Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 10th World Congress on Biomarkers & Clinical Research Baltimore, Maryland, USA.

Day 1 :

Biomarkers 2017 International Conference Keynote Speaker Frédéric Baribaud photo
Biography:

Frédéric Baribaud holds a PhD from the University of Lausanne and has conducted his Post-doctoral studies at the University of Pennsylvania. He has worked at Incyte Corporation in a discovery role on target validation and as a Compound Team Co-Lead for small molecular inhibitors. For the past ten years, he has been working at Janssen R&D in Imunology Biomarkers on various inflammatory diseases. In his current role as Scientific Director he is focusing on obtaining disease rational for targets and patient segmentation for inflammatory bowel diseases.

Abstract:

Objective markers of disease severity in inflammatory bowel disease that support clinical decision-making are still needed. We hypothesized that novel objective markers of tissue inflammation are best identified at the site of disease with a tissue-level assessment of disease activity. Biopsy samples were obtained from participants in the UNITI trials of ustekinumab in moderate-to-severe Crohn’s disease. Pairs of adjacent biopsies were taken from the rectum, splenic flexure and ileum. One biopsy from each pair was assessed by global histology disease activity score (GHAS) while the other was submitted for microarray analysis. Partial least squares regression and random forest were used to identify biomarkers associated with histological severity and robustness of the resulting models was assessed using cross-validation. A single multivariate model comprising 16 genes was identified that predicted histological activities in rectum or splenic flexure biopsies. This model was characterized by R2=0.78 for the training set, and R2=0.59, 0.54, and 0.32 on external validation sets. A separate 14-gene model capturing histological activity in ileal biopsies was characterized by R2=0.5 for the training set and R2=0.45 in the external validation set. In general, both models contained genes related to tissue degradation, barrier function, and immune regulation, including CXCL11 (I-TAC). Both models retained performance in external validation datasets from UNITI-2 but exhibited lower performance. Our analysis supports the ability of biopsy transcriptomics combined with machine learning approaches, to capture disease-relevant variability in Crohn’s disease and, more importantly, supports the use of similar approaches to identify additional surrogate markers. 

Biomarkers 2017 International Conference Keynote Speaker David Dongliang Ge photo
Biography:

David Dongliang Ge is the CEO and President of Apostle Inc., a Silicon-Valley-based Biotechnology Company developing a novel AI-enabled Nano Diagnostics (AID) Technology for early cancer detection. Previously, he was the President of BioSciKin Co. and Simcere Diagnostics Co., two global biotechnology companies headquartered in Nanjing, China. Between 2011 and 2016, he was the Director of Bioinformatics at Gilead Sciences, where he founded and provided Leadership to the Bioinformatics group.

Abstract:

The biotechnology industry has quickly entered an era when fast evolving genome technologies, historical precision medicine initiatives, and disruptive bioinformatics and artificial intelligence techniques synergistically start to provide pivotal and strategic support for new drug and diagnostics development. Unprecedented amount of data is being generated to help discover and develop new generations of medications. Using real-world examples, this presentation will cover several of the most important bioinformatics considerations in this strategy. How do we efficiently manage the massive amount of data at different levels of precision to ensure a seamless data flow? How do we annotate and present these data to make it more comprehensible and deliverable? How do we design and execute the new clinical trials more efficiently and improve the success rate? Where are we and where are we going in this new precision medicine era?

Keynote Forum

Kamala K Maddali

Cancer Genetics Inc, USA

Keynote: Integrated biomarker strategies in immuno-oncology

Time : 10:30-11:00

Biomarkers 2017 International Conference Keynote Speaker Kamala K Maddali photo
Biography:

Kamala K Maddali is currently the Vice President of Biopharma Collaborations, Market Development and Companion Diagnostics at Cancer Genetics Inc, Rutherford, NJ. Cancer Genetics, Inc., (CGI) is a leader in the field of Personalized Medicine, offering diagnostic products and services that enable precision medicine in the field of Oncology. She holds a DVM PhD, in Pharmacology from University of Missouri-Columbia and a DVM Veterinary Medicine from Acharya N G Ranga Agricultural University in India. She brings over 10 years of extensive experience of global P&L scientific and commercial management of clinical biomarker and companion diagnostics (CDx) services covering personalized medicine strategy. She brings a lot of strategic values from her previous roles at Quest Diagnostics, Quintiles and Merck Schering Plough in the arena of biomarkers and companion diagnostics. 

Abstract:

Immunotherapy enables the immune system to recognize tumors; insights into immunotherapy biomarker testing, especially PD-L1 IHC and; choosing the best patients for immunotherapy with the use of integrated biomarker panels. Combination regimens of immuno-oncology agents and targeted drugs may represent the next generation of cancer treatments and could result in improved outcomes and prolonged patient survival. This talk will focus on immunooncology advancements and a review of latest drug targets. In addition to the underlying science, we will focus on the practical aspects of targeting the PD1:PD-L1 interaction. We will discuss our perspectives of supporting PD-L1 as a pharmacodynamic end point and companion diagnostic. Additionally, we will focus on case studies, where we monitored PD-L1 expression and the variable sensitivity, specificity and dynamic range of three anti-PD-L1 antibodies in a cohort of 52 primary DLBCL patients. CGI believes that this work is essential in developing durable and reliable immune biomarkers and companion diagnostics for selecting lymphoma patients most likely to benefit from immune-checkpoint therapy.

