20^th Euro-Global Summit on Cancer Therapy& Radiation Oncology August 28-29, 2017 Brussels, Belgium

Jaime Tisnado graduated from Leoncio Prado Military Academy. He received his BM degree from San Marcos National University, College of Sciences. He received his MD degree summa cum laude from the same San Marcos National University Medical School. He was an Intern at GBMC, a division of John's Hopkins University Hospital in Baltimore, MD, 1965, and then an Intern and Resident in Surgery at The State University of New York, Upstate Medical Center in Syracuse NY, 1966-67. He was a Resident in Radiology for 4 years at Thomas Jefferson University Medical Center in Philadelphia, 1967-71. Then he took 2 years fellowships in Vascular and Interventional Radiology and Neuroradiology both at the same institution, Thomas Jefferson University in Philadelphia, PA, 1971-73. He then became an Assistant Professor of Radiology and Director of Interventional Radiology at Albany Medical College, Albany, NY, 1974-77. Thereafter he moved to Virginia Commonwealth University, in Richmond, VA, where he became Associate Professor of Radiology and Director of Interventional Radiology and eventually became Professor of Radiology and Professor of Surgery, at the same university from 1985 till 2010. Thereafter, he was named one of the few Professor Emeritus of Radiology and Surgery, all at the same Virginia Commonwealth University in 2010 till now. He has published more than 100 articles in peer reviewed journals, about 400 scientific posters and electronic exhibits all over the country and the world, and about 200 abstracts, 4 books, many chapters in books, and about 200 papers presented at meetings, at the local, national, and worldwide level. He has been selected many times to Who is Who in America, the Best Radiologists in America, the Best Physicians in USA, etc. Moreover, he is the only person in the country and in the world who has, at the same time and forever, more than 5 fellowships in the most prestigious professional organizations of USA.

Carotid blow out syndrome (CBOS) is a catastrophic neurovascular emergency associated with a high morbidity and mortality (M&M). The etiology of CBOS is: head and neck malignancies with tumor invasion, postoperative complications, inflammation, trauma, vasculitides, collagen diseases, and post radiation therapy for malignancies, among others. The conventional surgical management has been and is carotid artery and/or branch ligation or bypass, and is rather difficult and associated with significant M&M and could be ineffective in controlling the situation. At this time, the ideal management of this serious problem is the IR and INR endovascular: insertion of stents of ndifferent kinds (covered or uncovered, selfexpanding or balloon-expandable) and/or embolization of the carotid or vertebral arteries or branches, with temporary or permanent agents and/or devices. A permanent or temporary success is expected with stent insertion and/or embolization, or both procedures combined. We have managed many patients, not considered ideal candidates for surgery, at least during the acute phase, with stents from different manufacturers, mostly covered. In addition, we have embolized some patients as well and some other patients have had both methods. The procedures have been done in the IR suite by the IR, INR and surgeons as well, working in team, in a collaborative rather than in an adversarial manner. No major complications related to the procedures have been found. The patients have had a long-term or a temporary improvement in their condition. The emergent management of CBOS by stenting and/or embolization or both is a safe, effective and relatively easy procedure to temporarily manage these seriously ill patients. A longer follow up and many more patients studied are necessary to establish the definitive role of stenting and/or embolization in CBOS. In conclusion, the conventional surgical management of CBOS may be difficult and/or ineffective, therefore, the endovascular management is considered the first choice of therapy, at least for now, especially in clinically desperate situations.

Adhip P N Majumdar received his MS and PhD degrees from the University of London, England, and DSc (Doctor of Science) degree in Gastroenterology from the University of Aarhus, Denmark. He has been a Professor at Wayne State University since 1992. He also holds the post of Senior Research Career Scientist at the Detroit VA Medical Center. Over the past several years his work has been streamlined to uncover the biochemical and physiological pathways governing the growth of gastrointestinal (GI) tract. He has published 200 original scientific articles in peer-reviewed journals and a multitude of book chapters and review articles. He is particularly interested in elucidating the patho-physiology of age-related changes in the GI mucosa, specifically those that lead to malignancy. To this end, he has begun to investigate the role of pluripotent, self-renewing CSCs in the development and progression of GI malignancies. He has been continually funded by the VA and NIH and is considered one of the nation’s leading investigators in gastrointestinal aging and cancer.

