-viral drugs to treat this disease.

BiographyRoneet Choudhary is a student, who is pursuing his career in The Department of Bioinformatics (3rd year) in SRM University. He is from Mumbai (Maharashtra) and completed his schooling from Atmiya Vidya Mandir (Surat, Gujarat). He always allows himself to obtain a challenging position which gives him opportunity to apply his education and experience in the field of Bioinformatics and Computer Science. He is hard-working and career-oriented. He has been an icon of dedication and generosity for his fellow students. Furthermore, he has also been a part of many conferences such as International Cancer Conference (CANCERCON’14) and working on many projects related to his interest (Stats, Computer Programming).

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Roneet Choudhary et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitBAY 11-7082, an anti-inflammatory drug attenuates metastasis potential of Pak1 over expressing cells by modulating Pak1-NF-κB-p65–fibronectin signaling networkSankar Jagadeeshan1,2, Suresh Kumar Rayala2 and Raghunathan Malathi11University of Madras, India2Indian Institute of Technology Madras (IITM), India

p21-activated kinase 1 (Pak1) - a serine/threonine kinase, is a well-known regulator of cytoskeletal remodelling, cell motility, cell proliferation, and cell survival, which can induce phosphorylation and activation of NF-κB, that can accelerate growth

and survival of cells. Our previous study have implicated that Pak1 by itself can have an oncogenic role in pancreatic cancer through Pak1-NF-kappaB-p65–fibronectin pathway. Hence agents blocking downstream target of Pak1, namely NF-κB and its activation, may reduce the invasiveness of pancreatic cancer. To test this hypothesis, we used BAY 11-7082 a known NF-κB inhibitor and an anti inflammatory drug for the study. In the present study, we found BAY 11-7082 inhibited migration and invasive capability of Pak1 over expressing pancreatic cell lines through blocking p65 NF-κB- Fibronectin pathway. We also observed reduced fibronectin promoter activity on BAY 11-7082 treatment. Thus, the inactivation of NF-κB pathway, down-regulated fibronectin expression and reduces the metastasis potential of Pak1 over expressing pancreatic cancer, indicating targeting Pak1-NF-kappaB-p65–fibronectin pathway might be an efficient treatment modality for pancreatic cancer patients.

BiographySankarJagadeeshan is a graduate in Biotechnology, Chemistry and Zoology from University of Kerala and a post graduate in Biotechnology from Vellore Institute of Technology, VIT University,Tamil Nadu. He has seven years of research experience in molecular oncology, translational biology, nanomedicine and drug delivery as well as identification of novel drugs for cancer therapy. He had worked in premier institute of India viz., Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, Kerala and Indian Institute of Technology Madras, Tamil Nadu as research fellow. He has published nine papers in the field of microbiology, medicinal chemistry and oncology and has two book chapters to his account. Currently he is a research scholar in Department of Genetics in University of Madras working on the role of p21 activated kinase 1 in progression, metastasis, drug resistance and angiogenesis during pancreatic carcinogenesis.

[email protected]

Sankar Jagadeeshan et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitProgression and control of tumorigenesis in F1 mice from the ethylnitrosourea exposed mothers involve miR-21 and PI3K/PTEN/Akt pathway along with apoptotic eventsSatya Sahay, Prakash Tiwari and Krishna P GuptaIndian Institute of Toxicology Research, India

Lung cancer is a most common form of the cancer and is among the leading causes of cancer associated deaths in adults and is increasing in younger population as well. In view of this, we studied the transplacental lung tumor development in

the offspring’s from the ethylnitrosourea (ENU) exposed mothers and the preventive effects of inositol hexaphosphate (IP6) in the F1 mice at 30 and 240 days representing early and late stage of tumorigenesis. Progressive time-dependent increase was observed in the development of lung tumor in F1 mice. Number of tumors on the lung surface was 101(6.73 tumors/ tumor bearing mouse), and 378 (31.5 tumors/ tumor bearing mouse) at 30, and 240 days which was reduced to 81(5.06 tumors/ tumor bearing mouse), 201(15.46 tumors/ tumor bearing mouse) at 30 and 240 days in presence of IP6. During the tumorigenesis, overexpression of miR-21 activated the phosphorylation of Akt via targeting PTEN and inhibits apoptosis as revealed by down regulation of caspase-3 and cleavage of PARP1 in F1 mice. We also observed the upregulation of MMP-9 protein as well as its enzyme activity in F1 mice. Alterations in these molecular events were also prevented in presence of IP6. In conclusion, our findings show the progression and control of tumor development in F1 mice from the ENU exposed mothers possibly by affecting apoptosis via modulating the expression of miR-21, PI3K/PTEN/Akt pathways and MMP-9. The sensitivity of the molecular alterations to the IP6 makes them the potential targets for the cancer control.