Biomarkers 2017 International Conference Keynote Speaker Yoshiaki Omura photo
Biography:

Yoshiaki Omura received Oncological Residency Training at Cancer Institute of Columbia University and Doctor of Science Degree through research on Pharmaco-Electro-Physiology of Single Cardiac Cells in-vivo and in-vitro from Columbia Univ. He researched EMF resonance phenomenon between two identical molecules for non-invasive detection of molecules, at Graduate Experimental Physics Dept., Columbia Uni., for which he received US patent. He is also the Creator of Bi-Digital O-Ring Test. He published over 270 original research articles, many chapters, and nine books. He is currently working as Adjunct Prof. of Family and Community Medicine, New York Medical College; President and Prof. of Int’l College of Acupuncture and Electro-Therapeutics, NY; Editor-in-Chief, Acupuncture and Electro-Therapeutics Research, Int’l Journal of Integrative Medicine, (indexed by 17 major int’l Indexing Periodicals). Formerly, he was also Adjunct Prof. or Visiting Prof. in Universities in USA, France, Italy, Ukraine, Japan, Korea and China.

Abstract:

Using highly sensitive electro-magnetic field resonance phenomenon between two identical molecules with identical amount, which was discovered at Graduate Experimental Physics Department of Columbia University (for which US Patent was given under the name of Bi-Digital O-Ring Test for the imaging and diagnosis of internal organs), the author was able to non-invasively detect any molecules, including neurotransmitters, specific cancers of specific internal organs, virus, bacteria, fungus and toxic substances. Using this method, he developed the following three early diagnostic methods: 1) Accurate organ representation areas of face, including eyebrows, pupils, nose, upper and lower lips, upper and lower side of the tongue, hands, and feet which were accurately mapped using above-resonance phenomenon. The author often found in the presence of malignancy, deep crease or round projection appeared in the organ representation areas with or without discoloration. In addition, eyebrows where every organ is represented, in the presence of malignancy, color of the eyebrow changes to a white color and eventually hair disappears. In addition to these visible changes, in the presence of cancer, there will be invisible changes also, which can be detected rapidly using Bi-Digital O-Ring Test non-invasively without even touching a patient. These invisible changes were often found at different organ representation areas of nose, lips, tongue, and hands. 2) One page “Mouth, Hand, and Foot Writing Form”. Completion of the form takes about 5-10 minutes. From this one-page form, almost any malignancy can be detected. Any malignancy can be screened in one minute and the exact malignancy can be identified within 5-10 minutes non-invasively without knowing any medical history of the patient. 3) Detection of any cancer or malignancy from recorded ECGs; this method was recently discovered by the author and all the cancers and its related biochemical parameters can be estimated using rapidly changing QRS Complex as well as slowly changing, rising part of T-wave of ECGs. Using these three methods, almost any cancer can be screened rapidly and diagnosed in short time, non-invasively without biopsy or blood test or imaging devices. Our research indicated that human papilloma virus type 16 (HPV-16) infection was found in almost every cancer we examined. In the presence of the strong infection of HPV-16, high incidence of cancer was found and when one person in family has cancer with increased HPV-16 virus infection, almost every member of the family was often infected with same degree of the infection. HPV-16 can be transmitted very easily by talking with the infected person in short distance. As a result, our latest cancer treatment now includes safe, rapid elimination of HPV-16 virus. We tested many potential cancer treatments and also evaluated potential role of optimal dose of vitamin D3, taurine, and PQQ as well as DHEA and for safe, effective, individualized treatment of cancer patients. As a consequence, we found optimal dose of vitamin D3 to be most effective, safe, and economical treatment due to its unique seven beneficial effects, including its anti-cancer effect and efficient urinary excretion of microorganisms. Abnormal increase of 8-OH-dG, which is proportional to DNA mutation and its relationship with cancer metastasis and aggressiveness of cancer and factors inhibiting Vitamin D3 effects will also be discussed. 

Biomarkers 2017 International Conference Keynote Speaker Diana Anderson photo
Biography:

Diana Anderson holds the Established Chair in Biomedical Sciences at the University of Bradford. She has 450+ peer-reviewed papers, nine books, has successfully supervised 29 PhDs, and has been a Member of Editorial Boards of 10 international journals. She has been or is Editor in Chief of a book series on toxicology for J Wiley and Sons and the Royal Society of Chemistry respectively. She gives key note addresses at various international meetings. She is a Consultant for many international organisations, such as the WHO, NATO, TWAS, UNIDO and the OECD. Her h index =54.

Abstract:

Detection tests have been developed for many cancers, but there is no single test to identify cancer in general. We have developed such an assay. In this modified patented Comet assay, we investigated peripheral lymphocytes of 208 individuals: 20 melanoma, 34 colon cancer, four lung cancer patients, 18 suspect melanoma, 28 polyposis, 10 COPD patients and 94 healthy volunteers. The natural logarithm of the Olive tail moment was plotted for exposure to UVA through different agar depths for each of the above groups and analysed using a repeated measures regression model. Response patterns for cancer patients formed a plateau after treating with UVA where intensity varied with different agar depths. In comparison, response patterns for healthy individuals returned towards control values and for pre/suspected cancers were intermediate with less of a plateau. All cancers tested, exhibited comparable responses. Analyses of receiver operating characteristic curves, of mean log Olive tail moments, for all cancers plus pre/suspected-cancer versus controls gave a value for the area under the curve of 0.87; for cancer versus pre/suspected-cancer plus controls the value was 0.89; and for cancer alone versus controls alone (excluding pre/suspected-cancer), the value was 0.93. By varying the threshold for test positivity, its sensitivity or specificity can approach 100% whilst maintaining acceptable complementary measures. Evidence presented indicates that this modified assay shows promise as both a stand-alone test and as a possible adjunct to other investigative procedures, as part of detection programmes for a range of cancers.

