Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 2nd International Conference on Pancreatic Disorders and Treatment(10 Plenary Forums - 1Event) Dallas, Texas, USA.

Day 2 :

Keynote Forum

Nicholas Zavazava

University of Iowa, USA

Keynote: Human iPS cells ar e an alternative source of pancreatic beta cells

Time : 10:00-10:45

Conference Series Pancreas 2017 International Conference Keynote Speaker Nicholas Zavazava photo
Biography:

Dr. Nicholas Zavazava is currently working as a Professor and Director of Transplantation Research at University of Iowa, USA. His work primarily focusses on stem cells. His lab is interested in studying stem cell derived hematopoietic cell and insulin producing cells. 

Abstract:

Type 1 diabetes (T1D) is caused by autoimmunity whereby pancreatic beta cells are destroyed by autoimmune disease. Standard therapy is replacement of insulin by regular injections of recombinant insulin. However, T1D can be cured by the transplantation of pancreatic islets or that of the whole pancreas organ. Our approach is to generate iPS from the patient and derive pancreatic beta cells from those cells and transplant them back to the patient. The advantage of this approach is that we could potentially transplant patients early after diagnosis with no waiting times for the availability of organs and we would not require the use of immunosuppressant since the cells are self-derived. Fibroblasts from a healthy individual were transduced with the Yamanaka factors in a retroviral vector. After confirming that the cells were pluripotent, the cells were differentiated into the endoderm which co-expresses CXCR4 and Sox 17. Next the cells were exposed to growth factors that converted them into the foregut endoderm. The cells were further treated to form the pancreatic precursor cells which expressed Pdx1. After further treatment with GLP-1 and niconinamide, the cells formed pancreatic beta cells. These cells highly express GLP-1R and are responsive to high glucose by secretion of insulin. When transplanted in diabetic mice, they correct hyperglycemia within 3-4 weeks. Thus human iPS cells are an alternative source of pancreatic beta cells that can be harnessed for the treatment of diabetes.

  • Pancreatic Tumors & Cancers | Pancreatic Prognosis | Pancreatic Surgery | Pancreatitis

Session Introduction

Huocong Huang

UT Southwestern Medical Center, USA

Title: DDR1 inhibition as a strategy enhancing chemoresponse in pancreatic cancer

Time : 11:15-11:45

Speaker
Biography:

Huocong Huang has completed his MD degree from Sun Yat-sen University, China and PhD degree from Dr. Keith Johnson’s Lab at University of Nebreska Medical Center. He is now a Post-doctoral Researcher from Dr. Rolf Brekken’s lab at UT Southwestern Medical Center. He has been dedicated to studying pancreatic cancer microenvironment ever since his PhD study. He was involved in pancreatic cancer SPORE projects and tumor microenvironment network projects focusing on matrix-driven epithelial-mesenchymal transition in pancreatic cancer, and now he is developing many novel therapeutic strategies for the disease by targeting the tumor stroma and cancer-matrix interaction.          
 

Abstract:

The extracellular matrix (ECM), a principal component of pancreatic ductal adenocarcinoma (PDA), is rich in fibrillar collagens that facilitate tumor cell survival and chemoresistance. Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase that specifically binds fibrillar collagens and has been implicated in promoting cell proliferation, invasion, ECM remodeling, response to growth factors and epithelial-mesenchymal transition (EMT). We found that collagen-induced activation of DDR1 stimulated pro-tumorigenic signaling through protein tyrosine kinase 2 (PYK2) and pseudopodium-enriched atypical kinase 1 (PEAK1) in pancreatic cancer cells. Pharmacologic inhibition of DDR1 with an ATP competitive orally available small molecule kinase inhibitor (7rh) abrogated collagen-induced DDR1 signaling in pancreatic tumor cells and consequently reduced colony formation and migration. Furthermore, the inhibition of DDR1 with 7rh showed striking efficacy in combination with chemotherapy in orthotopic xenografts and autochthonous pancreatic tumors where it significantly reduced DDR1 activation and downstream signaling, reduced primary tumor burden, and improved chemoresponse. These data demonstrate that targeting collagen-signaling in conjunction with conventional cytotoxic chemotherapy has the potential to improve outcome for pancreatic cancer patients.

Vichin C Puri

The Liver Institute at Methodist Dallas, USA

Title: Transition from an open to a robotic pancreas surgery center

Time : 11:45-12:15

Speaker
Biography:

Vichin C Puri received his Medical training at the Maharashtra Institute of Medical Education and Research in Pune, India. He was trained as a General Surgeon at New York Hospital Queens in Flushing, NY and then completed a fellowship in abdominal transplant surgery at Cedar Sinai Medical Center in Los Angeles, CA. He served as an Assistant Professor at Methodist University Hospital Transplant Institute at the University of Tennessee in Memphis. Prior to joining The Liver Institute at Methodist Dallas, he served as Primary UNOS Transplant Surgeon and Surgical Director at St. Thomas Medical Center in Nashville, Tennessee. He is currently expanding the robotic hepatobiliary and pancreatic surgery program.