[email protected]

Satya Sahay et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitOral ingestion of Spondias pinnata bark extract trim down severity of small intestinal mucositis in etoposide treated rats: Histological sequelaeSudarshan Reddy C, Beena V Shetty and Gayathri M RaoManipal University, India

Chemotherapy-induced diarrhea (CID) is a common side effect of cancer treatment and can cause significant morbidity and mortality. Rat mucositis model was developed by injecting single dose of etoposide (i.p) and treated with S. pinnata

bark extract (100 & 200 mg/kg body wt.) for next 72 hrs. Treatment efficacy was determined by changes in the intestinal morphology and biochemical parameters such as intestinal GSH, Sucrase, NO, MPO and Interleukin-6 (IL-6) after 72 hr, with and without intervention. There was a significant decrease in reduced glutathione, sucrase and IL-6 levels and a significant increase in NO and MPO activities in intestinal tissue after etoposide injection. However, in the post treatment groups (in both 100 & 200 mg), reduced glutathione, sucrase and IL-6 levels reverted back to that of normal. NO levels reverted to normal levels in response to 100 mg/kg body wt. of S. pinnata extract; however it remained high in the group treated with 200 mg/kg body wt. MPO levels showed least response to the intervention during the study. Histological studies showed a good response to S. pinnata bark extract intervention. The results suggest that S. pinnata bark extract has some potential to prevent the toxic effects of etoposide which expedites to mucositis.

[email protected]

Sudarshan Reddy C et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitModeling the impact of magnetic fields in positron emission tomography R Vaitheeswaran Philips Radiation Oncology Solutions, India

The intrinsic spatial resolution of Positron Emission Tomography (PET) is known to be improved in the presence of strong magnetic fields due to the magnetic field induced curling of positrons. In this study a simple mathematical model has been

developed using the fundamental theories of electricity and magnetism that predicts the impact of applied external magnetic field strength on the PET image resolution for different radioisotopes. The proposed model accounts for the energy of the radioisotope, tissue density and range straggling effect. Moreover, the mathematical model can be directly incorporated into any Monte Carlo methods to get more accurate results. In order to validate the proposed model, we have compared our results with the experimental results obtained by Bruce E. Hammer et al. The comparative analysis reveals that the results obtained using the proposed model is consistent with the experimental observations. The proposed model can help understand the effect of magnetic fields in PET imaging accurately, which will be useful to optimize the use of magnetic fields for specific PET imaging studies. Moreover, the results obtained from the model theoretically augment the concept of integration of PET and MR scanners.

BiographyR Vaitheeswaran has completed his MS (Specialized in Medical Physics) from College of Engineering, Anna University, Chennai. He is working in Philips R&D Center (Healthcare division), Bangalore as Medical Physicist. He has published more than 9 papers in reputed journals and has about 10 US patents filed in his name. He has presented more than 25 research papers in national and international conferences. He is a reviewer for few international journals in the field of Medical Physics.

[email protected]

R Vaitheeswaran, J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitAnti-cancer potential of food extracts against oral and breast cancer cellsRam Prasad O G, Satish V and Vidudala V T S PrasadBasavatarakam Indo-American Cancer Hospital and Research Institute, India

In the present study, we have examined the anti cancer effects of plant extracts and curcumin on two oral cancer cell lines (SCC-9 and CAL-27), and a breast cancer cell line (MCF-7) and a non-cancerous breast epithelial cell line (MCF-10-A). The

cell lines were obtained from ATCC (USA) and were grown using an ATCC recommended media and supplements. The results revealed extracts (F-1 and P-1) induced cell death and the number of dead cells were found to be more at 48 hours compared to 24 hours. However, the extracts mediated cell death was found to be concentration and time dependent, and varied with the cell line, as expected. In addition to the cell death, we have also investigated the effect of the extracts and curcumin on the rate of proliferation, and on the cell cycle. We observed significant amount of cell death, following the exposure to the food extracts. In summary, the results of the present study indicate that the daily use of these extracts might help in preventing cancer and in sensitizing cells to anti-cancer therapeutic treatments.

