Biography:

Hem D Shukla is a Research Scientist in the Department of Pharmaceutical Sciences at University of Maryland and adjunct Professor of Genomics in Notre Dame of Maryland University. He has also worked as Research Faculty in Department of Biology at Johns Hopkins University. He has worked on proteomic analysis of oxidative stress response in BxPC-3 pancreatic cell lines and identification of biomarkers for early detection of pancreatic cancer. He has worked on “The Nrf2 mediated antioxidant defense against oxidative stress in pancreatic cancer cell lines and targets for therapeutic intervention”. He has shown elevated level of Nrf2 transcriptional factor in pancreatic cancer cell lines under oxidative stress, which is phosphorylated by protein kinase C and affects phosphatidylinositol 3-kinase and MAP kinase pathways. After phosphorylation, Nrf2 translocates to the nucleus, binds AREs and transactivates detoxifying enzymes and antioxidant enzymes, such as glutathione S-transferase, and superoxide dismutase. The IPA analysis has suggested a potential role of Nrf2 under oxidative stress conditions. His research interests are: proteomic analysis of oxidative stress response in BxPC-3 pancreatic cell lines, identification of biomarkers for pancreatic cancer and Nrf2 mediated antioxidant defense against oxidative stress in pancreatic cancer cell lines.

Abstract:

Pancreatic cancer is one of the most aggressive human malignancies and ninth leading cause of cancer death in the world. Estimated new cases and deaths from pancreatic cancer in 2013 in the United States would be 45,220 and deaths 38,460. Most patients diagnosed with pancreatic cancer die within 6 months, and only 4% survive 5 years after diagnosis. Pancreatic cancer is characterized by colossal local invasion and early metastatic growth to the liver and regional lymph nodes. Expression of Nrf2 was up-regulated in oxidatively stressed BxPC-3 cell line and ductal adenocarcinomas. Furthermore, the BxPC-3 cell line responds to stress signals and resist chemotherapeutic interventions and have shown drug resistance. The Nrf2 has also been implicated in proliferation in certain pancreatic adenocarcinomas. Normally, ROS levels are tightly controlled by an inducible antioxidant program that responds to cellular stressors and is predominantly regulated by the transcription factor Nrf2. We have also identified the presence of a number of gene products involved in integrin signaling pathways. The comparative proteomic analysis using Protein Center and Ingenuity Pathway Analysis have shown the activation of DNA repair pathway genes like RAD50, ApeX, damage-specific DNA binding protein, which have the capability to repair DNA damage. The activation of NRF2 transcriptional factor and its phosphorylation in BxPC-3 treated cells shows that it may bind to the DNA at the location of the Antioxidant Response Element (ARE) or also called hARE (Human Antioxidant Response Element), which is the master regulator of the total antioxidant defense system. The proteomic data have also shown the activation of INT-ILK-PT3K-ILKAP-AKT and Cav-1-GRB2-SOS-cRas-Raf-MEK cascades. These results may have some promise in therapeutic intervention in the treatment of pancreatic cancer adenocarcinoma.

Biography:

Dr. Praveen Sonkusre has completed his Ph.D. from CSIR - Institute of Microbial Technology, Sector 39A, Chandigarh, India and currently working in the same institute as Research Associate. He has published 4 research articles in the early stage of his scientific career and is a part of one patent (filed).

Abstract:

Selenium deficiency is associated with many physiological disorders including the high risk of cancer. The rehabilitation of selenium with different selenium supplements, however, fails due to their low therapeutic index. Therefore, it is advantageous to have a less toxic form of selenium for supplementation with potentially high anticancer activity. In this study, selenium nanoparticles were synthesized biologically by Bacillus licheniformisJS2, and a method was developed for extraction and purification of intracellular nanoparticles. Characterization of extracted nanoparticles with various biochemical, microscopic and spectroscopic techniques suggested that these 110 nm sized particles are composed of selenium and capped with a few functional groups that provide steric stability to them. These neutral charged, non-agglomerating selenium nanoparticles at a concentration as low as 2 µg Se/ml were inducing reactive oxygen species (ROS) mediated necroptosis in PC-3 cells by gaining cellular internalization without causing any significant toxicity to human peripheral blood mononuclear cells and RBCs. Real-time qPCR analysis showed increased expression of necroptosis associated tumor necrotic factor (TNF) and interferon regulatory factor 1 (IRF1). An increased expression of the RIP1 protein was also observed at the translational level upon SeNP treatment. Moreover, the cell viability was significantly increased in the presence of necroptosis inhibitor, Necrostatin-1. Furthermore, histopathological analysis showed the subsequent oral administrations of ten times higher concentration of these endotoxin free selenium nanoparticles in C3H/HeJ mice (50 mg Se/kg of body weight), induce significantly lower toxicity compared to the L-selenomethionine (5 mg Se/kg). Data suggest that these biogenic SeNP could be the safest form of selenium supplementation with potentially high anticanceractivity.