Colorectal cancer (CRC), whose incidence increases markedly after the age of 50 years, is a multi-step process resulting from accumulation of mutations during progression from normal epithelium to carcinoma. Loss or inactivation of the tumor suppressor gene in adenomatous polyposis coli (Apc) initiates genomic instability that is thought to produce the phenotypic appearance of an adenoma. Increasing evidence suggests that pluripotent cancer stem cells (CSCs) are involved in the development and progression of many types of malignancies, including CRC. Earlier, we reported that patients with ≥3 adenomas (High-risk for CRC) exhibit a marked increase in CSCs in the colon than those without adenomas. Although the regulatory mechanisms for this increase in CCSs are poorly understood, we have suggested a role for secondary bile acids in the intestine, specifically deoxycholic (DCA) and lithocholic (LCA) acids, bio-transformed by gut microbiota, in regulating this process. Indeed, we observed a marked rise in Fusobacterium nucleatum and Enterobacterium (in High-risk CRC patients. An opposite phenomenon was noted both are associated with CRC) for the anti-inflammatory Bifidobacteria and for probiotic Lactobacillus acidophilus. Among the secondary bile acids, DCA and LCA are thought to be the most significant with respect to the development of CRC. Interestingly, we found the levels of DCA and LCA in the colon of High-risk (HR) CRC patients to be markedly higher than those at lower risk (LR) for CRC. Interestingly, we found DCA and/or LCA to induce not only mutations of CRC initiating genes such as β-catenin but also CSCs in normal human colonic epithelial cells, as evidenced by increased colon sphere formation and elevated expression of several CSC markers as well as MMP-2, accompanied by an induction in drug exclusion and increased expression of multiple drug resistance (MDR) transporters ABCB1 and ABCG2. Our observations suggest that alterations in specific gut micro-organisms resulting in increase in DCA and LCA that induce stemness in colonic mucosal cells where CRC-initiating genes are mutated are responsible for the development of sporadic

CRC.

Junliang Liu underwent his Radiation Oncology Residency in University of Manitoba, Canada from 2000 to 2005. Since July 2005, he has been an attending Radiation Oncologist working at CancerCare Manitoba, Canada. He was the Radiation Oncology Residency Program Director from 2006 to 2012. He graduated from West China University of Medical Sciences (now is the Medical School Sichuan University), China in 1983 and pursued a Master’s Degree in Pediatrics from 1983 to 1986 in the same medical school. He was a Pediatrician working at Sichuan Provincial People’s Hospital, China from 1986 to 1991. He was a Guest Researcher supervised by Professor Hans Wigzell at the Department of Immunology, Karolinska Institute, Sweden, from 1991 to 1994. He earned a PhD in Immunology from La Trobe University, Melbourne, Australia in 1997, and conducted Post-Doctoral Research in Immunology at University of Alberta, Canada, from 1997 to 2000, before his residency training in Radiation Oncology. His publications included the ones in the prestigious journals of Nature Medicine and Proceedings of the National Academy of Sciences of the United States of America (PNAS). His current research interest is the treatment outcomes of gastrointestinal malignancies, breast cancer, and metastatic cancer.

Purpose/Objective: The prognosis of cancer patients with brain metastases has been dismal even with availability of stereotactic radiosurgery. This study is to explore the impact of post-whole brain radiotherapy (WBRT) systemic treatment.

Material & Methods: A consecutive cohort of patients with brain metastases were treated with WBRT with a dose-fractionation of mostly 30 Gy in 12 fractions, daily treatment, five days per week. Data was analyzed by dividing patients into group 1 patients who received post-WBRT systemic treatment and group 2 patients who did not have post-WBRT systemic treatment.

Results: Between July 1, 2005 to May 1, 2016, 65 patients’ male 31, female 34, aged 25 to 92 years old were identified. Eleven out of 65 patients received post-WBRT systemic treatment including chemotherapy (for 10 out of 11 patients) and target therapy (for 1 out of 11 patients). The median post-WBRT survival for patients who received post-WBRT systemic treatment was 14 months, compared to a much short median survival of only 3 months for patients who did not receive post-WBRT systemic treatment.

Conclusion: Post-WBRT systemic treatment increases the overall survival of patients with brain metastases.

Fikri Selcuk Simsek graduated from EskiÅŸehir Osmangazi University Medicine faculty. He completed his Master’s from EskiÅŸehir Osmangazi University Medicine faculty (2005) and Doctorate from Eskisehir Osmangazi University Medicine faculty (2011). Presently, he is working as Assistant Professor in Nuclear Medicine Department at the Firat University.

Introduction: DTC (Differentiated Thyroid Cancer) is most frequent endocrine malignancy, and after the surgery RA (Radioiodine Ablation) is the second step. But up to 20% of patients don’t have sufficient response to first dose. These cases mostly receive more than one doses. This increased patients and medical staff’s radiation exposure. In addition RA requires discontinuation of levotiroxin and this is really hard period psychologically and physically for patients. TSH>30 uIu/ml is a criteria for RA and some studies reported, if TSH is increased, TR (Theraphy Response) can be higher. In addition, tumor size

and TR rate have negative correlation in most of cancers. In this preliminary study, we assessed different TSH levels and sizes

relation between TR. Our hypothesis is, these findings can give us opportunity to individualised radioiodine theraphy and

more successful patient management.

Methods: We retrospectively reviewed DTC patients who received RA after surgery in 2011. Total 66 patients can be found. They assessed 6-12 months with I-131 (Iodine131) WBI (Whole Body Imaging) and stimulated Tg (Thyroglobulin) for TR. If Tg<0.2 and I-131WBI negative; 0.2

Findings: NR rate for TSH<30; 30-50 uIu/ml; >50 uIu/ml are 25%; 14.3%; 10.8% respectively. ER and HLR rate for TSH>50 uIu/ml and <50 uIu/ml are 75.6% and 83.4%. Tumor size have <10 mm; 1040 mm have 4.0%; 13.0% and 42.9% NR rate.

