Scientific Program

Day 1 :

Keynote Forum

Galina Migalko

CEO and President Quantum Medicine USA

Keynote: Is X-Ray Mammography Accelerating The Epidemic of Breast Cancer?

Time : 10:00-10:40


Galina Migalko, M.D., N.M.D. brings more than 30 years of excellence in non-invasive Diagnostic Medical Imaging. After graduating with her M.D. from Uzghorod Medical University, Ukraine in 1988, Dr. Magalko worked for years in wellness clinics and diagnostic medical centers as practitioner and administrator. She has pioneered and developed a revolutionary Full Body Comprehensive Medical Diagnostic Non-Invasive, Painless, Non-Radioactive Scan which includes a Full Body Medical Bio-Electric Scan, Interstatial Metabolic pH Testing, detailed medical reports and consultation to evaluate all physiological, anatomical and functional information about all tissues, glands and organ systems.

Dr. Migalko is the world’s leader in non-invasive, non-radioactive diagnosis treatment and early detection of cancer, heart disease, diabetes, metabolic acidosis, circulatory and lymphatic issues, infertility, and other preventable and treatable health challenges.

Dr. Migalko relocated to the United States in 1998. In 2011 she received her NMD from the University of Science, Arts & Technology in Montserrat, West Indies, and as CEO and President, founded Universal Medical Imaging Group that centers on the importance and principles of wellness and early detection.

Currently she is working on her dissertation in Quantum Medicine showing the benefits of combining the best from the conventional Western medicine with complementary and alternative diagnostic services and therapies.


While a growing body of research now suggests that x-ray mammography is causing more harm than good in the millions of women who subject themselves to breast screenings, annually, without knowledge of their true health risks, the primary focus has been on the harms associated with over-diagnosis and over-treatment, and not the radiobiological dangers of the procedure itself.

In 2006, a paper published in the British Journal of Radiobiology, titled “Enhanced biological effectiveness of low energy X-rays and implications for the UK breast screening programme,” revealed the type of radiation used in x-ray-based breast screenings is much more carcinogenic than previously believed.

Recent radiobiological studies have provided compelling evidence that the low energy X-rays as used in mammography are approximately four times – but possibly as much as six times – more effective in causing mutational damage than higher energy X-rays. Since current radiation risk estimates are based on the effects of high energy gamma radiation, this implies that the risks of radiation-induced breast cancers for mammography X-rays are underestimated by the same factor.

Keynote Forum

Robert O Young

Director PH Miracle Medical Association USA

Keynote: Alkalizing Nutritional Therapy in the Prevention and Reversal of Any Cancerous Condition

Time : 10:40-11:20


Over the past three decades, Robert O Young has been widely recognized as one of the top research scientists in the world in the nutritional sciences .  He has a PhD in Nutrition, an MSc and a DSc in biology and chemistry.  He also has a ND in the naturopathic sciences. Throughout his career, his research has been focused at the cellular level having a specialty in cellular nutrition, he has devoted his life to researching the true causes of "disease," subsequently developing The New Biology™ to help people balance their life. In 1994, he discovered the reality of biological transformation of red blood cells into bacteria and bacteria to red blood cells. He has documented several such transformations. His research findings have been published in several noted journals, including The Journal of Alternative and Complementary Medicine. (Sympathetic Resonance Technology, Scientific Foundations and Summary of Biologic and Clinical Studies, Dec. 2002, Vol. 8, No. 6: 835-842).  Metabolic and Dietary Acids are the Fuel that Lights the Fuse that Ignites Inflammation that Leads to Cancer!. Int J Complement Alt Med 3(6): 00094. DOI: 10.15406/ijcam.2016.03.00094 He is the author of numerous articles (Herbal Nutrition 1988) and author and co-author of many books including: Herbal Nutritional Medications (1988), One Sickness, One Disease, One Treatment (1992), Sick and Tired (Woodland Publishing, 1995), Back to the House of Health (Woodland Publishing, 1999), The pH Miracle (Warner Books, 2002), The pH Miracle for Diabetes, (Warner Books,2003), Back to the House of Health 2, (Woodland Books, 2003), The pH Miracle for Weight Loss (Warner Books, 2004), The pH Miracle revised and updated book 2 (Hachett Books 2010), The Cure for Type I and Type II Diabetes (Hikari Media 2013), Reverse Cancer Now (Hikari Media, 2014), The pH Miracle for Cancer (Hachett Books 2015) and The pH Miracle for Heart Disease. He has currently sold over 5 million pH Miracle books in 191 countries and his books are translated in 29 different languages.