Keynote Forum

Srinivas Pentyala

Stony Brook Medical Center, USA

Keynote: Translational approach to detect biomarkers bedside
Biomarkers 2017 International Conference Keynote Speaker Srinivas Pentyala photo
Biography:

Srinivas Pentyala is working as the Director of Translational Research and also as Associate Professor of Anesthesiology at Stony Brook University Medical Center, NY, USA. He has joint appointments in the Departments of Urology, Health Sciences, Physiology and Biophysics at SBUMC. He has 80 publications and several patents to his credit. He has received several honors and awards not only for his role as a Researcher but also as an Educator. He is the Founding Director of several biotech and health care companies. He serves on the Advisory Board of several national and international biotech and health care companies, and research institutes. 

Abstract:

Biomarkers are important tools for disease detection and monitoring. A highly effective, clinically useful biomarker for a specific disease should be measurable in a readily accessible body fluid, such as serum, urine or saliva. Translational approach based applications are now being widely utilized in the field of point-of-care diagnostics.  The search for biomarkers in early disease detection has included proteins, metabolites and other biological molecules that are altered and secreted as a consequence of the disease process and are shed into body fluids. After collecting these body fluids, the next step was to isolate and identify the marker that would give an indication of the disease process. Unfortunately, this approach is laborious and time-consuming, as specific candidate biomarker (s) must be identified from among the thousands of intact and altered molecules in the collected body fluids. In many disease manifestations, a marker can occur in trace amounts, yet large volumes of fluids are collected. Dipsticks and lateral flow devices that are availabale at present are limited for their ability to detect markers beyond a specific concentration and also the collection and application of sample to these existing diagnostic strips and devices have many limitations. We identified unique biomarkers for cerebrospinal fluid leaks, prostate cancer, diabetic nephropathy and other diseases and symptoms. We also designed and tested several point-of-care diagnostic detection methods and devices that can detect trace biomarkers in large volumes of samples. The translational approach to identify biomarkers and develop point-of care diagnostic methods and devices will be presented. 

Keynote Forum

Jianhua Luo

University of Pittsburgh, USA

Keynote: Cancer genomic biomarkers in human malignancies
Biomarkers 2017 International Conference Keynote Speaker Jianhua Luo photo
Biography:

Jianhua Luo has been studying molecular mechanism related to human malignancies in the last 24 years. Currently, he is a Professor of Pathology and Director of High Throughput Genome Center at University of Pittsburgh. In the last 16 years, he has been largely focusing on genetic and molecular mechanism of human prostate cancer and hepatocellular carcinomas. In this period, his group has identified and characterized several genes that are related to prostate cancer and hepatocellular carcinoma, including SAPC, myopodin, CSR1, GPx3, ITGA7, MCM7, MT1h and GPC3. He proposed prostate cancer field effect in 2002. He is one of the pioneers in utilizing high throughput gene expression and genome analyses to analyze field effects in prostate cancer and liver cancer. He is also the first in using methylation array and whole genome methylation sequencing to analyze prostate cancer. Recently, his group found that patterns of copy number variants of certain specific genome loci are predictive of prostate cancer clinical outcomes, regardless tissue origin. His discovery of several novel fusion transcripts and their association with aggressive prostate cancer has brought significant new insight into the field of prostate cancer research.

 

Abstract:

Cancer remains one of the most lethal diseases for human. In recent studies, genomic analysis has rapidly advanced the diagnostics of human cancers. Our result showed that combination of genome copy number variance, genome methylation pattern and novel fusion transcripts specific for cancer achieved high accuracy in predicting clinical outcomes of human cancers. Interestingly, some of these fusion genes are also present in a variety of human malignancies. Some of these fusion gene products trigger new pathways that are essential for carcinogenesis in multiple human cancers, and create novel functions that are not present in wild type gene counterparts. Some of these novel fusion genes are highly targetable. Treatment of cancers with drugs specific for these genes and their signaling pathways produced dramatic improvement of metastasis and survival rate of animals xenografted with cancers positive for these fusion genes. Our analyses suggest that targeting therapy for fusion genes holds promise as an effective treatment for human cancers. 

Biomarkers 2017 International Conference Keynote Speaker Michael Retsky photo
Biography:

Michael Retsky has done his PhD in Physics from the University of Chicago. He has made a career change to cancer research 30 years ago. He is on the Staff at Harvard TH Chan School of Public Health and Faculty at University College London. He was on Judah Folkman’s Staff at Harvard Medical School for 12 years. He is Editor of a Nature/Springer book on the breast cancer project to be published in 2017. He was the first person to use what is now called metronomic adjuvant chemotherapy and is a Founder and on the Board of Directors of the Colon Cancer Alliance. He has published more than 60 papers in physics and cancer.