[email protected]

Ram Prasad O G et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitDistribution of glucosylcerebrosidase (GBA) polymorphisms in oral cancer patients and possible functional implications of the SNPsSushma I1, Shiva SatishT1, Ravi L1, Sateesh N1, Padma K1, T Srivani, Sarika D1,2 and Vidudala V T S Prasad1

1Basavatarakam Indo-American Cancer Hospital and Research Institute, India2Acharya Nagarjuna University, India

The prevalence of the major polymorphisms in normal and oral cancer patients was investigated and analysed the data in a site specific way. The SNPs examined are; 1) G129T (Val394Leu), 2) G1497T (Val460Val), 3) G1342C (Asp409His), 4)

IVS 2+1 G>A, 5) A1226G (Asn370Ser), 6) c.1263-1317 del 55, 7) T1448C (Lys444Pro) and 8) G1604A (Arg496His). Analysis of the data revealed differential distribution of the polymorphisms in tongue and buccal cancer subjects and exhibited gender variations. In addition, it was also studied plausible implications of the SNP(s) on the structure and function of the GBA, using bioinformatics’ tools.

[email protected]

Sushma et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitStudy of genetic variants that result in loss of activity of major drug metabolizing enzymes such as CYP3A5, CYP2D6 and SULT1A1Dhanur A, Shiva Satish T, Kalyani M, Harpreet W, Padma K, Ravi L, Sateesh N Sarika D, Srivani N S S L, Sushma I and Vidudala V T S PrasadBasavatarakam Indo-American Cancer Hospital and Research Institute, India

We have carried out a comprehensive study on the occurrence of major SNPs in the genes encoding CYP3A5, CYP2D6 and SULT1A1. CYP3A5 and CYP2D6 are cytochrome P450 enzymes involved in phase I drug metabolism whereas

SULT1A1 sulphonates drugs and thus helps in the clearance from the system. CYP3A5 and CYP2D6 are known to metabolize 50% and 25% respectively of the currently prescribed drugs. Functional SNPs in these genes are known to impair the metabolism of commonly prescribed drugs apart from anti-cancer drugs. Hence, the objective of the study was to screen individuals for the presence of the SNPs; CYP3A5*3 (rs776746), CYP2D6*4 (rs3892097) and SULT1A1*2 (rs9282861). Our results indicate that a significant proportion of Indian population do carry SNPs of the enzymes and are likely to be poor responders to various commonly prescribed drugs, including tamoxifen, most widely used to breast cancer. The prevalence of the SNPs observed in the present study differed significantly from those reported by western countries. On a significant note one of the SNPs exhibited association with cancer. Our results therefore indicate a strong need for developing Indian/population specific databases for treating various ailments more effectively with fewer side effects.

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Dhanur A et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitRisk of tongue and buccal mucosa cancers may vary with FAS and FASL SNPs, in a gender dependent way Sarika D1,2, Sateesh N1, Saritha K1 and Vidudala V T S Prasad1

1Basavatarakam Indo-American Cancer Hospital and Research Institute, India 2AcharyaNagarjuna University, India

Background: Several reports have linked FAS (CD95 receptor) and FASL (CD95 ligand) aberrations with human cancers, including those of Head and Neck. However, expression pattern of these proteins vary among various tissues. Hence, we hypothesized that the role(s) of FAS and FASL together or independently may be specific to the site of the oral cancer and gender.

Objective: To test the hypothesis, we examined whether the promoter region polymorphisms of FAS (-1377 G>A; rs2234767 and -670 A>G; rs1800682) and FASL (-844 T>C; rs763110) have any association with cancers of tongue and buccal mucosa in males and females.

Materials and Methods: A case-control study of 535 oral cancer and 525 normal subjects were performed. Polymorphic variants were determined by subjecting genomic DNA isolated from peripheral blood to PCR-RFLP technique.

Results: We report a significant association between the FASL-844 T>C polymorphism and increased risk for buccal mucosa cancer in females. Protective effect of the combined genotypes of FAS -1377 GA and FAS -670 GG against tongue cancer (OR=0.28; P≤0.01) and increased risk of the cancer with the co-occurrence of FAS -1377 AA and -670 GG genotypes in males (OR=4.4; P≤0.03) was noted. In females, combined genotypes of FAS -1377GA and FAS -670 AA increased risk of buccal mucosa cancer (OR=3.27; P≤0.01). Increased susceptibility towards tongue cancer was observed in male carriers of the FAS -1377 AA + FAS -670 GG + FASL -844 CC variants. Our investigations also revealed gender bias in the distribution of the SNPs between normal males and females.