Due to the evident ineffectiveness of conventional cancer treatments (e.g. chemotherapy and radiation), more efficient alternatives are needed. The potential of Alkaline Nutritional Infusion (ANI) as a legitimate alternative to chemotherapy and radiation is examined. While largely ignored in conventional oncology, the pH of the interstitial fluids is suggested as paramount in identifying a cancerous condition. It is further suggested that cancer is an over-acidic condition of the body that can be reversed and prevented with alkalizing treatments such as ANI. Full Body Bio-Electro Scan (FBBES) is presented as a noninvasive means to examine body pH and the presence of pancreatic and liver cancer. In addition, non-invasive Full-Body Thermography (FBT) and Full-Body Ultrasound (FBU) are presented as a noninvasive means to examine the physiology and the anatomy of the organs, glands and tissues for inflammation, calcifications, cysts and tumors in the prevention and subsequent treatment of any cancerous condition. Finally, Live Blood Analysis (LBA) and Dried Blood Analysis (DBA) are non-invasive hematology tests for evaluating the health of the red and white blood cells and to view inflammatory and malignancy at the cellular level. In contrast to conventional cancer treatments, ANI methods such as Intravenous Nutritional Infusion (INI) and Rectal Nutritional Infusion (RNI) provide an alkalizing approach to cancer treatment and prevention.

Keynote Forum

Vincenzo Neri

Department of Medical and Surgical Sciences, University of Foggia, Italy.

Keynote: Complications In Biliopancreatic Surgery

Time : 11:40-12:20


Dr. Vincenzo Neri was born in Bari, Italy, on 15th March, 1946, graduated on 1970 in Medicine and Surgery in the University of Bari. He is full Professor of General Surgery in the Medical School of the University of Foggia, Polyclinic. He is Director of the Residency School of General Surgery and Department of General Surgery. He was President of the Course of Degree of Medicine and Surgery, University of Foggia, in the years from 1996 to 2002. He was Director of Department of Surgical Sciences , University of Foggia in the years from 2002 to 2008. He obtained the certificate of “Maitrise Universitaire en Pedagogie des Sciences de la Santè”on the Universitè Paris – Nord Bobigny. He is author of more than 330 scientific paper edited on national and international journals and chapters of books. His research interest is hepatobiliopancreatic surgery. He is member of scientific societies : SIC, IHPBA,AISP,EASL,NESA,SLS.


The complications of biliopancreatic surgery have a very variable range of incidence showing surgical procedures with low incidence of complications such as simple cholecystectomy and complex or very complex procedures such as pancreatic resections followed by high incidence of postoperative complications. The purpose of this editorial is to examine a number of specific complications unique to biliopancreatic surgery such as: pancreatic fistula in relation to the different types of pancreatic digestive anastomosis and biliary injuries after biliary surgery. Pancreatic and biliary surgical complications include a large range of conditions with overlapping clinical presentations and diverse therapeutic choices. The true incidence of pancreatic and biliary complications is difficult to determine due to selection and reporting bias. The treatment of these complications continues to evolve and patients may require endoscopic, surgical, and/or percutaneous techniques.

Keynote Forum

Mouad Edderkaoui

Cedars-Sinai Medical Center & University of California Los Angeles, USA

Keynote: Targeting metastasis and drug resistance for treating pancreatic cancer

Time : 12:20-13:00


Dr. Mouad Edderkaoui PhD has research goal to understand the mechanism of pancreatic cancer initiation and progression and to develop a treatment strategy for the disease. Edderkaoui focuses on the role of cells present in the tumor microenvironment and how histone deacetylases (HDACs) regulate the interaction between these cells. He currently  belongs to Cedars-Sinai Medical Center & University of California Los Angeles, USA.

He was awarded with career development award, national institute of health in 2011, Hirshberg foundation award in 2012 and at-present he is the Associate editor: Frontiers in science.


Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with no effective treatment. PDAC cells are highly proliferative and metastatic. We have developed a new drug called Metavert that targets, at the same time, the glycogen synthase kinase 3 beta (GSK-3β) and histone deacetylase (HDAC- class 1/2), important mediators of cancer progression.

We have designed and synthesized a novel drug that shows a significant anti-cancer effect in vitro in PDAC cells and patient-derived circulating tumor cells (CTCs) and in vivo in the most aggressive mouse model of experimental PDAC using the KrasLSL-G12D/+;Trp53LSL-R172H/+;Pdxcre (KPC) mice.

Metavert significantly (at nano-molar concentrations) decreased cancer cell survival and increased apoptosis in several PDAC cells lines and CTCs. The same doses of Metavert did not affect survival of normal hepatocytes and pancreatic ductal cells. Metavert decreased expression of markers of epithelial to mesenchymal transition (EMT) and cancer stemness, the two driving forces of metastasis and drug resistance. Metavert prevented invasion of the cancer cell lines. Furthermore, Metavert sensitized PDAC cells and CTCs to chemotherapy drugs gemcitabine and paclitaxel. Treatment with Metavert significantly increased KPC mice survival by ~50% and sensitized the tumors to gemcitabine. Distal metastasis was decreased from 29% in control KPC mice to 0% in Metavert treated KPC mice. Fibrosis, M2 macrophages, and pro-cytokine levels in the blood were decreased by Metavert treatment without affecting the function of healthy organs.

Avenzoar Pharmaceuticals has licensed Metavert and it has obtained the orphan drug status for it. The pre-clinical PK, PD, toxicity studies are ongoing and the drug is expected to be approved for clinical testing within one year.


Keynote Forum

Mohamed Gamil Ramadan

Ex-president of Egyptian Society of Surgical Oncology Cairo University Eqypt

Keynote: Pancreatic cancer can be diagnosed early

Time : 14:00-14:40


Dr. Mohamed Gamil A Ramadan MD, FACS Professor of Surgical Oncology Head of GI Endoscopy Unit NCI, Cairo University Ex-president of Egyptian Society of Surgical Oncology (EGSSO )




Pancreatic cancer is the forth cause of cancer death worldwide .Difficulty in early diagnosis is the main cause of its poor diagnosis. CT and MRI equally perform in diagnosis and evaluation of respectability of pancreatic cancer.  Ultra-sound had a lower sensitivity and specifity. EUS is a reference method for diagnosis and staging of different pancreatic disease. At this time no major professional groups recommended routine screening for pancreatic cancer in average risk people .The aim of this study is to compare EUS,CT and MRI in early diagnosis of pancreatic tumors .

Patients and Methods

Ninety eight patients with various pathological types of pancreatic mases were enrolled in this study. They were examined using the three diagnostic modalities and compared to the gold standard which is the cytological and histopathologic diagnosis of an EUS guided biopsy


EUS detected 100% of pancreatic tumors even those smaller than 1 CM in diameter .EUS detected nodal metastasis in 65% of cases verses 37.5% in MRI and 7.5% in CT.EUS detected vascular invasion in 50% of cases verses 32.5% in MRI and 7.5% in CT. EUS and MRI detected hepatic metastases in 20% of cases verses 7.5% by CT .EUS has sensitivity of 100% and specifity of 75% which is the highest values among the three diagnostic modalities


Endoscopic ultra sound is a very sensitive method for detection and staging of pancreatic cancer.


  • Pancreatic Tumor

Session Introduction

David Piquemal

Co-founder and Scientific Director of ACOBIOM Company

Title: Patient Stratification and Precision Medicine in Pancreatic cancer: a gene blood-signature for gemcitabine treatment

Time : 14:40-15:10


Dr. David Piquemal is the co-founder and scientifc Director of ACOBIOM company.  His main aim is to  develop innovative methods and  software to analyze, integrate and contextualize large-scale biological data in the fields of health, agronomy and environment. He completed  his PH.D in Molecular Biology from the institute of Human Genomic in the year 2000. His area of interest involves-Molecular Biology, Personalized Medicine,Translational Medicine and Bioinformatics.