Abstract:

A bimodal pattern of hazard of relapse among early stage breast cancer patients has been identified in multiple databases from US, Europe and Asia. We are studying these data to determine if this can lead to new ideas on how to prevent relapse in breast cancer. Using computer simulation and access to a very high quality database from Milan for patients treated with mastectomy only, we proposed that relapses within 3 years of surgery are stimulated somehow by the surgical procedure. Most relapses in breast cancer are in this early category. Retrospective data from a Brussels anesthesiology group suggests a plausible mechanism. Use of ketorolac, a common NSAID analgesic used in surgery was associated with far superior disease-free survival in the first five years after surgery. The expected prominent early relapse events in months 9-18 are reduced 5-fold. Transient systemic inflammation accompanying surgery (identified by IL-6 in serum) could facilitate angiogenesis of dormant micrometastases, proliferation of dormant single cells, and seeding of circulating cancer stem cells (perhaps in part released from bone marrow) resulting in early relapse and could have been effectively blocked by the perioperative anti-inflammatory agent. If this observation holds up to further scrutiny, it could mean that the simple use of this safe, inexpensive and effective anti-inflammatory agent at surgery might eliminate early relapses. We suggest this would be most effective for triple negative breast cancer and be especially valuable in low and middle income countries. Similar bimodal patterns have been identified in other cancers suggesting a general effect.

  • Biomarkers | Cancer Biomarkers | Novel Approaches to Cancer Therapeutics | Molecular Biomarkers | Biomarkers for Immuno-Oncology | Biomarkers in Clinical Research & Development | Biomarkers and Drug Discovery | Cancer Metastasis | Cancer screening & Diagnostics Session | Tumor & Cancer Immunology | Biomarkers and Pathology| Biomarkers for Disorders

Session Introduction

Wenzheng Zhang

Albany Medical College, USA

Title: Water channel AQP5 is a potential novel biomarker of diabetic nephropathy
Biography:

Wenzheng Zhang completed his PhD from MD Anderson Cancer Center, University of Teaxs Health Science Center at Houston in 1998. He performed his Post-doctoral studies at Howard Hughes Medical Institute in Baylor College of Medicine. His current work is focused on kidney fibrosis, renal progenitor cells and biomarkers in the context of diabetic nephropathy and polycystic kidney disease. He has published nearly 50 papers in highly reputed journals and served in over 10 NIH study sections in the past three years.

Abstract:

Diabetic nephropathy (DN) is the most common single cause of end-stage renal disease and one of the most significant long-term complications associated with diabetes in the US. Currently, there are no ideal biomarkers for DN. Water channel AQP5 is critical for the generation of saliva, tears and pulmonary secretions. It has little or no expression in normal mouse and human kidneys. We have reported that AQP5 is up-regulated in kidney biopsies from patients with DN. To investigate, if urinary AQP5 serves as a new potential biomarker of DN, we used an AQP5-specific enzyme-linked immunosorbent assay kit and measured serum and urinary AQP5 first in a cohort consisting of normal controls (n=26) and patients with diabetes mellitus (n=25) or diabetic nephropathy (n=33) and then in a validation cohort possessing normal controls (n=10), patients with diabetes mellitus (n=10) or diabetic nephropathy (n=14), and patients with chronic kidney disease of unknown etiology (n=10). We employed various statistical methods including Pearson's correlation coefficient, ANOVA, receiver operator curve and multiple logistic regression to analyze the data. Our results show that urinary AQP5/creatinine 1) is significantly higher in DN than in other two groups, and in DN stage V than in DN stage III; 2) correlates with serum creatinine, urinary albumin and multiple other known risk factors of the disease; and 3) improves the clinical models in distinguishing DN from normal controls and diabetic mellitus. Hence, urinary AQP5/creatinine may possess diagnostic and prognostic values as a biomarker of DN. 

Biography:

A-Lien Lu-Chang has completed her PhD from the University of North Carolina at Chapel Hill and has done her Post-doctoral studies from Duke University, School of Medicine with Paul Modrich (Nobel laureate in Chemistry in 2015). She is working as the Professor of Biochemistry and Molecular Biology at University of Maryland Medical School and a Member of University of Maryland Greenebaum Comprehensive Cancer Center. She has published more than 63 peer-reviewed papers in reputed journals, holds a patent, and has been serving as an Eeditorial Board Member for four journals. Her laboratory is currently studying the interplays among DNA repair, DNA replication, cell cycle checkpoint, transcription and chromatin remodeling. She investigates the impact of their co-ordination on telomere integrity and carcinogensis. Her team’s work highlights potential targets that can be exploited clinically for cancer therapies.

