2^nd International Conference on Pancreatic Disorders and Treatment(10 Plenary Forums - 1Event) September 13-14, 2017 Dallas, Texas, USA

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.

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.

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.

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. 

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.

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.

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 1^st 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 2^nd Asian to be awarded this prestigious DSc degree. He is the 5^th 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.

Biography:

Sorah Yoon has completed her PhD from Seoul National University, South Korea and Post-doctoral studies from Beckman Research Institute of City of Hope, USA. She is Staff Scientist of Department of Molecular and Cellular Biology at Beckman Research Institute of City of Hope. She has published more than 19 papers in reputed journals, one book chapter, and 15 patents including USA patents. She was awarded numerous travel awards including Meritorious Abstract Travel award in ASGCT, 2015 and travel award in OTS, 2016. She was also invited as a speaker to drug delivery conferences in China and Malaysia.

Abstract:

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies and the 4^th leading cause of cancer-related deaths in North America. The survival rate remains less than 5% at 5 years taking into account all stages of the disease. In contrast to other cancer types, the mortality rate of PDAC is increasing, with PDAC being predicted to become the second leading cause of cancer-related mortality by 2020. Despite great efforts to improve the treatment and outcome of patients with PDAC, limited progress has been made. Still, current therapeutic options are very disappointing. Genetic mutaions of tumor supperssor genes have been well characterized in pancreatic cancer. However, the pathophysical progression of PDAC doese not always correlate with these genetic changes, suggesting the possibility that unidentified genetic alterations or epigenetic factors might be involved in the progression of pancreatic maligancy. The loss of heteozygosity of lysine demethylase (KDM6B) encoding histone demethylase makes pancreatic cancer epigenetically silenced in the downstream target of CCAAT/enhancer binding protein alpha (C/EBPα), strong anti-proliferator by affecting p21, a cyclin-dependent kinase (CDK) inhibitor. The decreased expression of KDM6B and C/EBPα is well-correlated through the malignant progression of PDAC. For the precision medicine in pancreatic cancer, to activate the silened gene of C/EBPα for the therapeutics, small activating RNA(saNRA) to C/EBPα is developed. For targeted delivery of C/EBPα, RNA aptamers have been isolated via cell-SELEX, that showed the pancratic cancer cell specificity. The isolated RNA aptamers have been conjugated with C/EBPα-saRNA as targeting modalities. The targeted delivery of the C/EBPα-saRNA conjugates showed the increased expressionof C/EBPα in vitro with translational and transcriptional level. In vivo assay, the targeted delivery of C/EBPα-saRNA conjugates significantly inhibited the tumor growth without toxicity. Using pancreatic cancer specific aptamers, to reduce the non-specific absorption of cytotxic drugs in normal cells, aptamer-drug conjugates (ApDCs) were constructed with active metabolites of prodrugs, gemcitabine and 5FU, and chemotoxins, MMAE and DM1. The ApDCs with gemcitabine and 5FU showed the significant anti-prolieraction effects by inducing double-strand breask in nuclear without affecting non-targeting cells. Also, The ApDCs with MMAE and DM1 showed the stong anti-prolieraction effects by arresting the cycle without the cytotoxicity in non-targeting cells. Taken together, our studies prove the therapeutic strategies for precision medicine in pancrearic cancer by following firstly, targeting somatic mutaions for therapeutics and secondly, aptamer mediated targeted delivery of theapeutics with minimizing the side effects in normal cells.

Biography:

David G, PhD, is an Associate Professor of Biochemistry and Molecular Pharmacology at NYU School of Medicine. He received Graduation degree in Molecular Biology from the Pasteur Institute in Paris, studying the bases for acute promyelocytic leukemia. He then did his Post-doctoral work at the Dana Farber Cancer Institute, studying the interplay between chromatin modifiers and cancer using mouse models. His laboratory currently investigates the impact of epigenetic processes in early stages of prostate and pancreatic cancer progression. Recently, his work has focused on the contribution of chromatin modifiers on cell fate decisions, including cellular senescence, as modulators of tumorigenesis, and by inference the identification of epigenetic pathways that can serve as therapeutic targets to prevent cancer progression.