Biography:

Saganuwan Alhaji Saganuwan is working as an Associate Professor of Pharmacology, former HOD, Registration/Time Table Officer, College of Veterinary Medicine, University of Agriculture, Makurdi, Nigeria, Fellow, Institute of Industrial Administration, Licensed Member of Veterinary Council of Nigeria, Honorary Member, Nigeria Institute of Food Science and Technology, Member of Science and Technology Forum, Member of Institute of Research and Development Network, Editorial Board Member to many local and international journals of high repute. He received DVM degree in Veterinary Medicine, MSc in Pharmacology and PhD in Pharmacology from Usmanu Danfodiyo University, Sokoto, Nigeria. He received also PGD in Statistics and PGDE in Science Education from University of Agriculture, Makurdi, Nigeria. He received Medical International Noble Award in 2012. His areas of research interest are Pharmacology, Toxicology, Oncology and Medicinal Chemistry. Presently he teaches, carries out research and supervises undergraduate and graduate students of University of Agriculture, Makurdi, Nigeria. He has over 230 citations with 60 publications in local and international journals of high repute. He has presented conference papers in USA, UK, India, Spain, Japan, China, Cyprus, Australia and Nigeria.

Abstract:

The safety of anticancer dosing has become a serious concern due to high incidence of life-threatening toxicity signs. More so, dogs are used as models of research for human cancers. As such, a uniform body surface area (BSA) formula is developed for human and dogs with a view to having low safe effective therapeutic doses of anticancers.. The derived formula (BSA=BW^0.528×H^0.528×K) was used to calculate BSAs of greyhound, toy, companion, terrier, hunting and working dogs, yielded low doses of dacarbazine, asparaginase, streptozotocin, dactinomycin, epirubicine and prednisolone. Hunting and working dogs have high body weight, BMI and BSAs similar to that of human and may be prone to obesity and obesity associated diseases. Whereas BSAs and doses of anticancer agents of light and relatively tall dogs are relatively higher in comparison with that of short and light dogs. Greyhounds have higher BSA in comparison with toys, companions and terriers. Working breeds of dog: treeing walker coon haired (65.0 kg), great swiss mountain dog (59.0 kg), longhaired St bernard (55.0 kg), french mastiff (50.0 kg) and female komondor (59.0 kg) have same BSA values with humans weighing 51.3, 46.7, 44.8, 44.0 and 43.0 kg, respectively. Calculated exponent (0.528) may be the common relationship between basal metabolism of dog and human.

Biography:

Mr. Kamaju Suryahari and Ms. Sreevallika Immadi is working with Clinical Trials company for the past 3 years. Both are involved in active participation in running the company. The Basic profile related company is to provide Diagnostic tests in lower cost which help rural Indian Population. The Primary aim of the company is to promote low cost Biomarker Investigations for Rural Indian Population. Where they not able to afford for corporate pricing of the Bio Marker Investigations. Mr. Kamaju Suryahari is having almost 14 years of experience in Oncology Trials and well versed in Solid Tumor Test Based Investigations Related Studies. Ms. Immadi Sreevallika is having almost 2 years experience related to Oncology Therapeutic Area BasedStudies. 
 

Abstract:

Non-interventional, retrospective & anonymized data base study on  breast tumors for markers predictive of risk of recurrence: This is a non-interventional, anonym zed and retrospective research study. It does not involve enrollment of patients/administration of drugs. The study uses left over FEPE tumor blocks remaining after routine diagnosis for the patient is over. IHC/RTPCR based tests will be done on these blocks. Each patient will be de-identified with a unique code, by the hospital. No contact between patient and researcher at any point of time, thus study will have no side effects on the health of the patient. Main aim the study To carry out a non -intervenaial, retrospective & anonymized  study on 2000 breast cancer tumors to assess biomarkers for :

i) Prediction of risk of cancer recurrence

ii) Usefulness of chemo/radio therapy

iii) Overall effective cancer treatment planning.

Benefits :

1) Patients will avoid excessive therapy/ side effects & enjoy improved quality of life & save resources.

2) Medical oncologists can prescribe most effective therapy and targeted drugs .

Cancer and Recurrence:

*ASCO report: 1M new cancer cases in India per year. 12 Million Breast cancer survivors in US. In India 2.4M  breast cancer cases.

*Cancer recurrence is the most feared aspect of cancer as it is responsible for the Morbidity and mortality associated with the disease.