Abstract:

Melanoma is the deadliest form of skin cancer. Mutational activation of the protein kinase BRAF accompanied by loss of the tumor suppressor PTEN is the most common cause of melanomagenesis. Targeted therapy against BRAF mutation represents one of the most significant advances in the treatment of melanoma. However, response to BRAF inhibitor (BRAFi) PLX4032 (vemurafenib) is not durable because many patients acquire drug resistance. Thus, therapies that can overcome resistance to the drug are urgently needed. We have demonstrated that a specific inhibitor of protein deacetylase SIRT1 (SIRT1i) and BRAFi synergistically reduces the viability of melanoma cells and SIRT1i slows melanoma tumor growth in mouse xenografts. Cell cycle checkpoints are very promising targets for anticancer therapies because they control cancer cell responses to chemotherapy and radiation. Currently, Chk1 inhibitors (Chk1i) are being tested clinically for several cancers. Our novel findings show that a specific Chk1i significantly decrease cell proliferation, but even more impressively, triggers PLX4032-resistant melanoma cells regaining the sensitivity to the drug. We hypothesize that SIRT1i and Chk1i will augment the potency of BRAFi against melanoma. The use of combinatorial therapies will improve the outcomes and curtail the resistance to BRAFi in melanoma. Our work holds promise for finding novel targets for anti-cancer therapies and will provide new therapy options for melanoma patients.

Biography:

Sherry A Bradford has attended undergraduate school at SUNY at Buffalo and has done her PhD in Biochemistry from the University of Buffalo. During her clinical laboratory vocation, she was solicited by the Chief of Surgery at Millard Fillmore Hospital, Buffalo, NY, to direct the Surgical Research Laboratory. She was awarded for Excellence in Research by the American Federation for Clinical Research, and for the Excellence in Research – SUNY at Buffalo. Currently, she sits on the Editorial Board of many reputed national and international journals and has authored and co-authored a number of scientific peer-reviewed manuscripts. She is also a member of many professional organizations including: International Metabolic Cancer Group, AACR, ASCO and GLIFCA.

Abstract:

Despite significant increases in the numbers of persons surviving cancer, there yet exists a vast rift in the number who dies each year despite treatment. It remains a challenging disease to treat, in part, due to the heterogeneity of the malady. It is widely accepted that virtually all cancers are highly heterogeneous and that subpopulations of cells within a single tumor can exhibit distinct genomic, protein and metabolic divergent profiles. These profound and complex profiles develop into and result in an individualistic shrewd and capricious phenotype leaving an imprint, established and ascribed to that specific tumor. Furthermore, tumor cells experience a range of microenvironmental cues, which would in turn, translate into a range of phenotypic manifestations, contributing to morphologically dissimilar cellular lineages and tissues, within the tumor milieu. Thus, interactions of tumor cells with their microenvironment mutually shape tumor behavior and phenotype. Likewise, plasticity of tumor cell phenotypes would necessarily also influence the apoptotic and autophagic responses. The clinical relevance is that this disparate and divergent heterogenicity contributes significantly to the efficacy of drug therapy and therefore imparts considerable inter-individual variation in pharmacotherapy and clinical response to a myriad of agents. Accordingly, this tumor intra-/inter- incongruence in breast cancer patients, underscores the necessity to personalize therapeutic regimens favoring more personalized patient care throughout monitoring disease progression, relapse and remission states. Our lab briefly delineates a reliable in-vitro test that employs a more scientific and logical approach to identify drug(s) and drug combinations that may be efficacious against a specific patient’s tumor in-vivo. The patient’s own tumor mass is fully disaggregated and as such, all cells (microenvironment) that compose the tumor are subjected to cytotoxic/cytolytic agents. The end-point is cell death which correlates to clinical outcomes of progression-free and overall survival in cancer patients. In summary, our studies do validate that in-vitro testing does qualify as a tool that can assist and guide oncologists to the most efficacious therapy(s) for their patients but also further demonstrates the necessity to individualize chemotherapeutic regimes. Nonetheless a randomized controlled clinical trial must be designed to further correlate and validate our studies and to fully appreciate the impact of in-vitro chemoresistance and sensitivity testing on cancer recurrence and survival rates.

Biography:

Tamaki Ikuse has completed his MD and PhD from Juntendo University Graduate School of Medicine. He is working as an Assistant Professor in the Department of Pediatric and Adolescent Medicine, Juntendo University Graduate School of Medicine and also acts as a Visiting Assistant Professor in the Department of Pediatrics, University of Maryland School of Medicine. He has published more than 10 papers in reputed journals.

Abstract:

Background: Chronic Helicobacter pylori (H. pylori) infection in children induces lymphoid hyperplasia called nodular gastritis (NG). The aim of this study was to evaluate gene expression in pediatric antral mucosa with NG by microarray analysis to identify molecules closely associated with NG when compared to NG-negative pediatric and adult tissue with H. pylori infection.

Methods: Eight pediatric and six adult H. pylori-infected patients, as well as six pediatric and six adult uninfected patients were evaluated. All infected adults had atrophic gastritis (AG). Nodular gastritis was observed in the antrum of all eight pediatric patients and in the corpus of three patients. Adult and uninfected patients were free of NG. Total RNA was purified from gastric biopsies and microarray analysis was performed to compare gene expression between groups. The three infected children with NG in both the antrum and corpus were excluded from analysis of corpus samples.

 

Results: The total number of genes significantly up- or down-regulated (fold changes>3, P<0.01) compared to uninfected controls varied widely with 72 in pediatric antrum, 45 in pediatric corpus, 104 in adult antrum and 77 in adult corpus. Nineteen genes had significantly altered expression in the antrum of NG tissue compared to NG-negative pediatric corpus tissue and adult AG tissue. Although many molecules known as regulators of lymphoid follicle development were not predominantly upregulated in the NG mucosa, the CD20 B cell specific differentiation antigen demonstrated the most pronounced increase.