Abstract:

Pancreatic ductal adenocarcinoma (PDAC) is virtually invariably a fatal disease, and is characterized by invasive and metastatic progression, as well as a striking resistance to conventional therapeutic approaches. In addition, recent reports have demonstrated that inflammation is a key component of precancerous lesion initiation and progression. However, the downstream events linking oncogenic activation KRAS to inflammation are not yet fully understood. Here, we report that the chromatin associated Sin3B co-repressor, previously shown to be required for oncogene induced senescence, promotes KRAS driven pancreatic lesions formation and progression in the mouse. At the molecular level, Sin3B is necessary for KRAS induced or chemically-induced inflammation of the pancreas. Importantly, we have now extrapolated these results to pancreatic human cells and have correlated Sin3B expression levels and inflammation in pre-neoplastic and neoplastic human pancreatic samples. Together, these results point to an unexpected tumor promoting function of senescence associated secreted cytokines. Furthermore, our preliminary results indicate that senescence-associated inflammation depends on the activation of the Interleukin (IL)-1alpha pathway. Thus, we have tested the impact of targeting this pathway in a mouse model of pancreatic cancer and will present the outcome of this study. Together, these studies indicate that senescence and its associate may represent potent therapeutic targets for the prevention of pancreatic cancer and other inflammation-driven cancers.

Biography:

Dong Tang has completed his PhD from Nanjing Medical University and Post-doctoral studies from Nanjing University of Medicine. He is a 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 Visiting Scholar in the National Cancer Center in Japan from December 2012 to January 2013. He has published more than 20 papers in reputed intanational journals.

Abstract:

Pancreatic cancer is one of the most common malignant tumors with poor prognosis due to extremely high malignancy, low rate of eligibility for surgical resection and chemoradiation resistance. Increasing evidence indicate that the interaction between activated pancreatic stellate cells (PSCs) and PDAC cells plays an important role in the development of PDAC. By producing high levels of cytokines, chemotactic factors, growth factors and excessive extracellular matrix (ECM), PSCs create desmoplasia and a hypoxic microenvironment that promote the initiation, development, evasion of immune surveillance, invasion, metastasis and resistance to chemoradiation of PDAC. Our founding suggested that Galectin-1 expression was highest in poorly differentiated pancreatic cancer cells and lowest in well-differentiated pancreatic cancer cells, and was associated with tumor size, lymph node metastasis, differentiation, and UICC stage short survival. High expression in PSCs contributes to immune privilege in the pancreatic cancer microenvironment by enhancing apoptosis and anergy of T cells and skewing the Th1/Th2 cytokine balance. Further more, TGF-β1 from pancreatic cancer cells upregulated Galectin-1 expression in PSCs, and in turn to promotes the proliferative activity, MMP2 and MMP9 expression, and invasion of pancreatic cancer cells, as well as the tumor establishment, growth, and liver metastasis. High expression of Galectin-1 in pancreatic stellate cells may provides a therapeutic target for the treatment of pancreatic cancer.

Biography:

Sally Hodges is currently working in a University of Kentucky Markey Cancer Center, USA

Abstract:

Pancreatic cancer is the most aggressive, most lethal cancer in medicine today. The American Cancer Society has estimated that there will be 53,670 new diagnoses of pancreatic cancer and 43,090 deaths in 2017. Those numbers will propel pancreatic cancer to the number three cancer killer, which spot has been held by breast cancer for many years. The overall 5-year survival is less than 10%, but in patients who have received curative resection, the 5-year survival extends to 20%. Pancreas Cancer Action Network has estimated that as a result of the aging population, it will be the number 2 cancer killer by 2025, second only to lung cancer. It has long been accepted that pancreatic cancer is a disease of the elderly. However, there is a subset of much younger individuals who are being diagnosed well before the age of 60. It appears that approximately 10-15% of all individuals diagnosed with pancreatic cancer are below the 60-year-old assumed minimum. The objective of this study is to determine whether there are common genetic mutations, common risk factors, or common past medical factors. The common risk factors in older patients are age and coronary artery disease, but younger patients would not have these diseases. It is important to determine what the younger onset individuals have in common. This will be a secondary analysis of genomic data in the largest cohort of pancreatic cancer patients ever assembled to ferret out the similarities and differences between early onset and normal onset of pancreatic cancer.

Biography:

Pradeep Kumar Vaitla has completed his Medical School from Osmania Medical College, India and Internal Medicine Residency from Texas Tech Univeristy followed by Nephrology Fellowship at Ochsner Clinic in New Orleans and later Transplant Nephrology Fellowship at Emory University, Atlanta. He has served as Living Donor Kidney Program Director and is currently serving as Medical Director for Kidney- Pancreas Trasnplantation at University of Mississippi Medical Center, Jackson, MS. He is an active member of the American Society of Nephrology, the American Society of Hypertension and the American Society of Transplantation. He is the author or coauthor of 13 abstracts in peer-reviewed professional publications.

Abstract:

Objective of the talk is to discuss the evaluation of potential pancreas transplant reciepients, transplant lisitng criteria from UNOS (United Network of Organ Sharing), early and late complications of pancreas transplantation, immunosuppression and bascis of allograft rejection, treatment of pancreas rejection and combined kidney-pancreas transplantation. Presented information will be collected from UNOS guidelines, highly respected and peer reviewed journals like American Journal of Transplantation (AJT), Clinical Journal of the American Society of Nephrology (CJASN), Transplantation, American journal of kidney diseases (AJKD) and established medical facts.

Biography:

Pamela L Paris, PhD, received her undergraduate degree from John Carroll University, where she obtained a degree in Chemistry magna cum laude. She was awarded two fellowships, the Sherman Clarke Fellow and Merck Fellow, while conducting her advanced education in Biophysical Chemistry at the University of Rochester. Upon completion of her PhD, she did a Post-doctoral fellowship at the Cleveland Clinic in Prostate Cancer Genetics. She joined the Department of Urology in 2001 as an Associate Researcher, received support from the Prostate Cancer Career Development Program from 2001 to 2003, and was promoted to Associate Professor in the Department of Urology in 2009.  She received a joint appoint in the Division of Hematology-Oncology in 2010 and was advanced to Professor in 2012.

Abstract:

Intraductal papillary mucinous neoplasm (IPMN) is a precursor cystic lesion to pancreatic cancer. With the goal of classifying IPMN cases by risk of progression to pancreatic cancer, we undertook an exploratory next generation sequencing (NGS) based profiling study of miRNAs (miRNome) in the cyst fluids from low grade-benign and high grade-invasive pancreatic cystic lesions. Thirteen miRNAs (miR-138, miR- 195, miR-204, miR-216a, miR-217, miR-218, miR-802, miR-155, miR-214, miR-26a, miR-30b, miR-31, and miR-125) were enriched and two miRNAs (miR-451a and miR-4284) were depleted in the cyst fluids derived from invasive carcinomas. Quantitative real-time polymerase chain reaction analysis confirmed that the relative abundance of tumor suppressor miR-216a and miR-217 varied significantly in these cyst fluid samples. Ingenuity Pathway Analysis (IPA) indicated that the genes targeted by the differentially enriched cyst fluid miRNAs are involved in five canonical signaling pathways, including molecular mechanisms of cancer and signaling pathways implicated in colorectal, ovarian and prostate cancers. Our findings make a compelling case for undertaking in-depth analyses of cyst fluid miRNomes for developing informative early detection biomarkers of pancreatic cancer developing from pancreatic cystic lesions.