*Current means to predict risk of recurrence are limited. Treatment can be planned optimally if recurrence information is available.

Mission: To develop novel diagnostic tests for prediction of risk of recurrence for ALL cancers, first focus on breast cancer.

Clinical Trials Company Established in Year 2015. Currently the company is working with leading Medical Oncologists in India. Involving the Clinical Trials as well as the Molecular testing and Bio Marker Investigations. Most of the Trials involved in Medical Oncology related areas such as (Breast Cancer, Metastatic Colorectal Cancer, Head & Neck Cancer and other Lymphomas.

Biography:

Mirjana Maletic-Savatic is a Board-Certified Neurologist and a Physician/Scientist interested in the interactions between genes and environment, particularly those that affect learning and memory. The new concepts and analytic algorithms she and her team have developed at the bench have the potential to change the standard of clinical care, ultimately leading to improved diagnosis, prognosis and individualized treatment of our patients. She is the Recipient of numerous awards and has published extensively in top-tier journals.

Abstract:

The discovery of adult neurogenesis has opened a new era in modern neurobiology: the brain, after all, has the capacity to regenerate. In the mammalian brain, new neurons are continuously formed in the hippocampus, the center for learning and memory. In animal models, newborn neurons are important for cognition, mood and stress regulation. In humans, it is estimated that about 700 new neurons are integrated daily into the hippocampus, but their functional importance is not known because of the lack of a live and non-invasive measure. Based on a series of experiments using magnetic resonance spectroscopy (MRS), we identified a fatty acid-related metabolite that is highly enriched in neuroprogenitors and visible at 1.28 ppm on the resonance spectrum. To enable detection of the neuroprogenitors in the human brain, we developed an analytical algorithm that allows automated and objective quantitation of the 1.28 ppm spectroscopic signal obtained by 3T MRS. Using this method, we can distinguish neurogenic and non-neurogenic areas in the human brain. Further, we discovered that the neurogenic signal is associated with age and depression. Strikingly, in medication-resistant depressed individuals, electroconvulsive treatment provokes a two-fold signal increase–a leading indicator that predicts subsequent hippocampal plasticity and clinical outcome. Overall, we now have the means to study neurogenesis in the live human brain and provide new insights on the role of this process in human brain function, dysfunction and treatment response. Moreover, this method may be used to trace activated and/or stem cells transplanted into the human brain, already in clinical trials for stroke and multiple sclerosis.

Biography:

Erin Sharkawy has completed her Bachelor’s degree of Science (Biochemistry) in 2012, Diploma of Medical Tests–Biochemistry Analysis in 2013, Master’s degree in Biochemistry from Cairo University of Science. She is a Member of Presedential Leadership Programme. She is currently waiting to publish three papers on cancer researches. She has also worked as a Bio-Analytical Chemist and Medical Representative, but now she works as a Demonstrator and Molecular Biologist at National Cancer Institute. She has participated in Summer Training courses at NCI of Basics of Cancer and Molecular Biology.

Abstract:

Hepatitis C virus (HCV) is a single stranded RNA virus, of the Flaviviridae family. It is the main cause of chronic HCV diseases like fibrosis, cirrhosis, HCC and end stage liver disease. Worldwide, about 71 millions of individuals have HCC resulting from HCV chronic infection with about 790 thousands annual deaths. A major cause of high mortality rate due to HCC is the lack of early diagnostic resources. There is a great need for a sensitive, specific and non-invasive diagnostic marker to detect HCC in the earlier stages. We studied four protein markers in serum (SAA2, KNG1, PON1 and GAL3) that were significantly elevated in HCV-related HCC patients in previous study in our lab using C-MS/MS screening analysis and separated by SDS-PAGE gel electrophoresis. Estimation of protein concentrations were done in 52 patients infected with HCV-free HCC, 51 with HCV-related HCC in addition to 40 healthy participants as a control group. Analyses of protein concentrations were performed using sandwich ELISA technique. From the studied biomarkers, SAA2 provided the highest diagnostic accuracy (AUC=0.925) for HCC patients at (p<0.001). Morever, the diagnostic accuracy increased slightly when we used the panel of SAA2 with AFP, together with AUC=0.946, for HCC patients. SAA2 may have a considerable use in early detection of HCC in both normal population and high-risk patients.

