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.
ABSTRACT:
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.
ABSTRACT:
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.
Universal Medical Imaging Group
USA
ABSTRACT TITLE: Is X-Ray Mammography Accelerating The Epidemic of
Breast Cancer?
ABSTRACT:
Universal Medical Imaging Group
USA
ABSTRACT TITLE: Is 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
USA
ABSTRACT TITLE: p38 MAPK signaling and pancreatic
tumorigenesis
ABSTRACT:
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 p38knockout 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
ABSTRACT:
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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