Conclusion: SNPs of the FAS and FASL might be associated with tongue and buccal mucosa cancers differentially and in a gender dependent manner.

[email protected]

Sarika Det al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitPromoter polymorphism of FASL confers protection against female specific cancers and those of FAS impact the cancers divergentlySateesh Nallapalle1, Sarika Daripally1,2 and Vidudala T S Prasad1

1Basavatarakam Indo-American Cancer Hospital and Research Institute, India2Acharya Nagarjuna University, India

Breast, ovarian, cervical and endometrial tissues, and the malignancies of these tissues are sensitive to estrogen/estradiol, age at menarche, child bearing and menopausal age. Moreover, hormonal therapy and anticancer drugs also have been shown

to predispose these patients to cancer. In view of the commonalities among female specific tissues and cancers of these tissues, we hypothesized that similar mechanisms may be operating in the female specific cancers. To begin to test the hypothesis, it was investigated and compared the association of FAS (-1377 G>A and -670 A>G) and FASL (-844 T>C) promoter polymorphisms with breast, ovarian, cervical and endometrial cancers. The genotype AA of FAS -1377 G>A polymorphism was associated with an increased risk for breast cancer alone while the GA variant of the polymorphism enhanced the risk of both breast and cervical cancers (P≤0.005). In contrast, FAS -670 AG variant was significantly associated with lowered risk of breast cancer alone but not that of other cancers. On the other hand, the prevalence of CC variant of FASL-844 T>C was lower in cases and was found to be protective towards breast, ovarian, cervical and endometrial cancers (P≤ 0.01). We also report that the effect of combined genotypes of FAS and/or FASL SNPs differed from that of individual polymorphisms. Although, risk and protective haplotypes of FAS SNPs were observed across the cancer phenotypes, the association of the haplotypes was significant for breast cancer alone with a 3-fold enhanced risk. Our results indicate that FASL-844 T>C polymorphism (CC genotype) is protective against female specific cancers, whereas the FAS -670 AG variant lowers risk of breast cancer alone. In contrast, FAS-1377 G>A polymorphism was found to elevate risk of breast and cervical cancers, significantly. The protective effect of the FASL SNP seen in this study is in line with the proposed hypothesis and suggests similar bio-molecular mechanisms involving FASL and/or FAS may play a role in female specific cancers.

[email protected]

Sateesh Nallapalle et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitIdentification of potential dna elements that may regulate sphingolipid metabolizing enzymes and ceramide transport protein using bioinformatics toolsSaritha Katta, Srivani N L S S, Sarika Daripally and Vidudala V T S PrasadResearch and Development, BIACH & RI, India

Sphingolipid pathway plays a major role in anti-cancer drugs and radiation induced cell death. Ceramide, a pro-apoptotic molecule is central to sphingolipid metabolism. Ceramide released from sphingomyelin by sphingomyelinase in response

to various stimuli, has been shown to induce cell death in variety of cells, including those of cancer. However, the presence of intra-cellular ceramide is transient as the ceramide gets metabolically converted in to various other sphingolipids that are either pro or anti-apoptotic. This suggests the importance ofmaintaining the ratio of sphingolipids in inducing cell death.

We hypothesize that down regulating the enzymes that convert ceramide in to either C-1-P and / or S-1-P keep the intracellular ceramide levels high thus increasing the sensitivity to anti-cancer treatment modalities. To test the hypothesis, we have been looking at various factors like DNA elements, mutations in the genes, small molecule inhibitors and activators, and ceramide transfer protein (CERT) that may contribute to upregulation or down regulation of these enzymes.

In this regard, we are investigating for the possible presence of DNA elements that may regulate expression of genes involved in ceramide synthesis and its metabolism. Investigations of the present study included genes which encode ceramide kinase (CERK), sphingosine kinases (SPHK1&2), sphingosine-1-phosphate lyase (SGPL1), ceramidases (1,2 &3), glucosidase-β- acid (GBA) and galactocerebrosidase (GALC).

The data obtained so far reveals the presence of DNA regulatory elements in ceramide synthases and enzymes involved in ceramide conversion but not in ceramide transfer protein.