Biography:

Nina Mezu-Nwaba is working as a Captain with the United States Public Health Service and a Senior Compliance Officer in the Center for Devices and Radiological Health (CDRH) at the Food and Drug Administration. She has over 20 years of clinical, retail, and regulatory experience, with expert knowledge in OB/GYN, Gastroenterology, Surgical and Urology products. She has been with the FDA for 17 years and has held positions at the Office of Generic Drugs, the Center for Drug Evaluation and Research, CDRH Office of Device Evaluation, and CDRH Office of Surveillance and Biometrics. She obtained her Doctor of Pharmacy from the University of Maryland at Baltimore, a Master’s in Biomedical Science from Georgetown University and a Master’s in Public Health from the John Hopkins Bloomberg School of Public Health. She has represented the FDA in Berlin, Puerto Rico, and the US as the Liaison for International Standards Committees. She actively participates in community health outreach, mentoring, as well as international humanitarian missions. She seeks to bridge gaps in health-disparities through voluntary service with the Commissioned Corps, Health and Human Services, MI Foundation in Nigeria, Rotary Club and serving the USPHS in Indian Health Reservations and other US locations.

Abstract:

The US Food and Drug Administration (FDA) defines a biomarker as “a defined characteristic that is measured as an indicator of normal biological processes, pathogenic processes, or responses to an exposure or intervention, including therapeutic interventions.” The increasing worldwide trend in the utilization of biomarkers has shown to be a significant element in the field of healthcare. Biomarkers have been integrated as measuring outcomes in the regulation of drugs, devices and biologics. Biomarkers in drug and medical device development provide information concerning detection of disease states in early stages as well as efficacious treatment options. For example, non-specific biomarkers such as WBC, D-dimers, C-reactive protein and criteria to diagnose sepsis have also played a part in therapy. In a recent study, biomarkers were utilized for a mice model of retinopathy of prematurity to ultimately benefit premature neonates in the early detection of this disorder. Based on the current trend, biomarkers offer an optimistic, yet challenging perspective on the future of its incorporation into personalized medicine. Clinicians can potentially measure and identify positive and negative responses to therapies benefitting both providers and patients. However, there have been several challenges in application of biomarkers due to lack of regulations in developing these biomarkers. In order to address these challenges, the FDA developed the Biomarker Qualification Program to establish the regulatory framework in biomarker evaluation and acceptance. As part of this program the FDA is working together with external stakeholders to develop a list of qualified biomarkers that can be applied in development of any drug, biologic or medical device. With more regulations put in place to assess and verify a biomarker’s value, the integration of biomarkers will continue to expand our understanding of human health.

Biography:

Mangilal Agarwal received his MS (2002) and PhD (2004) in Engineering from Louisiana Tech University (Ruston, LA). After his PhD, he was a Post-doctoral Research Associate at Louisiana Tech’s Institute for Micromanufacturing, which was followed by an appointment as Research Assistant Professor there. He joined IUPUI in 2009 as the Associate Director for Research Development in the Office of the Vice Chancellor for Research. He is currently working as Associate Professor of Mechanical Engineering and Director of Integrated Nanosystems Development Institute (INDI) at Indiana University-Purdue University Indianapolis (IUPUI) and directs the development of interdisciplinary research and education initiatives.

Abstract:

It is well recognized that trained canines can identify hypoglycemic lows in patients with type 1 diabetes (T1D) from smell alone. In order to build a noninvasive breath sensor to mimic canines’ ability to detect hypoglycemia in breath, we’ve collected breath samples from people with T1D and at the same time we’ve been developing cross-selective polymer and nanoparticle-based sensors for constructing a nanosensor array. Gas chromatography/mass spectrometry (GC/MS) was used to detect volatile organic compounds (VOCs) in the breath samples, and the GC/MS results were then aggregated and subsequently analyzed using statistical models to identify the specific panel of VOC biomarkers co-related to hypoglycemia. The analysis shows that from the panel of seven identified biomarkers one can detect hypoglycemia in breath with 91% sensitivity and 84% specificity (cross-validated results). Concurrently, we have been developing polymer and nanoparticle-based resistive sensors that can differentiate VOCs specific to the types of VOCs identified by results from the first summer. We have shown how poly(vinylidene fluoride-hexafluoropropylene) (PVDF-HFP)-based sensors can have increased sensitivity and cross-selectivity by modifying specific sensors in an array to increase or decrease both adsorption and transduction efficiency for specific classes of VOCs including alcohols (detector response can be varied by 200%) and ketones (response changes of up to 89%).

