Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 12th World Cancer Conference London, UK.

Day 2 :

Keynote Forum

Ella L Kim

Johannes Gutenberg University Medical Centre, Germany

Keynote: The role of stem-like glioma cells in GBM progression and post-treatment recurrence

Time : 09:30-10:05

Conference Series World Cancer 2016 International Conference Keynote Speaker Ella L Kim photo
Biography:

Ella L Kim has completed her PhD from the Institute of Molecular Biology and Genetics, Kiew, Ukraine and Post-doctoral studies from the Barrow Neurological Institute, Phoenix, AZ, USA. She is directing the Laboratory of Experimental Neurooncology at the Johannes Gutenberg University Medical Center.

Abstract:

Glioblastoma multiforme (GBM) is the most malignant intrinsic brain tumor. Th e current standard of care for newly diagnosed GBMs involves maximum safe resection, radiation therapy and concomitant/adjuvant chemotherapy with DNA alkylating agent temozolimide (TMZ). Th e effi cacy of existing therapies is unsatisfactory with a rather modest survival advantage compared to radiation treatment alone (median survival 14.6 vs. 12.2 months, respectively), <10% of the highest 5-years survival rate and inevitable post-treatment recurrence. Developing eff ective therapies for GBM previously based on the paradigm for the pathogenesis and therapeutic resistance of this devastating disease is ongoing. A new conception of GBM has emerged aft er the identifi cation of a distinct population of glioma stem-like cells (GSCs). GSCs are thought to have the highest tumorigenic potential among all cell types comprising the tumor and responsible for tumor growth aft er treatment. However, there is still considerable uncertainty regarding the precise role of GSCs in the initiation, maintenance and progression of GBM with some fundamental questions remaining. Is there a universal type of stem-like glioma cells? What criteria defi ne glioma cell stemness? How does the degree of glioma cell stemness relate to the clinicopathological criteria of glioma aggressiveness? Our research indicates that, in GBM, the type of cells collectively called GICs comprise heterogeneous subtypes of phenotypically
and functionally distinct cells with varying tumorigenic potential. Our findings urge a reconsideration of some of the key assumptions of the GIC paradigm and provide important insights into the roles of diff erent types of stem-like cells in GBM.

Keynote Forum

Qingyong Ma

Xi’an Jiaotong University, China

Keynote: Perineural invasion in pancreatic cancer

Time : 10:05-10:40

Conference Series World Cancer 2016 International Conference Keynote Speaker Qingyong Ma photo
Biography:

Qingyong Ma has completed his PhD from Queen’s University of Belfast during 1992 to 1996. He is the Professor and Head of Department of Surgery, First Affi liated Hospital of Xi’an Jiaotong University, Xi’an, China. He has published more than 100 papers in reputed journals and has been serving as an Editorial Board
Member of repute

Abstract:

Perineural invasion (PNI) is a signifi cant pathologic feature of pancreatic cancer (PCa). As an another route of tumor spread besides vascular and lymphatic channels, PNI is considered to be an independent prognostic factor of PCa and is associated with the abdominal pain sensation and a higher risk of local recurrence aft er tumor resection. It is estimated that up to 90% of
patients have intra-pancreatic nerve infi ltration by tumor cells and that 69% have involvement of the extra-pancreatic nerve terminations. Despite increasing recognition of this metastatic process, there has been little progress in the understanding of molecular mechanisms behind PNI and, to date, no targeted treatment modalities aimed at this pathologic entity. However, it is generally believed that tumor microenvironment created a favorable environment for PNI in PCa. During the past, we have done a series of studies about PNI in PCa. Our data shows that the expression of sonic hedgehog (SHH), CXCR4, and hyperglycemia is correlated with PNI in PCa. Paracrine SHH protein derived from PCa cell could activate Hh pathway of PSCs, and increase MMP-2, MMP-9, and NGF expression in stellate cells to promote PCa growth, PNI, and peritoneal metastasis. CXCL12 derived from the peripheral nerves stimulated the invasion and chemotactic migration of CXCR4-positive PCa cells in a paracrine manner, eventually leading to PNI. Hyperglycemia could upregulate the expression of nerve growth factor in
PCa cells and inhibit the migration of Schwann cells, leading to neurites exerted pathological regeneration, thus to increase PNI. In conclusion, the internation between tumor cells and stromal cells plays a critical role in PNI of PCa.