 

Abstract:

The pancreas has traditionally been considered one of the more challenging organs to work with and only a small percentage of surgeons across the world choose to dedicate their carriers treating patients with pancreatic pathology. Pancreaticoduodenectomy (PD) is considered one of the most challenging operations associated with pancreatic surgery. It was first performed in 1935 by Allen O Whipple. Over the years improving technology and science has allowed us to adopt minimally invasive techniques towards pancreatic surgery. Laparoscopic assisted PD was reported in 1994 with subsequent application of robot assisted PD in 2001 with over 400 cases reported by 2015. Review of the literature has shown steady improvement in operative outcomes, decreased mortality and morbidity, blood loss and length of stay with oncological equivalent outcome with the application of the robot compared to open surgery. Adopting the robot for pancreatic surgery has been slow and controversial however there is more evidence to support improved outcomes in select group of patients with pancreatic disease. Our early experience demonstrated decreased length of stay consistent with the data from 11.3 to 6.9 days post PD (p<0.002) in an older cohort of patients (66.2 years vs. 60.8 years; p<0.03), at equivalent cost compared to open surgery. Transition from a center that mostly performed open pancreatic surgery to a center of excellence for robotic surgery has been a challenging process however it is possible by investing the right resources and developing stringent protocols by a multi-disciplinary team. We will discuss the process involved in making this transition at a community hospital and will share some of our earlier results.

Speaker
Biography:

Dr. Deepthi Rao, M.D., FCAP, FASCP is an accomplished Gastrointestinal and Pancreatobiliary Pathologist. She has completed her medical schooling from Rajiv Gandhi University of Medical Sciences with high honors followed by her residency training at the University of Kansas Medical Center. She has completed her fellowship training in Oncological Gastrointestinal and Pancreatobiliary pathology from prestigious Memorial Sloan Kettering Cancer Center. Additionally, she has dedicated extra time in one of her interest areas, hepatic pathology, reading a large volume of liver biopsies at Weill-Cornell Medical Center during her fellowship training. She already has a decorated academic record in her young career with more than a dozen peer reviewed articles published and an even greater number of abstracts. Her interest in gastrointestinal pathology began early and is particularly unique as she spent two years doing clinical gastroenterology research in addition to her time in pathology residency and GI/Liver fellowship. She is currently working at one of the finest physician owned pathology practice - ProPath and continues to serve a large and diverse patient population. Dr. Rao has received numerous accolades during her career including meritorious acclaim for research, teaching and pure scholarship.

Abstract:

High-grade neuroendocrine neoplasms (World Health Organization Grade 3) classification of the pancreas include both well-differentiated neuroendocrine tumor (WD-NET) and poorly differentiated neuroendocrine carcinoma (PD-NEC). Previously, the diagnosis of this group of tumors was based on both the histopathology of the tumor and the assessment of proliferation fraction. However, it is extremely challenging to differentiate the  WDNET Grade 3 from the PDNEC due to the lack of well-defined histologic criteria, and the utilization of guidelines with mitotic count and immunohistochemistry for Ki-67 (>20 mitoses/10 high-power fields or Ki67>20%) shows significant overlap. However, there can be major differences in treatment strategies and clinical outcome. Thus, there is a growing need for additional practical modalities to consistently facilitate the accurate differentiation between the two categories among the high-grade pancreatic neuroendocrine neoplasms. In the age of precision medicine and molecular biomarkers, the evaluation of immunohistochemical staining for surrogate biomarkers of known genotypes of WD-NET and PD-NEC, can be crucial in establishing a final definitive classification. These biomarkers are DAXX, ATRX, Tp53 and Retinoblastoma protein. The loss of DAXX or ATRX protein expression supports the diagnosis of WD-NET, whereas the abberant expression of  Tp53,  and/or  Retinoblastoma protein aids the diagnosis of PD-NEC which can result in the appropriate clinical management and prognosis.

Speaker
Biography:

Haitao Shen has completed his PhD from China Medical University and currently he is working as a Visiting Scholar at the Temple University. He is the Medical Doctor of Shengjing Hospital of China Medical University. He has published more than 10 papers in reputed journals and has been serving as a group member of Emergency branch of Chinese Medical Association. 

Abstract:

Objective: To observe the therapeutic effects of somatostatin administered in different speeds on the severe acute pancreatitis during hemoperfusion.