Biography:

Mohammad Obaidul Hoque is working as an Associate Professor of Otolaryngology-Head and Neck Surgery, Urology and Oncology at Johns Hopkins University School of Medicine. He completed Dental and Oral Surgery Training at the Dhaka Dental College, Dhaka University, Bangladesh. He then moved to Japan for the completion of PhD degree, where he also completed Advanced Clinical Training in Oral and Maxillofacial Surgery and Oncology. After training in Japan, he worked in the Head and Neck Cancer Research Division as a Post-doctoral Fellow under the mentorship of David Sidransky. He joined as a Faculty Member in 2006 in the Department of Otolaryngology-Head and Neck Surgery. His research interests includes: a) understanding the molecular biologic basis of head and neck, lung and genitourinary cancer b) developing and validating genetic and epigenetic approaches for early cancer diagnosis, cancer risk assessment and cancer prognosis and c) identifying molecular alterations due to environmental exposures such as active smoking, passive smoking and arsenic.

Abstract:

Bladder cancer (BCa) is classified as non-muscle-invasive BC (NMIBC) or muscle-invasive BC (MIBC). Because the recurrence and mortality rates of BCa are high, suitable biomarkers for early detection and targeted therapy are needed. Cancer stem cells (CSCs) have been shown to contribute to tumorigenesis and therapeutic resistance. In a recent study we found that CSC factors can be detected in the urine of BCa patients with high sensitivity and specificity and targeting CSC pathways elicits a long-lasting therapeutic response by limiting CSC expansion following chemotherapy and EGFR inhibition in BCa.

Biography:

Obaidi I is currently a final year PhD Student at the Conway Institute, School of Biomolecular and Biomedical Sciences, UCD, Ireland. He is also a Pharmacist, and has an MSc in Pharmacology and Toxicology, from the School of Medicine, University of Babylon, Iraq. He has more than eight published papers/abstracts. He is currently a Member of the International Cell Death Society.

Abstract:

Renal cancer is the ninth most common cancer in the world. In 2012 there were 337,860 newly diagnosed renal cancer cases worldwide, with 121,629 cases in Europe alone. In 2013, the number of deaths in the USA due to renal cancer was 13,680 out of 65,150 total cancer deaths (21%) cancer cases. Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, responsible for approximately 95% of cases. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), is a trimeric ligand, which binds to death receptors. Upon incorporation with DR4 (TRAIL-R1) and/or DR5 (TRAIL-R2), it activates the death inducing signaling cascade (DISC) in which fas associated death domain (FADD) recruits and activates the initiator procaspase 8 to active caspase 8, which in turn, amplifies the death signal by cleaving and activating many caspases including procaspase 3. Micro-RNAs (miRNAs) are a class of a highly conserved, small (~19-25 nucleotides) non protein-coding RNA. They silence gene expression by the induction of mRNA degradation or translational inhibition. Following the exposure of cancerous human renal cells (ACHN) to 25 µM curcumin for 24h, an miRNA screening test was performed for an estimated number of 84 apoptosis-regulating miRNA. The results revealed that let-7C was significantly upregulated. Several bio-informatic tools were used to identify let-7C gene targets. The results of the search revealed that genes regulating cell cycle phases and those controlling tumor metabolism are the primary targets of let-7C. Inhibition of let-7C using antagomirs was associated with the abbrogation of curcumin effects on cell cycle and cancer cell metabolism. 

Biography:

Hediye Nese Cinar has completed her MD degree from Dokuz Eylul University in Turkey. After completing her Post-doctoral studies at University of California Santa Cruz she joined Food and Drug Administration as a Research Fellow. She works as a Staff Scientist/ Research Biologist at FDA. 

Abstract:

Cyclospora cayetanensis is a coccidian apicomplexan parasite causing large outbreaks in different countries, including the US. The surveillance data collected by the CDC between 1996-2015 indicated that C. cayetanensis is the second most common cause of illness and outbreaks in the U.S. associated with imported foods regulated by FDA. Cyclosporiasis outbreak investigations are limited by the absence of molecular epidemiological tools for tracebacks. Due to difficulties in the recovery of the oocysts from produce and clinical samples, the unculturable nature of the organism, and limitations in efficient DNA extraction, until recently very little C. cayetanensis genomic information was available. In different apicomplexan parasites, multicopy organellar DNA such as mitochondrial and apicoplast genomes have been used for detection and molecular epidemiology analysis. We developed genomic workflows to obtain complete mitochondrial and apicoplast genome sequences from contaminated foods and clinical samples, for differentiation of C. cayetanensis isolates. The 6274 bp C. cayetanensis mitochondrial genome was amplified by PCR in four overlapping amplicons from genomic DNA extracted directly from cilantro spiked with oocysts, and from clinical stool samples. DNA sequence libraries of pooled amplicons were prepared using the Ovation Ultralow System library kit (NuGEN technologies) and sequenced using MiSeq. To obtain larger apicoplast genomes (34 kb), oocysts were purified from clinical stool samples. Genomic DNA was extracted from purified oocysts, NGS libraries were prepared using the Ovation Ultralow System library kit and sequenced using Miseq. Sequence reads were assembled using CLC Genomics WorkBench, and Geneious programs, to map to a reference C. cayetanensis mitochondria or apicoplast genome. The PCR amplification combined with NGS sequencing approach allowed us to sequence complete mitochondrial genomes directly from produce samples seeded with C. cayetanensis oocysts, and from stool samples. We were able to obtain whole apicoplast sequences from purified oocysts isolated from clinical stool samples. SNP profiles of both mitochondria and apicoplast genomes exhibited discriminatory power based on geographical metadata. C. cayetanensis isolates from different states grouped together in an evolutionary tree, suggesting that genomic analyses of mitochondria and apicoplast sequences may help to link outbreak cases to the source. The described approaches will facilitate the application of genomics tools to epidemiologically link C. cayetanensis identified in clinical and food samples during outbreak investigations. 