 

Conclusions: CD20 over expression may play an important role in developing lymphoid follicle enlargement and NG.

Biography:

Xichun Sun is a practicing Surgical Pathologist and Cytopathologist. He graduated from Medical School in China. He completed his PhD, Post-doctoral and Residency Training and Fellowships in the USA. His current research interest centers on cancer diagnosis, carcinogenesis and cancer metastasis. He is the author of one monograph and has proposed a new theory on cancer metastasis.

Abstract:

In parallel to the appearance of primordial germ cells during early embryogenesis, the cancer reproductive saga starts with the separation of metastasis initiating cells (MICs) from cancer initiating cells when the primary cancer is still in its infancy. Prime MICs embark on a journey to the host bone marrow where they undergo further development and regulation. Migrating MICs are guided by the same CXCR4/CYCL12 axis as used in the migration of primordial germ cells to the genital ridge. Like the ovary, the host bone marrow features immune privileges, coolness, hypoxia and acidity which are essential for stemness maintenance and regulation. Opportune activation of the MICs via fusion with bone marrow stem cells triggers a frenzy of cellular proliferation and sets them on the move again. This scenario is akin to oocyte fertilization in the Fallopian tube and its subsequent journey towards the decidum. Just as the human reproductive process is plagued with undesirable outcomes so is the cancer metastasis highly inefficient. The climax of the cancer metastatic drama (colonization) is reached when proliferating MIC clusters attempt to settle down on decidum-like premetastatic sites. Successfully colonized clusters blossom into overt macrometastases only after the execution of sophisticated immunomodulation, angiogenesis and vascular remodeling. Similarly, the implanted blastomere needs to orchestrate these feats before flourishing into a new life. What is more, the cancer reproductive drama seems to be directed by a primordial hypothalamus-pituitary-gonad axis. Pursuing this reproductive trail could lead to new frontiers and breakthroughs in cancer research and therapeutics. 

Biography:

Dr. Michael A Tainsky is associated with Wayne State University, USA and his research interest in Molecular genetic mechanisms by which normal cells become malignant, Pathway analysis of gene expression changes leading to cellular immortalization, Development of novel cancer diagnostic tests for early detection of cancer in the form of a complex blood test.

Abstract:

Routine disease monitoring of ovarian cancer patients is generally recommended by gynecologic oncologists for women from high-risk families and for ovarian cancer patients during after the completion of primary surgery and first-line chemotherapeutic treatments. The recurrence is determined by measuring the level of serum CA125, one of the most extensively used tumor biomarkers in standard clinical practice for disease surveillance. Numerous studies have shown the role of tumor autoantibodies as biomarkers for ovarian cancer diagnosis and its recurrence. These autoantibodies to tumor associated antigens (TAAs) arise due to the generation of humoral immune response before evidence of clinical symptoms in cancer patients. Previously we showed that three biomarker panel predicted ovarian cancer recurrence at a median lead time of 9.07 months with 94.7% sensitivity, 86.7% specificity, and 93.3% accuracy, in a cohort of ovarian cancer patients where normalization of CA125 had occurred after the surgery and completion of chemotherapy. One of those biomarkers was a peptide epitope from a known paraneoplastic antigen, HARS. Paraneoplastic antigens can elicit a humoral immune response in cancer patients as these antigens are expressed in the cells of nervous system and tumor. The appearance of these onconeural antibodies in ovarian cancer patients leads to the development of various neurological disorders called paraneoplastic syndromes, particularly dermatomyositis or polymyositis but can precede the occurrence of dermatomyositis or polymyositis. Although the clinical implication of these onconeural antibodies as biomarkers for early diagnosis of ovarian cancer has been reported in many case studies, the usefulness of these antibodies has yet to be evaluated in monitoring disease status in ovarian cancer patients after cytoreductive surgery and chemotherapy treatments. In the present study, we evaluated the role of a panel of three recombinant paraneoplastic antigens, HARS, CDR2 and Ro52 in combination with three of our previous biomarkers in predicting recurrence in new and independent cohort of ovarian cancer patient population in which most of the patients had no elevation in CA125 level months before their clinical recurrence. Our results indicate that autoantibodies to HARS, Ro52 and CDR2 and 5H6 antigens predicted ovarian cancer recurrence 5.03 months before the clinical or symptomatic relapse in 21 ovarian cancer patients with a sensitivity of 90.5% when CA125 levels were below the standard cutoff (35 U/ml).

Biography:

Vanessa Bellat received her PhD in Chemistry from the University of Burgundy in France in 2012. After completing her degree, she joined Welience, the private valorization subsidiary of the University of Burgundy, and oversaw the development of a new technological platform called “NanoCare”, which was devoted to the toxicological analysis of nanoparticles. In 2014, she moved to New York and became a member of the Molecular Imaging Innovations Institute (MI3) in Weill Cornell Medicine where she is currently working as a Post-doctoral fellow. Her work focuses on the development of nanomedicine for cancer drug delivery.