Pancreatic cancer (PC) kills 98% of those it afflicts and is one of the most lethal cancers worldwide: patients diagnosed with PC have a poor prognosis partly because the cancer usually causes no symptoms early on, leading to metastatic disease at the time of diagnosis. The high mortality rate is partly due to the difficulty to diagnose and due to the lack of stratified patients to effective treatments. The capability of biomarkers to improve treatment and to reduce healthcare costs is potentially greater than in any other area of current medical research. Otherwise, Healthcare stakeholders are facing two major issues: the reduction of global Healthcare system expenditures and the growing need to improve the efficiency of therapies. Diagnostics are one of the most efficient solutions to respond to these needs by supporting physicians in the selection of the best treatment.

In a without a priori analysis and from a whole blood collection, from clinical trial phase III and based on a high throughput analysis of NGS data using the proprietary ACOBIOM genomics platform (Big Data system dedicated to Biomarker discovery), we identified a set of genes in a pre-discovery phase. Using Real-Time PCR, candidate genes were selected for test significance and a Gene Expression-based Score was established.

Acobiom developed a new In Vitro Diagnostic for patient stratification based on molecular analysis. The GemciTest® assay is an IVD associated with gemcitabine drug in PC treatment. GemciTest® is currently a prototype in an operational environment through a 15 Clinician Peer Network. This IVD is a quantitative real-time PCR assay and is intended to quantitatively aid in the determination of high probability Progression- Free Survival and Overall Survival rates of patients diagnosed with pancreatic cancer and treated with gemcitabine as first-line therapy.

In this context, Acobiom is always looking for new partnerships, public or private, the right way to really open the opportunity to develop safe/better solution in PC for the patient (Bench-to-Bedside), assisting physicians in routine patient care.


Sangeeta Choudhury

Sir Ganga Ram hospital, India

Title: Role Of Vitamin D In Modulation Of Muc-1 In Pancreatic Cancer

Time : 15:10-15:40


Sangeeta Choudhury is Associate Professor & Senior Consultant @ Sir Ganga Ram hospital, New Delhi, INDIA. She has obtained her Doctoral degree from one of the premier institute of the country, Bhabha Atomic Energy Research Centre, Mumbai, India. Thereafter she was a Research Fellow at Department of Anatomy, Division of Cell Biology, University of New South Wales (UNSW), Sydney, AU and also did her Post Doctoral Fellowship at Division of Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, USA. On returning to the country, she was positioned as Research Scientist (Indian Council of Medical Research), National Institute of Immunology, New Delhi, India. She has been the recipient of national awards (Lady Tata Grants, Department of Atomic Energy, INDO-US Vaccine Action Program). Her major areas of interests are solid tumor biology and stem cell, cancer & obesity related metabolic disorders, transplantation immunology. She is in the review board of national journals and also scientific committee. She is a member of Cancer bodies and also Immunology & biochemistry national bodies [American Association for Cancer Research (USA); Indian Society of Oncology (India); American Society for Microbiology (USA), Society for Biological Chemists, India (India), Association of Clinical Biochemists India]. She has authored about 28 scientific articles and 3 book chapters too.                                                                                  


Over the years, pancreatic cancer has been established as a complicated disease with poor prognosis and survival rate. Standard chemotherapeutic agents/drugs have not shown any significant advancement in its regression. Several studies have indicated anti-angiogenesis and blocking the cancerous growth of breast, prostate, lung and colon by micronutrients like vitamin D, E, B12. Although, pancreatic cancer tissue expresses Vitamin D (VitD) receptor, the potential mechanism to exert anti-cancer effect remains underexplored.

Thus, our study aimed to find out the mechanistic effect caused by the VitD analogue (Calcitriol) in pancreatic cancer cells. Pancreatic cancer cells (PCC lines; MiaPaCa2 and PanC-1) treated with calcitirol for longer duration (24hrs-to-96hrs) showed decreased expression of metastatic phenotype, CXCR4/CCL12, EpCAM/Vimentin along with decreased chemoresistant-MUC-1 expression, although no inhibitory effect was observed on their proliferative capacity. But, addition of Gemcitabine (Gem) to calcitirol-treated PCC lines increased their apoptotic capacity than cells treated only with Gem, suggesting that calcitirol treated-PCC cells are susceptible to chemotherapeutic drug. Further, with the emergence of stroma playing a major role in pancreatic cancer, we attempted to elicit the involvement of VitD in Sonic Hedgehog (SHH) signaling. Enhanced apoptosis was observed when salinomycin (SHH inhibitor) was administered to calcitirol treated-PCC cells. Copy numbers of transcription factors C-myc, SMO, PTCH1, PTCH2, and hypoxia-induced factor (HIF1-α) were observed to show increased expression in treated PCC lines in comparison to untreated cells.