Biography:

Shyam Mohapatra is a distinguished USF Health Professor, Director of the Division of Translational Medicine (Internal Medicine) and Associate Dean of Graduate Programs at the College of Pharmacy in the University of South Florida. He also directs the USF Center for Research and Education in Nanobio-Engineering and is a Research Career Scientist at the James A Haley VA Hospital in Tampa. He has published over 200 papers and holds over 30 US and foreign patents. He is a Fellow of the AAAAI, NAI, AIMBE and AAAS and a 2014 Inductee of the Florida Inventors Hall of Fame.

Abstract:

Considerable technological success has been achieved in this burgeoning field of nanomedicine, but there remain substantial challenges, from this becoming a new paradigm in modern and evolving human needs for diagnostics and therapeutics. These include the complexities and heterogeneity of biology of chronic diseases, an incomplete understanding of nano–bio interactions and the challenges regarding chemistry, manufacturing and controls required for clinical translation and commercialization. This presentation will highlight the progress, challenges and opportunities in nanomedicine and discuss novel engineering approaches that capitalize on our growing understanding of biology and nano–bio interactions. Advances in knowledge of tumor microenvironment and the realization that the use of cancer cell cultures in 2D-monolayer format for anticancer drug discovery are responsible for the high attrition rate of drugs in clinical trials have led to use of 3D cell culture platforms that closely mimic in vivo tumors. Herein, we review the difference between 2D and 3D cultures and provide use of various nanotechnology platforms that are used not only to explicate the development of novel drug candidates that target tumor microenvironment, but also facilitate in personalizing cancer treatment.

Biography:

WassilNowicky obtained Diploma and is the Director of “NowickyPharma” and President of the Ukrainian Anti-Cancer Institute (Vienna, Austria). He has finished his study at the Radiotechnical Faculty of the Technical University of Lviv (Ukraine) with the end of 1955 with graduation to “Diplomingeniueur” in 1960 which title was nostrificated in Austria in 1975. He is the inventor of the anti-cancer preparation on basis of celandine alkaloids “NSC-631570”.

Abstract:

Another important feature of NSC-631570 is the inhibition of the formation of the new blood vessels supplying a tumor. Due to these antiangiogenic properties NSC-631570 administered before surgery brings about better demarcation of the tumor from surrounding tissue and the tumor encapsulation. This alleviates the surgical removal of tumors what has been confirmed in breast cancer studies [67, 71, 103-106, 140]. In tests in vitro, NSC-631570 inhibited in a dose-dependent manner the proliferation of human endothelial cells without exerting cytotoxic effect. The angiogenesis inhibition was observed on the capillary formation model [134]. This inhibition of the neoangiogenesis prevents the metastasis formation as well.

The length of the total capillary tubes after the incubation with NSC-631570 in given concentrations. 1 – HUVEC were incubated with NSC-631570 for 4 h. 2 – HUVEC were preincubated with NSC-631570 for 4h and then incubated for 2 h in fresh medium without NSC-631570. HUVEC – human umbilical vein endothelial cells

Biography:

Dan Yan received her MD and PhD degrees from Tongji Medical College in China. She has published 22 research papers in journals including Science Translational Medicine, Proceedings of the National Academy of Sciences (PNAS), and Journal of Biochemistry. She has reviewed multiple journals and is an Editorial Board Member for Results in Immunology and Gavin Journal of Blood. She joined the Emory Faculty in 2015 as a newly appointed Instructor focusing on characterization of roles for MERTK in non-small cell lung cancer (NSCLC) with an emphasis on identification of other pathways that cooperate with MERTK to promote tumorigenesis. 