Abstract:

A drug delivery system that can cross multiple biological barriers, penetrate solid tumors, and prevent nonspecific body accumulation is in demand for precision treatment. We introduce a smart self-assembling peptide nanofiber that can overcome these challenges by using an approach that combined shape-controlled tumoral uptake, chargeassisted tissue penetration, and enzyme-induced retention approach to improve the delivery efficacy of anticancer agents. The nanofiber displays a high aspect ratio to promote tumoral delivery. Multimodal imaging studies reveal the tumor infiltration, invasion, and saturation properties of the nanofibers. In situ activation by tumorassociated proteases structurally transforms the fibers into networks that are more than ten times larger, leading to a weeks-long local retention. Specific examples are given on delivering aldoxorubicin, proceeding as a novel treatment for triple negative breast cancer. The drug-loaded nanofibers release the active metabolites under the acidic tumor microenvironment and display an enhanced antitumor efficacy with minimal host toxicity in immunodeficiency mice bearing tumor explants compared to the free drug and the liposomal formulation. 

Porunelloor A Mathew

University of North Texas Health Science Center, USA

Title: CS1 (CD319) is an effective immunotherapeutic target for multiple myeloma
Biography:

Porunelloor A Mathewcompleted his PhD from University of Pune, India and postdoctoral studies at University of Medicine and Dentistry of New Jersey and UT Southwestern Medical Center, Dallas. Dr. Mathew, Associate Professor at UNT Health Science Center, Fort Worth, is a world-renowned Cancer Immunologist who identified and cloned human NK cell receptors, 2B4 (CD244), CS1 (CD319) and LLT1. Research in his laboratory showed that anti-CS1 antibody activates NK cell cytotoxicity against various cancer cells. Research in Dr. Mathew’s group has lead to the development of novel NK cell based immunotherapy for cancer. He has published over 60 papers in reputed journals and serving as an editorial board member of repute.

Abstract:

Multiple Myeloma (MM) is a cancer of the plasma cells and is fatal without treatment due to anemia, renal failure, hypercalcemia, and bone destruction. Natural killer (NK) cells, a component of the innate immune system, function against infection and cancer. Identification and characterization of NK cell receptors lead to a better understanding of the molecular basis of  Natural Killer cell recognition and activation by cancer cells. NK cell functions are regulated by a delicate balance between signaling through activating receptors and inhibitory receptors. We have identified and characterized CS1(CD319, SLAMF7, CRACC) as an NK cell receptor activating its function through homophilic interactions. A monoclonal antibody against CS1 induced both Natural cytotoxicity and ADCC (Antibody-dependent cell-mediated cytotoxicity) by NK cells. CS1 is overexpressed on MM cells and anti-CS1 mAb enhance the killing of MM by NK cells. Elotuzamab (Empliciti) isa humanized monoclonal antibody against CS1, and has been aproved as a breakthrough drug against MM. During clinical trails, Empliciti in combination with chemotherapeutic drugs showed more effective than antibody treatment alone. However, the underlying mechanism for this is not known. We hypothesize that chemotherapeutic drugs induce the expression of CS1 on MM cells making them more susceptible to NK mediated killing. To investigate this property, MM cells were incubated with various combinations of chemotherapy and immunotherapy drugs in order to observe any change in surface expression of CS1. Our results indicate that treatment with anti-CS1 in combination with lenalidomideor doxorubicin and dexamethasone increased the cell surface expression of CS1. Thus enhancing the expression of molecular targets for NK cells is an effective strategy for immunotherapy ofcancer.

Biography:

Hajime Orita graduated and completed Surgical Training from Juntendo University, School of Medicine in Japan. Currently, he is working as Associate Professor of Dept. of Upper GI and especially Laparoscopic Surgery. He has done his Post-doctoral studies and received the Adjunct Associate Professor position from Johns Hopkins University School of Medicine. He has published more than 10 papers in reputed journals and has been serving as an Editorial Board Member of repute.

Abstract:

Gasdermin (Gsdm) family was originally identified as a candidate causative gene for mouse hair follicles, recombination-induced mutation 3 (Rim3). It has four human homologs; A, B, C, and D. All Gsdm family members are located in amplicons; genomic regions often amplified during cancer development, and are considered to be involved in the regulation of epithelial apoptosis. Gsdm A is mainly expressed in the upper gastrointestinal tract. In contrast, Gsdm D is expressed in the colorectal tract. In this study, we researched those expressions in colorectal cancer and evaluated them for tumor marker, comparing between those expression and clinical pathological status. We analyzed expressions of Gsdm A and D, using thirty colorectal cancer cases which were surgically treated at our institution 2013(Stage I; 10 cases Stage II; 10 cases and Stage III; 10cases. Then retrospective analysis of the connection, between Gsdm expression and clinic-pathological data was done. GsdmA is not expressed in normal colorectal epithelium, but is overexpressed and gradually-rising in carcinoma, meanwhile, GsdmD showed precisely the opposite results. The results of the expression analysis suggest that GsdmA and GsdmD works parallel, and relate to clinical stage.

Biography:

Kai Fu has completed his PhD from the University of Science and Technology of China. He started his Post-doctoral training in the Department of Biochemistry and Molecular Biology at Johns Hopkins Bloomberg School of Public Health since 2012. 