Methods: A total of 112 severe acute pancreatitis patients with routine treatment in emergency intensive care unit were divided into control group and experimental group according to the speed of somatostatin injection during hemoperfusion. Patients of experimental group (n=56) received accelerated injection of somatostatin, while the patients of control group (n=56) got somatostatin in a steady speed injection. The time required for relieving clinical symptoms, time consumed for resuming normal results of laboratory tests, changes of inflammatory mediators, morbidity and mortality rate were compared between two groups.

Results: The levels of Serum C-reactive protein, tumor necrosis factor and interleukin-6 in experimental group were significantly decreased compared to those of control group (P<0.05). There were shortened hospital stay, and reduced the time required for relief of abdominal pain and distention, and for normalized WBC and amylase found after accelerated injection of somatostatin in experimental group compared with control group. Compared with control group, the acute physiology and chronic health evaluation (APACHE) II scores after treatment for one week were significantly lower in the experimental group (P<0.05). The incidence of morbidity in experimental group was significantly lower than that in control group (P<0.05). Additionally, OR value for morbidity was 0.429, and OR value for death was 0.65.

Conclusions: The accelerated injection of somatostatin during hemoperfusion could obviously improve the therapeutic effect and decrease the serum inflammatory mediators in severe acute pancreatitis, as well as reduce the incidence of morbidity and mortality. 

Dong Tang

Clinical Medical College of Yangzhou University, China

Title: High expression of galectin-1 in pancreatic stellate cells induced T cell apoptosis and skewed Th1/Th2 balance

Time : 14:15-14:45

Speaker
Biography:

Dong Tang has completed his PhD from Nanjing Medical University and Post-doctoral studies from Nanjing University of Medicine. He is Supervisor and Assistant Chief Physician of Clinical Medical College of Yangzhou University (Subei People's Hospital of Jiangsu Provinc). He got a chance of being a Visiting Scholar in the National Cancer Center in Japan from December 2012 to January 2013. He has published more than 20 papers in reputed international journals.

Abstract:

Pancreatic cancer microenvironment is composed by stromal cells and extracellular components, in which the main stromal cell includes activated pancreatic stellate cells (PSC, one of the most important stromal cells). PSC in pancreatic cancer microenvironment can promote tumor cell growth, and increase the tumor cells resistance to chemical drugs in vitro. Galectin-1 is a lectin protein with high affinity to β-galactose, which can inhibit T cell proliferation and induce tumor infiltrating T-cell apoptosis. Recently, it has founded that Galectin-1 was significantly expressed in cultured activated PSC. As a lot of activated PSC existing in pancreatic cancer microenvironment, the relationship between endogenous Galectin-1 of PSC and the pancreatic cancer immunosuppression is unclear. PSC were isolated from resected fresh pancreatic tissue and Galectin-1 was knocked down using a small hairpin RNA (sh RNA) or overexpressed using recombinant lentiviruses. In order to investigate the relationship between Galectin-1 expression and tumor immune suppression in pancreatic cancer, the impacts on T cells function and apoptosis by primary PSC with different levels of Galectin-1 expression were studied, and the expression of Galectin-1 and CD3 in pathological specimens of pancreatic cancer, chronic pancreatitis and normal pancreas tissues were analyzed. Compared with normal PSCs, PSCs with Galectin-1 over-expression significantly induced apoptosis of CD3+T cells (p<0.01), CD4+T cells (p<0.01) and CD8+T cells (p<0.05), and CD3, CD4 and CD8 T cells apoptosis was significantly decreased in PSCs with Galectin-1 silenced (p<0.05). Compared with normal PSCs, PSCs with Galectin-1 over-expression significantly inhibited secretion of Th1 cytokines (IL-2 and INF-γ) (p<0.01), and induced secretion of Th2 cytokines (IL-4 and IL-5) (p<0.01), and PSCs with Galectin-1 silenced increased Th1 cytokines (IL-2 and INF-γ) secretion (p<0.01) and decreased Th2 cytokines (IL-4 and IL-5) secretion (p<0.01 and p <0.05, respectively). Expression of Galectin-1 and CD3 in pancreatic cancer tissues were located around the pancreatic cancer cells and significantly high than chronic pancreatitis and normal pancreas tissues (p<0.01). Our study suggests that PSC with Galectin-1 high expression promoted the T-cell apoptosis, and significantly inhibited the secretion of Th1 cytokines (IL-2 and INF-γ) and induced secretion of Th2 cytokines (IL-4 and IL-5) which skewed Th1/Th2 balance. High expressed Galectin-1 of PSC in pancreatic cancer microenvironment might form a tumor immunosuppression barricade which induced apoptosis of T cells and inhibited the infiltration of T cells, and results in development of immunosuppression of pancreatic cancer.