Abstract:

Lung cancer is the leading cause of cancer-related death with poor survival rates worldwide. Non-small cell lung cancer (NSCLC) accounts for 85% of all lung cancers and 60% of these have wild-type EGFR (wtEGFR) overexpression, which portends a poor prognosis. However, agents targeting EGFR have limited utility in preclinical models with wtEGFR overexpression. Our laboratory previously identified MERTK receptor tyrosine kinase as a potential therapeutic target in NSCLC and developed MRX-2843, a novel MERTK-selective small molecule inhibitor with favorable properties for clinical translation. MRX-2843 mediated potent anti-tumor effects in the wtEGFR-expressing A549 NSCLC line in vitro and in vivo. In addition, we screened a library of 378 kinase inhibitors in various development stages and identified favorable interactions between MRX-2843 and multiple irreversible EGFR TKIs, including CO-1686 and Osimertinib/AZD-9291. Synergistic inhibition of cell expansion was observed in a spectrum of wtEGFR-expressing NSCLC cell lines. Further, we found that wtEGFR and MERTK were frequently co-expressed and co-immunoprecipitated from NSCLC cell lysates. Mechanistically, combined treatment with CO-1686 and MRX-2843 inhibited MERTK and EGFR phosphorylation and downstream PI3K-AKT and MAPK-ERK signaling. In contrast, MERTK, EGFR, and downstream signaling were not efficiently inhibited in response to treatment with single agents. Furthermore, tumor size was reduced in response to treatment with combination therapy relative to single agent treatments in a wtEGFR-expressing xenograft model. Taken together, our data provide rationale for combined treatment with MRX-2843 and an irreversible EGFR inhibitor as a novel strategy for treatment of NSCLC with wtEGFR overexpression. 

Biography:

Bhuvarahamurthy V has gained his research and teaching experience at prestigious institutions including Harvard Medical School (Boston, USA), Weizmann Institute of Science (Israel), and Humboldt University (Berlin, Germany). His research areas are Cancer Genetics, Metabolic Disorder, Cardiovascular and Neurobiology. He is skilled in assay development, cell culture, molecular biology, biochemistry, KO mouse model creation and human genetics and genomics. He has excellent skills in teaching, presentation, collaboration and working in a team. He also has experience of working in a supervisory role (experiment planning and oversee the plan execution), highly inquisitive, creative, resourceful and a fast learner. Due to vast knowledge in research field, he gained experience in writing validation protocols for biotech, medical devices and managing the protocol to completion.

Abstract:

Despite recent advances in pancreatic islet isolation techniques and changes in the regimen of immunosuppressive drugs, between 50-70% of islet cells are lost to hypoxic cell death within the first 10 to 14 days after isolation and subsequent transplantation. Islet survival must be increased, during the ischemic period between isolation and revascularization if islet transplantation is to succeed as a preferred treatment modality. The present study directly addresses the problem of isolated and transplanted islet survival. The use of exogenous growth factors has decreased the period required for islet revascularization, potentially reducing the total time of ischemia, however the resultant blood vessels surround but do not penetrate the islets sufficiently to prevent prolonged ischemia and central islet cell death. Therefore, it must be recognized that revascularization is only part of the islet survival equation in islet transplants. Cytoglobin (CYGB) is a recently discovered intracellular oxygen binding protein inducible in islet beta cells during hypoxia. Transfection of islet cells with CYGB DNA induces the production of CYGB and increases islet survival and preserves insulin secretion in cultured and immunoisolated islets, and significantly reduces the generation of toxic reactive oxygen species (ROS). Our results also suggest that the increased survival of islets by the overexpression of CYGB promotes increased vascular density in transplanted islets and surrounding immunoisolation chambers. This result is of prime interest as CYGB induces VEGF either directly or indirectly as a consequence of enhanced islet survival. The hypothesis examined by the present study is that the induction of cytoglobin will increase islet survival in isolated islets and islet transplants, thereby reducing the number of islets required to prevent the reoccurrence of diabetes in the recipient. World population contains a significant percentage of diabetic patients or those at risk to develop diabetes from aging and diet, and from pancreatitis or pancreatic malignancy. The present study will provide new information relevant to the prevention of diabetes in those patients.

Biography:

Aurora Esquela-Kerscher completed her MS in Biotechnology and PhD in Biochemistry, Cellular and Molecular Biology at the Johns Hopkins University School of Medicine. She conducted a Post-doctoral Fellowship in Frank Slack’s laboratory at Yale University where she began her studies on the role of microRNAs during development and disease. She is currently working as an Associate Professor in the Department of Microbiology and Molecular Cell Biology and Member of the Leroy T Canoles Jr. Cancer Research Center at Eastern Virginia Medical School in Norfolk, Virginia. Her lab aims to develop novel diagnostic and therapeutic targets for aggressive forms of prostate cancer.