In conclusion, our experimental evidence postulates a potential mechanism by which VitD- analogue, calcitirol modulated its stromal interaction via its action on the cell-membrane protein MUC-1.

Guan Chen

Department of Pharmacology and Toxicology,Medical College of Wisconsin,USA

Title: p38γ MAPK signaling and pancreatic tumorigenesis

Time : 16:00-16:30


Ras is the most established oncogene in human cancer, with its mutation (K-Ras) occurring in about 50% human colon cancer and its hyperexpression (H-Ras) in more than 50% of human breast cancer. Ras oncogene activity, however, is determined by downstream effectors and elucidation of this regulation is essential to understand why not all Ras mutations can lead to human malignancies. MAPKs (mitogen-activated protein kinases), including ERK, JNK, and p38, signal downstream of Ras by converting extracellular and Ras signals into specific cellular response through a group of transcription factors. Our previous work established that Ras-induced p38 alpha phosphorylation/activation inhibits the oncogene activity by negative feedback. Results from our recent studies further showed that p38 gamma, a p38 family protein, is induced by Ras and in turn required for Ras transformation in rat intestinal epithelial cells and for Ras-invasive activity in human breast cancer. These results together indicate that signaling integrations among p38 family members determine Ras oncogene activity in a given tissues and p38 proteins regulate Ras activity by isoform-dependent mechanisms. Currently, we are investigating mechanisms by which Ras induces p38 gamma expression and by which p38gamma is required for Ras-induced transformation / invasion.
Nuclear receptors are group of transcription factors that play an important role in reproduction, homeostasis, and cancer development through regulating gene expression in response to their ligand. Our second research interest is to study signal cross-talks between Ras/MAPK pathways and nuclear receptors. Studies from our lab have established a c-Jun/AP-1 dependent trans-activation for stress-induced vitamin D receptor (VDR) expression and an anti-apoptotic activity of VDR by a K-ras-dependent mechanism. Our results further showed that another nuclear receptor ER (estrogen receptor) inhibits stress MAPK-mediated cell death independent of its transcriptional activity by converting pro-apoptotic c-Jun activity into a c-Jun-dependent AP1 transcription. These results together suggest that nuclear receptors may cooperate with Ras/MAPKs to regulate stress-response independent of their transcription activity. We are currently investigating whether regulation of nuclear receptors represents a novel strategy for human cancer treatment.


Pancreatic ductal cancer (Pda) lacks established therapeutic targets and is consequently among the deadliest malignancies with near-universal K-Ras mutations. Here, we report that a Kras effector p38g (MAPK12) is required for pancreatic tumorigenesis through stimulating metabolic reprogramming. Both conditional p38g knockout and pharmacological inhibition decrease pancreatic tumorigenesis and inhibit Pda growth. Mechanistically p38g binds PFKFB3 dependent of mutated Kras and phosphorylates this glycolytic activator at S467, which is required for aerobic glycolysis and Pda growth. Activation of the p38g/p-PFKFB3 pathway in clinic specimens further correlates with decreased patient survival. Thus, p38g MAPK is essential for Pda tumorigenesis by linking K-Ras oncogene activity and metabolic reprogramming and may be targeted for therapeutic intervention

  • Pancreatic tumours and cancers

Session Introduction

Omar Sabeeh

King Abdulaziz University, Jeddah, Saudi Arabia

Title: Mapping of the Superior Mesenteric Vessels for Artery First Pancreatoduodenectomy in Patients with High Visceral Fat

Time : 16:30-17:00


Dr. Omar Sabeeh was born in Jeddah, Saudi Arabia. He obtained his medical degree at King Abdulaziz University in Jeddah.
Currently he is a resident at King Abdullah Medical Complex, with special interest in Hepatobiliary and Pancreatic Surgery