Abstract:

Nuclear factor kappa B (NF-κB) is a transcription factor that controls genes for cell survival and NF-κB signaling has emerged as one of the most important mediators of the cellular response to genotoxic stresses. Genotoxic agents trigger a ‘nuclear-to-cytoplasmic’ NF-κB activation signaling pathway; however, the early events controlling the initiation of the signaling pathway is poorly understood. Our data demonstrate that Src-associated-substrate-during-mitosis-of-68 kDa/KH domain containing, RNA binding, signal transduction associated 1 (Sam68/ KHDRBS1) plays a key role in genotoxic stress-initiated NF-κB signaling pathway. Sam68 directly binds to Poly (ADP-ribose) polymerase 1 (PARP1) and regulates PARP1 enzymatic activity in vitro. Sam68 deficiency abolishes DNA damage-stimulated polymers of ADP-ribose (PAR) production and the PAR-dependent NF-κB transactivation of anti-apoptotic genes. Sam68 null cells are hypersensitive to genotoxicity caused by genotoxic agents. Up-regulated Sam68 coincides with elevated PAR production and NF-κB activation in human and mouse colon cancer. Interference with Sam68 protein sensitizes human colon cancer cells to genotoxic stress-induced apoptosis and the hypersensitivity is abolished by ectopic expression of constitutively activated NF-κB. Further, genetic deletion of Sam68 substantially alleviates colon tumor burden in mice model. Taken together, our findings reveal a novel function of Sam68 in the genotoxic stress-initiated nuclear signaling, which is critical for colon tumorigenesis.

 

Tijen Atacag

Near East University, Turkey

Title: Early detection of ovarian cancer
Biography:

Tijen Atacag is associated with Near East University, Turkey.

 

Abstract:

Many cancer patients are in a hypercoagulable state. The association between thrombocytosis and the presence of an underlying solid tumor has long been recognized, prompting investigation of the role of platelets in disease progression. The pathogenesis of the hypercoagulable state of malignancy involves the interplay of multiple variables. Thrombotic episodes may precede the diagnosis of malignancy by months or years. In gynecologic cancers, pre-operative elevations in platelet counts have been described for endometrial, vulvar and cervical cancer and studies suggest that thrombocytosis may be an independent poor prognostic factor in locally advanced cervical carcinomas. The recent studies indicate that platelets are actively involved in tumour growth and metastasis, especially in ovarian cancer. Ovarian cancer is the deadliest gynecologic malignancy. Early detection decreases the mortality. But, because of the anatomic location within the peritoneal cavity, ovarian cancer may be very advanced or even distantly metastatic before a patient experiences symptoms. Further, these symptoms are often initially vague and non-specific, and may mimic a variety of benign conditions. Platelet count is an easy and cheap parameter. It can be done everywhere. Thrombocytosis can help us in the differential diagnosis of adnexal masses especially if combined with CA-125. The aim of this present paper is to emphasize that thrombocytosis when combined with CA-125 can be used as an early detection parameter in the diagnostic evaluation of suspicious pelvic masses.

Biography:

Dr. Manikonda Prakash Rao, a self-made Healthcare specialist, excellence in Mucus related respiratory Health, Hyderabad, Telangana has completed his Master’s Degree, International Law and Legal Studies, and was a Gold Medalist in International law and Constitutional law. He presented papers at various international Medical conferences. So far he participated in about 20 conferences including All India Institute of Medical Sciences, New Delhi for Geriatric conferences, WAO of US for conferences in immunology and allergy etc. He was also made the Chairperson at Multi disciplinary healthcare conferences organized by All India Institute of Medical Sciences, New Delhi in the year 2014 and 2016. Recently he presented papers at Indo global health summit and expo at Hyderabad and other summits on Throat and Lung cancers – prevention and Management through exercise interventions.

Abstract:

Background: The objective of the paper is to create awareness among people about alternative and complimentary methods to protect themselves from various respiratory diseases including Throat and Lung cancers.  The diseases cause the following changes in Airways.1) Inflammation: Acute inflammation is a defense process whereas chronic inflammation is a diseases process. 2) Hyper secretion of mucus:Chronic mucus hyper secretion is a potential risk factor for an accelerated loss of lung function. The thick viscous mucus in the lungs will be conducive to pathogens. Currently available medicines and methods are not able to meet the needs of the sufferers. Continued inflammation and mucus hyper secretion may significantly contribute to transformation of normal cells into cancer cells i.e. the scope for series of mutations may get increased. 3) Bronchospasm: is an additional factor in asthma patients.

 

Methods: Exercise is a potent medication in history.  It can be used as a tool to manage various respiratory diseases including throat and lung cancers. a)  Cleaning Upper airway passages, mouth, nose and pharynx, the primary sites of colonization of pathogens and the sinuses, the way stations to the brain. These exercises should be practiced with hypertonic solution i.e., a solution having greater osmotic pressure than that of cells or body fluids and draws water out of cells thus inducing plasmolysis.b)Physical, aerobic and yogic exercises: help in strengthening the Inspiratory and Expiratory muscles.

 

Conclusions: Any mucus related respiratory health problem commences from upper airway passages and spread to tracheo bronchial tree as they constitute only one path way. The mucociliary clearance mechanism becomes defunct when excess and sticky mucus forms. Once the upper airway passages are cleaned of it, the defunct cilia become active and ciliate mucus towards mouth and it can be pushed out easily. The upper airway passages and the bronchial airways get cleaned from excess and sticky mucus.  The diseases originating from its pathway come under control. The exercises are based on the concept “ Once the offending factor, excess mucus is removed, the origin of it, Inflammation  gets resolved “ As a result of management of the above two  factors,  the gene damaging effect may get  reduced i.e., the scope for  series of  mutations  on genes  may get reduced.