[email protected]

Saritha Katta et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitAssociation between female cancers and aberrations in genes encoding 12- and 15 lipoxygenasesSaritha Katta, Srivani N L S S, SarikaDaripally and Vidudala V T S PrasadBasavatarakam Indo-American Cancer Hospital and Research Institute, India

Both, 12- and 15-lipoxygenases play a key role in inflammatory pathways and generation of reactive oxygen species (ROS), and are linked with cancer. However, investigations on the association between the polymorphic variants of the

lipoxygenases and cancers are limited and hence their association with cancer risk remains to be understood. Earlier, we reported increased risk of breast cancer with a functional polymorphism of 12-lipoxygenase. In the present case-control study, we have explored the risk association between the polymorphic gene variants of 12- and 15-lipoxygenases and female cancers. Genes encoding 12- and 15-lipoxygenases are located on chromosome 17 at loci, p13.1 and p13.2, respectively. The sequence similarity between these two genes is reported to be 86%. The SNP examined for 12-lipoxygenase is located in exon 6 (mRNA, A835G; Glu261Arg; rs1126667). This non-synonymous SNP which substitutes glutamine with arginine impairs the enzyme activity. For 15-lipoxygenase a promoter region SNP (C>T; -292C/T; rs11568070) which is known to up regulate the gene expression was examined. The C to T substitution of the polymorphism creates a novel transcription factor binding site for SPI1. A two-fold increased expression of 15-lipoxygenase was reported with the promoter variant containing ‘T’ allele. The patients studied were affected with either of the cancers of breast, ovaries, endometriumor cervix. The examinations revealed varied association between the cancers and the polymorphisms.

[email protected]

Saritha Katta et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitHaplotype analysis of TP53 polymorphisms in oral cancer patientsSrivani N L S S1,2, Padma K1, Saritha K1 and Vidudala V T S Prasad1

1Basavatarakam Indo-American Cancer Hospital and Research Institute, India2Acharya Nagarjuna University, India

P53 is a tumor suppressor protein. The protein has been reported to be defective, leading to complete or partial loss its functionality in about half of the human cancers, including those of oral cavity. P53 is encoded by TP53 gene located on

the short arm of chromosome 17 (17p13.1). Hence, we investigated association of the three major polymorphisms of TP53 gene with tongue and buccal mucosa cancers in males and females. Further we have also performed haplotype analysis of the data to understand whether the occurrence of these polymorphisms is independent or not, and co-occurrence of these polymorphisms of the genes alters the risk of the oral cancers. Therefore we have investigated the prevalence of the variants and their association with tongue and buccal mucosa cancers. The polymorphisms investigated are; intron-3 16bp duplication (rs17878362), intron 6 G>A (rs1625895) and Exon-4 G215C (R72P, rs1042522), in a case-control study. Results obtained revealed significant variations in the distribution of the polymorphisms between tongue and cancer patients. Further, we also observed gender based variations in the polymorphisms.

[email protected]

Srivani N L S S et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitCytotoxic potency of plant extracts varies with breast cancer cell linesSatish, Vemuri, Ram Prasad, O G and Vidudala V T S PrasadBasavatarakam Indo-American Cancer Hospital and Research Institute, India

Cell lines derived from tissues and immortalized, played a crucial role in understanding disease mechanisms and identifying potential drug targets, and for evaluating potency/toxicity of various xenobiotic and bioactive molecules.

In view of the pre-clinical utility of the cell lines, we wanted to determine whether the response of various established breast cancer cell lines to cytotoxic agents would be similar or not? For this study, we chose to test cytotoxic effect of two plant extracts (FE and PE) against three widely used breast cancer cell lines (MCF- 7; MDA-MB-435 and ZR-75) derived from three different Caucasian females afflicted with breast cancer. The breast cancer cell lines utilized for the investigations were reported to be either positive or negative for Estrogen and/or Progesterone receptors which play role in breast cancer and in determining mode of anti-cancer strategy. MCF-7 and ZR-75 are positive for the presence of while MDA-MB-435 is negative for the presence of Estrogen and Progesterone receptors.

We report, that the breast cancer cell lines were differentially susceptible to both the extracts (FE and PE). Cell lines, MCF-7 and ZR-75 were more prone to death mediated by these cytotoxic agents when compared to MDA-MB-435. Our study also demonstrated the presence of apoptotic cells in the cultures exposed to these cytotoxic agents, indicating a role for apoptosis in the cell death. We are also examining the impact of these pro-apoptotic extracts on the cell cycle events of the breast cancer cell lines.