Conclusion: TSH<30 uIu/ml isn’t sufficient for RA. But there is no significant differencies between 30-50 uIu/ml and >50 uIu/ml. If tumor size>40 mm NR rate is very high. In these patients radioiodine doses maybe increased. But these preliminary findings needs to be supported by high scale studies.

Oleg V Gerasimenko completed his PhD in 1991 at BogomoletzInst, Kiev, Ukraine before moving to Liverpool, UK in 1993 to join research group lead by Prof. Ole H Petersen. He became Lecturer in 2000 and Reader in 2005 before moving to Cardiff School of Biosciences in 2010. Since then he is a Team Leader of wellequipped MRC funded research group together with Prof. Ole H Petersen (Head of School of Biosciences) and Dr. Julia Gerasimenko.

Asparaginase is an essential element in the successful treatment of childhood acute lymphoblastic leukemia, the most common type of cancer affecting children. However, in about 5–10% of cases this treatment causes acute pancreatitis (AP) as a side-effect. In AP, a potentially fatal human disease, the inactive pancreatic pro-enzymes become active enzymes inside the pancreatic acinar cells, digesting the pancreas and its surroundings. Under physiological conditions intracellular calcium signalling and Mg-ATP level are the key elements needed for stimulant-evoked exocytotic enzyme secretion from pancreatic acinar cells. Physiological Ca2+ signals stimulate ATP production, whereas sustained global cytosolic Ca2+ elevations decrease ATP levels and cause necrosis leading to AP. Alcohol and gallstones are the major causes of the disease. Recently we have investigated in vitro the mechanism by which L-Asparaginase evokes AP.For the first time, we have shown that like other

pancreatitis-inducing agents, L-Asparaginase evoked excessive intracellular Ca2+ release followed by Ca2+ entry, decreased the intracellular ATP levels and reduced Ca2+ extrusion. The toxic Ca2+ signals induced by L Asparaginase caused extensive cell necrosis. Our data suggest that the L Asparaginase-induced pathology depends on protease activated receptor 2. The inhibition of PAR2 receptor prevented the toxic L-Asparaginase-elicited Ca2+ signals and cell necrosis. Inhibition of Ca2+ entry with GSK-7975A markedly reduced L-Asparaginase-induced cellular pathology. We have demonstrated a decreased rate of Ca2+ extrusion due to the reduction in the intracellular ATP level limiting the energy supply to the Ca2+ ATPase in the plasma membrane. Supplementation of the medium with sodium pyruvate provided a similar degree of protection against pancreatic necrosis as PAR2 inhibition or GSK-7579A. The established mechanism of action of L-Asparaginase has been confirmed for several sources of asparaginase, including drug Elspar, PEG-asparaginase and asparaginase from both and Erwinia. We have now developed model of asparaginase-induced AP that allows us to fully test our previous findings and develop protection from the side effects of Asparaginase. Both Ca2+ overload and ATP loss play key roles in Asparaginase-induced AP and therapeutic strategies must take both target points into account. We suggest that a combined pharmacological control of intracellular calcium and ATP levels will prevent or alleviate AP and improve childhood cancer treatments.

Omnia Abd El-Fattah is an Assistant Professor of Clinical Oncology, Faculty of Medicine Tanta University Hospital, Egypt, member of the Egyptian Association for Cancer-based National Cancer Institute, Cairo, Egypt and Patients' Friends Society tumors in Gharbia based Department for Clinical Oncology, Tanta University Hospital, Egypt. She has Master’s and MD degrees in Clinical Oncology in 2002 and 2009 respectively from Faculty of Medicine Tanta University Hospital, Egypt. Her Master’s and MD theses focused on non-Hodgkin's lymphomas. She is teaching postgraduate students and is interested in participating in a therapeutic service in university hospitals. She attended many courses in the capabilities of faculty development and supervised multiple Master’s and MD theses. She has attended multiple national and local conferences of Clinical Oncology and has multiple international published papers in Clinical Oncology.

Purpose: The purpose is to analyse the factors that determine quality-of-life (QOL) scores among successfully treated locally advanced laryngeal squamous cell carcinoma patients and clarify their impact on survival.

Patients & Methods: A study was conducted to determine the relationship between QOL scores (Physical and mental component of short form SF-36 questionnaire and the pain, eating, speech, and mood domains from University of Washington Quality of Life (UW-QOL) questionnaire and all-cause survival among 62 locally advanced laryngeal cancer patients.

Results: The physical and mental component of short form SF-36 score and the pain, eating and mood domains from UWQOL score were significant survival predictors. The speech domain of UW-QOL score was not associated with survival.

Conclusion: QOL scores were valuable in predicting and detecting those patients with poor survival who had low score to improve survival by close follow up, early treatment of recurrence and any detected deterioration in one or more of QOL domain in those patients.