Soriba Naby Camara

Gamal Abdel Nasser University of Conakry, Guinea

Title: Epidemiology of pancreatic carcinoma in Guinean population a multicentric and retrospective study

Time : 14:45-15:15

Speaker
Biography:

Soriba Narby Camara has completed his Master’s in Surgery from Union Hospital, Tongji Medical College and PhD in Pancreatic Surgery in Union Hospital Huazhong University of Science and Technology. In 2004, he served as Teacher in Medical College and Physician in the Department of Visceral Surgery of the National Hospital Donka Conakry, Guinea. He has published more than 15 papers in reputed journals and has served as Head of Departments in Fundamental Sciences, in University Gamal Abdel Nasser of Conakry Guinea. He was also Assistant Chief in Department of Visceral Surgery at the Hospital of Friendship Sino-Guinea of Kipe.

Abstract:

This study aim to investigate, the epidemiologic aspects, the diagnosis procedure, the pathological characteristic, the management and the prognosis of pancreatic carcinoma in Guinean population

Methods: The unuversitary hospital of Donka, of Ignace and friendship Hospital Sino-guinean of Kipe were used as frameworks for the realization of this work. However, 358 patients with pancreatic carcinoma were retrospectively studied. All patients were of Guinean nationality and were hospitalized from January 2011 to December 2016. Their ages ranged from 34 to 85 years. Of 358 patients there were 179 from Ignace Deen Hospital, 173 from Donka Hospital and 4 patients from friendship Hospital Sino-Guinean of Kipe.

Results: The abdominal pain, the jaundice and weight loss were the main symptomatology encounter with our patients. The NSE, was elevated in 259 patients, never elevated in 99 patients, CA19-9, was elevated in 321 patients, never elevated in 37 patients. CYFRA21-1, was systematically elevated in in 242 patients, and never elevated in 116 patients. The CT scan had highlighted, hyper density located in the region of head (n=304), the neck (n=22), the body (n=27) the tail (n=4), and whole pancreas (n=1) influenced the choice of surgical procedures. The diameter of cancer mass was 4.3±2.2. Cytopatholgy results show us the carcinoma grade I in 200 patients and grade II in 134 patient’s. According to the pain scale of European Organization for Research and Treatment of Cancer (QLQ-C30) a decrease from 82±28 to 24±12 was observed.

Conclusion: In guinea the management of pancreatic carcinoma is difficult, of because of the late step.

  • Special Session

Session Introduction

Purujit Choudhury

Gauhati Medical College, India

Title: Is chronic pancreatitis an unsolved enigma of pancreatic milestone? An observation Purujit Choudhury

Time : 15:15-16:15

Speaker
Biography:

Purujit Choudhury is currently working as Associate Professor of Surgery at Gauhati Medical College. After completion of MBBS, he completed MS (Master of Surgery) from Gauhati Medical College. Later he completed his Research work in Surgical Gastroenterology and 1st Indian Surgeon to be awarded PhD in SGE under famous Gauhati University. After that in 2008, he was selected to continue research work in pancreaticobiliary cancer and successfully completed in 2016 and was conferred DSc (Doctorate of Science) from Gauhati University under University Grant Commission of India and was the first Indian Surgeon to get DSc and 2nd Asian to be awarded this prestigious DSc degree. He is the 5th Surgeon across the globe to get Doctorate of Science under UGC and was conferred FMAS (Fellowship Minimal Access Surgery) by AMASI (Association of Minimal Access Surgery of India) headed by Dr. C Pallanivelu, legend in the field of Laparoscopic Surgery of the world. He was selected for prestigious PhD Guide and Supervisor of two eminent universities of India- Gauhati University and Srimanta Sankaradeva University of Health Sciences. 

Abstract:

Introduction: Chronic pancreatitis is a disease of varied aetiology with high morbidity and remarkably significant mortality if intervention is late and improper. It was said to be a non-surgical disease. No surgical procedure can restore its function or it is unlikely to prevent further glandular destruction. Avoidance of alcohol is determinant of outcome after all operation striving to improve quality of life which is also dismal. There are many surgeries but no one can cure pain in totto which is the main symptom to affect quality of life.

Materials & Methods: Thorough history, physical examination, laboratory data and imaging are used to diagnose the cases. CT and MRCP are the imaging commonest used though CT guided FNAC was advocated in doubtful cases of pancreatitis involves head. Conservative and surgical procedures are adopted for the management of the cases according to extent of pathology.

Results: Quality of life is dramatically improved when treated early. Long time follow-up shows recurrence and high morbidity who presented late. Surgical procedures are unable to cure symptoms in totto. Improve quality of life was achieved by surgeries. Recurrence of ductal stones in small percentage of cases could manage with improved function.

Conclusion: Chronic pancreatitis is a progressive disease with massive parenchymal destruction of both exocrine and endocrine system and replaced by fibrous tissue. Many of the cases might develop carcinoma. Early surgical intervention favors its prognosis. Counseling is mandatory before starting treatment.