Background No studies have reported the impact of visceral fat on anatomy of the superior mesenteric vessels. We aim to clarify the anatomical relationships between the superior mesenteric artery, vein and their tributaries relative to levels of patient visceral fat to assess applicability of artery first pancreatoduodenectomy in obese patients. Methods 176 triple-phase computed tomography scans were retrospectively analysed to determine the positioning and distance of the superior mesenteric artery relative to the superior mesenteric vein at varying levels, and to jejunal veins. Patients were categorised into high and low visceral fat groups based on mean sagittal abdominal diameter. Hypothesis testing was performed to highlight anatomical differences. Results No statistical significance was found to suggest that either the distance between superior mesenteric artery and superior mesenteric vein (at gastrocolic trunk level), or the distance between superior mesenteric artery and ventral jejunal vein varied with level of visceral fat (p=0.26 and 0.08, respectively). Superior mesenteric artery originating caudal to the spleno-mesenteric confluence was significantly more prevalent.

  • Pancreatic Enzymes & Hormones

Session Introduction

Hildegard M. Schuller

Experimental Oncology Laboratory, USA

Title: Targeting the neurotransmitter receptor-driven regulation of pancreatic cancer

Time : 17:00-17:30


Hildegard M. Schuller, D.V.M., Ph.D. is Distinguished Professor Emeritus, College of Veterinary Medicine, University of Tennessee Knoxville, TN, USA.


Dr. Schuller held positions at the Medical School Hannover (Germany), the Frederick Cancer Research Center and National Cancer Institute before joining the University of Tennessee Knoxville TN in 1985 as Director, Experimental Oncology Laboratory. She was promoted to Distinguished Professor in 1994. Dr. Schuller’s research has pioneered the concept that neurotransmitter receptors regulate lung cancer and pancreatic cancer and are promising targets for the prevention and therapy of these cancers. She has published 248 articles in national and international professional journals.



Pancreatic ductal adenocarcinoma (PDAC), is the leading histological type of pancreatic cancer with incidence rising and a very high mortality within one year of diagnosis. We have pioneered the concept that the highly coordinated hyperactivity of pancreatic cancer stem cell self-renewal, cell proliferation, angiogenesis, metastatic potential and drug resistance is regulated by neurotransmitter receptors that are the recipients of signals from the autonomic nervous system. We as well as others have thus shown that either stress or drug-induced hyperactivity of the sympathetic branch of the autonomic nervous system, resulting in systemic increases of the catecholamine neurotransmitters epinephrine and norepinephrine, significantly stimulated the growth of PDAC in mouse xenografts via hyperactive cAMP-dependent signaling downstream of Gs-coupled beta-adrenergic receptors. Treatment of the animals with -aminobutyric acid (GABA) completely reversed this effect via inhibition of cAMP formation in response to binding of GABA to Gi-coupled GABAB receptors. The general beta-blocker propranolol had similar effects via inhibition of cAMP formation downstream of Gs-coupled beta-adrenergic receptors. Using a hamster model of pancreatitis-associated PDAC, we additionally showed that treatment of the animals with GABA effectively prevented the development of PDAC. Stress reduction via environmental enrichment also significantly reduced the development and progression of PDAC xenografts in mice. In each of these animal models, the observed inhibition of PDAC growth and progression was accompanied by decreases in cAMP-dependent signaling of  multiple proteins associated with cell proliferation, cell migration, stem cell self-renewal and angiogenesis. In vitro investigations with human PDAC cell lines confirmed the central role of cAMP hyperactivity downstream of Gs-coupled receptors as the driving force of PDAC growth suggested by the animal experiments. Collectively, these findings identify the opposing roles of PDAC stimulating Gs-coupled neurotransmitter receptors and PDAC inhibiting Gi-coupled neurotransmitter receptors as promising novel targets that can be successfully used for the prevention and therapy of PDAC by restoration of  cAMP homeostasis via psychological as well as pharmacological agents that are already widely used for the therapy of several non-neoplastic diseases.




Day 2 :

  • Lunch time@ Hotel Restaurant