Biography:

Jose R Torrealba has completed his MD in 1994 from the Central University of Venezuela. He then did a Post-doctoral fellowship in Molecular Biology at the University of Wisconsin, in Madison, Wisconsin and obtained his degree in Anatomic and Clinical Pathology from the Univeristy of Wisconsin. He specialized in Immunopathology of Transplantation at the University of Toronto, Canada in 2005. He held a job as Assistant Professor of Pathology at the University of Wisconsin until 2010 and currently is the Dr. George and Anne Race Distinguished Professor of Pathology at the Department of Pathology, UTSW Medical Center in Dallas, Texas. 

Abstract:

The histopathologic parameters associated with acute cellular rejection (ACR) of the pancreas allograft have been well defined and have undergone modifications over the years to reflect the latest diagnostic and prognostic updates. Antibody-mediated rejection, in the other hand, is a relatively recently identified entity that we are yet learning how to diagnose and manage. This presentation will cover both the latest Banff approved diagnostic criteria for ACR and AMR with emphasis on our own research findings on incidence, risk factors, pathologic diagnosis, treatment and outcomes of pancreas AMR. Briefly, we have found that pancreatic AMR occurred in about 10% of patients by 1-year post-transplant. The most important risk factors associated with AMR included non-primary simultaneous pancreas-kidney (SPK) transplant, primary solitary pancreas (PAN) transplant and race mismatch. After pancreas rejection, patient survival was 100% but 20% of pancreas grafts failed within one year. Graft survival after acute cellular rejection (ACR), AMR and mixed rejection was similar. Of biopsies that stained >5% for the AMR surrogate marker C4d, 80% were associated with increased Class I donor specific antibodies (DSA). AMR occurs at a clinically significant rate after pancreas transplantation, and the diagnosis should be actively sought by staining the allograft biopsy using C4d staining and screening for DSA levels in patients with graft dysfunction, especially after nonprimary SPK and primary PAN transplantation.

Biography:

Filipa Ribeiro Crespo Lucas has completed her Medicine Master degree from the University of Lisbon, Portugal. She is now working as a Physician at the Cascais Hospital, Portugal, where she has started her Internal Medicine Internship last January. Her master thesis was about the impact of tobacco and its components on the cervix cancer. 

Abstract:

The critical acute pancreatitis (CAP) has recently emerged as the most sever acute pancreatitis. The shock is a complex pathophysiological process that often results in multiple organ dysfunction syndrome (MODS) and death. The MODS, though newly described, was observed in intensive care unit (ICU) patients for several decades. However, the cardiogenic shock-related acute pancreatitis is a rare event. A 53-year-old Caucasian man with a critical shock-related acute pancreatitis (distributive and hypovolemic/cardiogenic) was admitted in our ICU. He had a chronic pancreatitis medical history. He had alcohol drinking and cigarette smoking habits and a chronic HCV (serum anti-HVC antibodies were positive and serum RNA HCV was negative) history and past HBV infection (serum anti-Hbs and Hbc antibodies were positive and Ag Hbs were negative). The patient developed a cardiovascular, a renal (AKIN 3), respiratory MODS and a compartmental syndrome too. The patient recovered over a few days with invasive support by transpulmonary thermodilution, with a cardiogenic shock evolved to distributive shock, norepinephrine support, invasive-ventilation-support and dialysis (CRRT). Emergency operations were undertaken: A total colectomy (sigmoid ischemia) is an ileostomy and a cholecystectomy. Afterwards, after 5-months internment in the hospital, with some nosocomial infections, the clinic evolution was good enough for the patient to leave the hospital with hemodynamic stability. Patients with severe acute pancreatitis require intensive care. Within hours to days, a number of complications (e.g., shock, pulmonary failure, renal failure, gastrointestinal bleeding, or multiorgan system failure) may develop. The goals of medical management are to provide intensive supportive care, to limit infection and to identify and treat complications whenever appropriate.