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J Med Oncl Ther 2017 | Volume 2 Issue 4
Oncology and Biomarkers Summit
November 27-28, 2017 | Atlanta, USA
Annual Congress on
Hepatocellular carcinoma: The role of host immunity in the regulation of proliferative responses
Natalyn N Hawk
Winship Cancer Institute, USA
H
epatocellular carcinoma (HCC) is the most common
primary liver malignancy, with over 600,000 cases
annually around the world. Less than 20% of cases are not
amenable to curative therapy either surgery or transplant,
so the overall outcome of patients with HCC is poor. Cirrhosis
of the liver is a major driver in the pathogenesis of HCC in
addition to direct proliferative stimuli from hepatitis viruses.
The nature of the influence of cirrhosis has emerged as
an area of intense study, where the long-term effects of
chronic inflammatory states might include creating a host
environment drivenby aperpetual activationof inflammatory
responses which may lead in some cases to abnormal cell
proliferation or inappropriate persistence of activation of
inflammatory states culminating in malignancy. Recently,
PDL1 ligand inhibition with novel therapies that up regulate
MHC-1 targeted markers on the malignant cells has shown
exceptional promise for various malignancies including
melanoma, lung cancer, renal cell carcinoma and sub-classes
of colon cancer as well as in hepatocellular carcinoma. The
mechanisms remain to be clarified in HCC. However, the
impact of cirrhosis in creating the frameworkwithinwhich the
host’s immune system can benefit from these therapies may
be critical in determining how effective these therapies can
be. Future study in the area of HCCwill highlight how survival/
proliferative and immune signaling pathways communicate
in the background of cirrhosis compared other conditions
and what may be the impact on the ability of driving the key
pathogen etic events in the development and progression of
HCC as well as influence the therapeutic approaches that are
being actively studied to achieve control of this disease and
thereby improve survival. In our discussion we will: Provide
an overview of the major etiologic factors associated with
the development of HCC; Review the major biological and
molecular pathways that have been shown to be important
in the pathogenesis of HCC and review the current therapies
that are in use or in study for treatment; Review the data
which demonstrates the impact of host inflammation on the
pathogenesis of HCC in the absence versus presence of liver
cirrhosis; and summarize the widely used systemic therapies
in HCC and refractory HCC and highlight the more promising/
actively studied therapies that show reasonable promise in
improving the outcomes of patients with advanced and or
refractory HCC.
Speaker Biography
Natalyn N Hawk obtained her MD and PhD from Brown University in Providence, Rhode
Island, earning her doctorate in molecular pathology as a visiting scientist at M.D.
Anderson Cancer Center in Houston, Texas where she identified a molecular complex
important in the pathogenesis of chronic myeloid leukemia. She completed residency
training in internal medicine at Johns Hopkins Bayview Medical Center in Baltimore,
MD. She completed fellowship training in hematology and medical oncology at Emory
University which included a one year post-graduate fellowship where she studied
the efficacy of dual inhibition of mTOR and EGF receptor pathways as a potential
therapy in Non small cell lung cancer. She is an Assistant Professor of Hematology
and Medical Oncology at Emory University and is a member of the Gastrointestinal
Oncology Working Group of Emory Winship Cancer Institute. She is also a member of
the Discovery and Developmental Therapeutics Research Program at Winship Cancer
Institute of Emory University.
e:
nhawk@emory.edu