Friday, 6 April 2018

Pre-Posting #Speakers Abstract #Medical Meet #Most awaited update is out now #Prepare yourself to question the experts #We are ready to answer for all your doubts #Join us @Rome, Italy #June 18-19, 2018

Group of Speakers from different parts of the world attending this conference as a Speaker/Delegate/ Organizing Committee Member.  Here comes the list of Speaker along with their title in which they are gonna present in our conference!

NAME: Dr.David Piquemal

AFFILIATION: Co-Founder & Scientific Director at ACOBIOM company

ABSTRACT TITLE: Patient Stratification and Precision Medicine in Pancreatic Cancer: a gene blood-signature for gemcitabine treatment.


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

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

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

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


   Universal Medical Imaging Group


ABSTRACT TITLEIs X-Ray Mammography Accelerating The Epidemic of Breast Cancer?


While a growing body of research now suggests that x-ray mammography is causing more harm than good in the millions of women who subject themselves to breast screenings, annually, without knowledge of their true health risks, the primary focus has been on the harms associated with over-diagnosis and over-treatment, and not the radiobiological dangers of the procedure itself.
In 2006, a paper published in the British Journal of Radiobiology, titled “Enhanced biological effectiveness of low energy X-rays and implications for the UK breast screening programme,” revealed the type of radiation used in x-ray-based breast screenings is much more carcinogenic than previously believed.
Recent radiobiological studies have provided compelling evidence that the low energy X-rays as used in mammography are approximately four times – but possibly as much as six times – more effective in causing mutational damage than higher energy X-rays. Since current radiation risk estimates are based on the effects of high energy gamma radiation, this implies that the risks of radiation-induced breast cancers for mammography X-rays are underestimated by the same factor [1].


NAME: Dr. Guan Chen  

AFFILIATION:  Department of Pharmacology and Toxicology
                                   Medical College of Wisconsin

 ABSTRACT TITLE: p38 MAPK signaling and pancreatic tumorigenesis


Pancreatic ductal cancer (Pda) lacks established therapeutic targets and is consequently among the deadliest malignancies with near-universal K-Ras mutations. Here, we report that a Kras effector p38 (MAPK12) is required for pancreatic tumorigenesis through stimulating metabolic reprogramming. Both conditional p38knockout and pharmacological inhibition decrease pancreatic tumorigenesis and inhibit Pda growth. Mechanistically p38 binds PFKFB3 dependent of mutated Kras and phosphorylates this glycolytic activator at S467, which is required for aerobic glycolysis and Pda growth. Activation of the p38/p-PFKFB3 pathway in clinic specimens further correlates with decreased patient survival. Thus, p38 MAPK is essential for Pda tumorigenesis by linking K-Ras oncogene activity and metabolic reprogramming and may be targeted for therapeutic intervention.
NAME: Dr. Mouad Edderkaoui

AFFILIATION:  Cedars-Sinai Medical Center & University of California Los Angeles

ABSTRACT TITLE: Targeting metastasis and drug resistance for treating pancreatic cancer


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

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

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

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

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