[email protected]

Satish et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitIdentification of cfr positive Staphylococcal aureus isolate from an ICU caseGuru Prasad Manderwad1, Vidudala V T S Prasad1, Lunavath Ravi Kumar1 and Ashok Kumar Reddy2

Basavatarakam Indo-American Cancer Hospital and Research Institute, India

Introduction: A Multidrug resistant bacterium poses a formidable challenge in effectively treating infections and is significant factor infection related mortality. The cfr (Chloramphenicol-flrofenicol resistance) gene encodes methyltransferase which methylates 23S rRNA at A2503, conferring resistance to various classes of antibiotics, such as oxazolidinone, phenicols, lincosamides, pleuromutilins streptogramin A.

We report, presence of cfr related drug resistance in methicillin resistant Staphylococcus aureus isolated from septisemic patient.

Material and Methods: A total of 59 bacterial isolates obtained from ICU (20) and ocular (39) cases from hospitals across the Hyderabad region were screened for the presence of cfr gene, using PCR with specific primers, and a positive control (The plasmid containing cfr gene was a gift from Dr. Gopegui ER, Hospital Universitari Son Espases, Palma de Mallorca, Spain).

Result: Our investigations, revealed presence of cfr positive Staphylococcal isolate obtained from an ICU case. The presence of the multidrug cfr gene is a rare in the humans. The bacterial isolate was also found to have higher MIC to linezolid. The presence of the gene is being validated by sequencing.

Conclusion: The present study demonstrates the presence of a cfr positive Staphylococcus aures. The particular isolate had a higher MIC for linezolid.

Acknowledgement: The study was supported by Fast Track Scheme for Young Scientist (to Dr. GPM) by SERB under DST SB/FT/LS-321/2012).

[email protected]

Guru Prasad Manderwad et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038

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September 15-17, 2014 Hyderabad International Convention Centre, IndiaGlobal Cancer Conference & Medicare SummitTrans-ferrulic acid induces down-regulation of BCL2 and up-regulation of BAD and Tp53 genes in smokeless tobacco induced human head and neck cancer cellsVishwas Tripathi, Rajvardhan Singh, Nikhil Khurana and Anjana SinghGautam Buddha University, India

Head and neck cancer is among one of the most common cancers worldwide. In India, Head and neck cancer accounted for 30% of all cancers. Tobacco consumption has been linked with the high incidence of head and neck cancer. Trans-

ferulic acid is a naturally occurring dietary component found in rice bran, vegetables and fruits. It has been previously reported to have anti-cancer activity in different cancer cells. This neutraceutical has a good bioavailability. Ferulic acid stays in blood for longer than other antioxidants such as vitamin C. The effect of trans-ferulic acid against smokeless tobacco induced head and neck cancer is not yet explored. We investigated the anti-cancer effect of trans-ferulic acid on smokeless tobacco induced head and neck cancer cells. We observed that trans-ferulic acid inhibited the proliferation of SCC4 head and neck cancer cells in a dose and time dependent manner. Furthermore, we observed the effect of trans-ferulic acid on apoptotic marker genes. Our study suggests that trans-ferulic acid induces down regulation of BCL2 and up Regulation of BAD and Tp53 in smokeless tobacco induced human head and neck squamous cell carcinoma (SCC4) cells. Taken together, these results support further investigation of trans-ferulic acid as a potential therapeutic agent in the treatment of head and neck cancer.

BiographyVishwas Tripathi is currently working as Assistant Professor in the School of Biotechnology, Gautam Buddha University, Greater Noida, India. He has done his doctorate under the collaboration of All India Institute of Medical Sciences, (AIIMS) New Delhi and Panjab University, Chandigarh. During his doctorate work at AIIMS, New Delhi, he reported for the first time the differential expression of one of the novel co-receptor of HIV-1 called CXCR7. Further, He also elucidated the signaling pathways triggered by the interaction of CXCl12 (A ligand of CXCR7) with CXCR7 suggesting the hypothesis that this receptor may play a crucial role in the growth and development of the human placenta. At present, his lab is involved in Screening and identification of the potent anti-cancer natural compounds found in the routine diet (e.g. vegetables, fruits, spices cereals etc.) and elucidation of the molecular pathways triggered by these compounds in the Head and neck cancer cells. Dr Tripathi has been recently granted the DST-Young scientist award. He has supervised eight M.Tech students for their dissertation work and is currently supervising three PhD students. He is reviewer of several important international journals.

[email protected]

Vishwas Tripathi et al., J Cancer Sci Ther 2014, 6:9http://dx.doi.org/10.4172/1948-5956.S1.038