Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 34th Euro-Global Summit on Cancer Therapy & Radiation Oncology | Park Inn by Radisson Hotel & Conference Centre London Heathrow Bath Road Heathrow Middlesex UB70DU.

Day 2 :

Keynote Forum

Xinzhong Li

Teesside University, UK

Keynote: An integrated platform for developing brain cancer diagnostic techniques

Time : 10:00-10:40

Conference Series Euro Cancer 2019 International Conference Keynote Speaker Xinzhong Li photo
Biography:

Xinzhong Li has completed his education from Xi'an Jiaotong University, China. He is a Reader in System Biology and Bioinformatics at Teesside University School of Science, Engineering and Design, UK. He has broad research interests with a focus on biomarker discovery for early disease diagnosis including dementia and cancer. He is the Scientific Coordinator of EU H2020 Marie Skłodowska-Curie Action AiPBAND project aiming to train 14 PhD students in the field of early diagnosis of brain cancer.

 

Abstract:

There were 17 million new cases of cancer and 8.2 million deaths from cancer worldwide in 2018. It’s estimated that there will be 27.5 million new cases of cancer each year by 2040. Th is causes huge social, political and financial pressures. Different from other cancers, brain tumors deaths are rising, representing 2.6% of all deaths from cancer and kill more children and people under 40 than any other cancers. Every two hours, someone is diagnosed with a brain tumour in England alone. Despite intensive eff orts, there are currently no effective disease-modifying treatments or preventive strategies for brain cancer in part due to the lack of effective early diagnostic techniques. Developing a reliable, less expensive diagnostic technique with short time intervals is utmost important and required for personalized therapy, which may potentially help patients to avoid harmful biopsy. Th e long-term fight against cancer and the lack of young interdisciplinary talents in the brain cancer diagnostic field highly requires intensive training of a new generation of researchers. AiPBAND is proposed to provide such an excellent triple-i (interdisciplinary, intersectoral and international) research and training platform with multidisciplinary expertise and advanced technologies for developing innovative diagnostic techniques for brain cancer. Through this platform, a new generation of innovative, entrepreneurial and creative early-stage researchers (ESRs) will be trained with triple-i knowledge/skills and broad vision to maximize their ability of knowledge transformation and employability, and become the future leaders in both academia and industry. Fighting against cancer and other complex human diseases requires complementary interdisciplinary research eff orts and intensive intersectoral collaborations.

Keynote Forum

Qingyong Ma

First Affiliated Hospital-Xi’an Jiaotong University, China

Keynote: HSF1 inhibition sensitizes pancreatic cancer to Gemcitabine via the suppression of cancer stem cell-like properties

Time : 10:40-11:20

Conference Series Euro Cancer 2019 International Conference Keynote Speaker Qingyong Ma photo
Biography:

Qingyong Ma has his expertise in pancreatic cancer for both scientific research and clinical studies. He has published more than 150 papers in reputed journals and has been serving as an Editorial Board Member of reputed journals. He has completed his PhD from Queen’s University of Belfast during 1992 to 1996. He is the Professor and Head of the Department of Surgery, First Affiliated Hospital, Xi'an Jiaotong University, Xi’an, and China.

 

Abstract:

Pancreatic cancer is a fatal disease with poor prognosis. Gemcitabine has been regarded as the mainstay of chemotherapy for pancreatic cancer; however, it is accompanied with a high rate of chemoresistance. We have previously reported that heat shock factor 1 (HSF1) is involved in the invasion and metastasis of pancreatic cancer, a highly conserved transcriptional factor that mediates the canonical proteotoxic stress response. Here, we further investigate whether HSF1 contributes to the chemoresistance of pancreatic cancer cells caused by gemcitabine and to explore the underlying mechanisms. Genetically engineered mice (LSL-KrasG12D/+; Trp53fl /+; Pdx1-Cre mice), which spontaneously develop pancreatic cancer, were used to examine the sensitivity of pancreatic cancer to gemcitabine in vivo. Sphere formation assays were employed to assess the tumor sphere-forming ability of pancreatic cancer cells. Th e expression of cancer stem cell (CSC)-associated markers was determined by Western blotting and quantitative real-time PCR. Small interfering RNA targeting HSF1 was used to down-regulate the expression of HSF1. MTT assays were performed to determine the sensitivity of pancreatic cancer cells to gemcitabine. We found that HSF1 was enriched in sphere-forming cancer cells. Panc-1 and MiaPaCa-2 cells treated chronically with gemcitabine displayed increased transcription and expression of CSC-associated markers. In addition, gemcitabine-surviving Panc-1 and MiaPaCa-2 cells showed an increased ability to form tumor spheres. Moreover, we observed that gemcitabine treatment increased the activity and expression of HSF1, as well as transcription of its downstream targets. Finally, HSF1 inhibition significantly suppressed the expression of CSC-associated markers, augmented the cancer-killing property of gemcitabine, and increased chemosensitivity to gemcitabine in vivo. Our study reveals a novel mechanism in which HSF1 promotes the chemoresistance of pancreatic cancer to gemcitabine by modulating CSC-like properties. Targeting HSF1 could be thus a rational strategy to improve treatment outcomes.