Abstract:

Prostate cancer (PCa) is the 2^nd leading cause of cancer-related male deaths in the US. Clinicians lack effective clinical options for advanced disease and metastatic PCa remains incurable and lethal. MicroRNAs (miRNAs) are often dysregulated in human PCa. It is poorly understood how these small non-coding RNAs function in the prostate to promote cancer progression. In a screen for miRNAs correlating with advanced disease, we found miR-888 was enriched in aggressive, castration-resistant human PCa cell lines and in tumors from PCa patients. This miRNA was elevated in an innovative prostatic fluid biomarker source called expressed prostatic secretions in urine (EPS urine) from PCa patients with high-grade disease. We postulated that miR-888 plays an oncogenic role in the prostate. Indeed, we noted miR-888 promoted prostate cell proliferation, migration and colony formation in vitro. miR-888 belongs to a genomic cluster of seven miRNAs (miR-892c, -890, -888, -892a, -892b, -891b, -891a) located on chromosome Xq27.3 and lies within HPCX1 (hereditary PCa, X-linked 1), a region associated with hereditary PCa. miR-888 cluster members were similarly elevated in aggressive PC3 cell lines and enriched in EPS urine exosomes from high-grade PCa patients. Our in vitro assays indicated that this cluster modulated prostate cell growth, migration, invasion, and ability to grow in soft agar. miR-888 and miR-891a were validated as bona fide pro-oncogenic factors and accelerated prostate tumorigenesis in mice. We are testing if miR-888 cluster inactivation using antimir reagents blocks disease progression in animal models. This work will lead to effective clinical tools for aggressive PCa.

Biography:

James McNamara had studied Chemical Engineering at the University of Virginia (BS in 1992), Neurobiology at Duke University (PhD in 2003) and then completed a Post-doc at Duke University where he developed RNA based therapeutic approaches for cancer. He joined the Department of Internal Medicine at the University of Iowa in 2007. His research is focused on developing rapid clinical diagnostic assays for bacterial infectious diseases based on selective detection of pathogen-derived nuclease activities.

Abstract:

Rapid and sensitive methods are currently needed for the detection of many important bacterial pathogens. The diversity of nucleases and their presence in all living organisms make them an attractive class of biomarkers for such applications. Moreover, in contrast to most biomarkers, the enzymatic activity of nucleases can be used for signal amplification in assays that detect them. An important advantage of this approach is that it is not subject to the background that results from the non-specific adherence of exogenous enzymes (e.g., HRP-coupled antibodies binding to ELISA plates). We have developed various rapid and ultrasensitive assays that detect target bacterial species with quenched fluorescent oligonucleotide substrates that are selectively digested (and thereby activated) by their nucleases. The author will discuss applications that have been developed with this platform, including rapid culture-independent detection of 1) urinary tract infections via detection of endonuclease I (of E. coli) and 2) S. aureus bacteremia via detection of micrococcal nuclease. 

Biography:

Umashanger Thayasivam has completed his PhD from the University of Georgia in 2009. He is currently working as an Associate Professor of Statistics at Rowan University, Mathematics Department. His interdisciplinary research spans diverse areas including data mining, robust estimation and network security. He collaborated with Biomarker Discovery Center at Rowan School of Osteopathic Medicine and optimizing and verifying the utility of autoantibody biomarkers for early diagnosis. He has published several papers in reputed journals and conference proceeedings. He has been PI/co-PI for several internal and external grants. He won the Best Research Paper Award for his work on robust estimation (GSTF 2017).

Abstract:

Analyzing biomarkers is a rapidly emerging study that helps answering a wide range of biological questions. Modern biology has experienced an increasing use of data mining techniques for large scale and complex biomarker analysis. There is an urgent need to identify biomarkers that can accurately detect and diagnose rare diseases. One of its greatest potentials is, the development of criteria that allow us to diagnose a disease or to classify patients according to their risk for a clinical outcome of interest. Metabolite profiling data and omics data in general, pose several statistical challenges for classification and prediction. Metabolomics, like most ‘omics’ technologies, suffer from the problem of having huge quantities of data without the ability to efficiently process them and gain valuable knowledge. Random Forest (RF) technique, which includes an ensemble of decision trees and incorporates feature selections and interactions naturally within the learning process, is a popular choice for omics data. Recent work in computational biology has shown an increased use of random forest, owing to its unique advantages in dealing with small sample. The focus of this presentation is two-fold. First, to provide an overview of data mining in particlulur Random Forest (RF) technique in biomarker discovery, including feature selection. Second, to briefly introduce application by presenting results from different biomarker studies.