Break: Networking & Refreshments 11:20-11:40 @ Foyer

Keynote Forum

Gabor Somlyai

HYD LLC for Cancer Research and Drug Development, Hungary

Keynote: Hydrogen/Deuterium ratio is a key regulator of energy production and cell proliferation – submolecular dimensions of drug development

Time : 11:40-12:20

Conference Series Euro Cancer 2019 International Conference Keynote Speaker Gabor Somlyai photo
Biography:

Gabor Somlyai graduated as a biologist at József Attila University (now University of Szeged) in 1982. Between 1982 és 1990 he worked for the Department of Plant Pathology, Plant Protection Institute of the Hungarian Academy of Sciences. From 1983 to 1986 he had a scholarship of the Hungarian Academy of Sciences as a postgraduate student for obtaining PhD. In 1988 he defended his thesis in molecular biology. In the same year dr. Somlyai spent 6 months at the Georg-August University in Göttingen with a DFG scholarship and from the end of 1988 he held a postdoctoral fellowship at the University of Missouri (Columbia, Missouri, USA), where he worked in the field of genetic engineering and gene mapping. Gábor Somlyai is the inventor of numerous international patents granted in most developed countries.

 

Abstract:

The concentration of deuterium (D) is about 150 ppm (over 16 mM/L) in surface waters and 12-14 mM/L in living organisms, which is clearly a biologically relevant ion considering that circulating Ca2+ is only 2.24-2.74 mM/L. In order to reveal the possible role of naturally occurring D in living organisms, the replacement of normal tap water with deuterium depleted water (DDW) in a range from 25 ppm to 135 ppm was investigated in cell cultures, animal studies, as well as in prospective blinded and retrospective clinical trials. DDW inhibited cell growth of multiple cancer cell lines in

In vitro culturing studies and readily induced tumor xenograft regression in mice [1-3]. Double blind, controlled, human Phase II clinical trial with prostate cancer, in compliance with GCP principles exhibited a significant difference between the control (n=22) and DDW treated (n=22) patients with respect to end point parameters and confirmed significant antitumor efficacies [4]. To gain additional information on DDW efficacy, the data matrices of 1827 cancer patients consuming DDW were evaluated in an open label retrospective study. Th e cumulative follow-up period of patients covers over 6881 years from the diagnosis of the disease, with DDW consumption of 2265 cumulative years. Median survival time (MST) of the 1827 control patients treated with standard oncotherapy, which represent all major tumor types, was 121.2 months (10.1 years). MST correlated with the length of DDW consumption in treated groups. Th e MST of small, homogenous prostate-, breast-, lung- and pancreas cancer populations was also calculated. Th e MST was 64.8 months in prostate cancer patients (n=20) having bone metastases within one year after diagnosis, which is a 3-fold increase when compared to 15-20 months in patients with standard oncological care without DDW [4].The 74 breast cancer patients with stage IV disease with distant metastases in 135 cumulative number of organs the DDW treated group showed an MST of 4.3 years in comparison with ~2.0 years MST [5] of control patients. Th e MST was 25.9 months in male patients (n=78) and 74.1 months in female patients (n=51) with lung cancer which is a 3 to 7-fold increase in comparison with control patients receiving conventional oncotherapy [6]. Unresectable pancreatic cancer patients entering DDW trial within or after 60 days of diagnosis were also evaluated. Th e MST for patients starting the DDW treatment within 60 days after diagnosis (n=18) achieved 39 months MST. In contrast, patients joining the DDW trial 60 days or later after diagnosis (n=14) showed a 16 months’ MST [7]. Th e basic concepts of dosing DDW as part of standard oncotherapy will be discussed. Thirty volunteers with decreased glucose tolerance underwent 90 days long DDW treatment. Fasting glucose decreased significantly after 90 days DDW treatment (6.06±0.66 mmol/L at day0 and 5.74±0.94 mmol/L at day 90, p=0.029). Evaluation of individual cases showed that glucose uptake increased in 11 volunteers (6.9±2.4 mg/kg/min at day 0, 8.6±2.5 mg/kg/min at day 90, p=0.0014). We suggest that the cells can regulate the D/H ratio and the changes in the D/H ratio trigger certain molecular mechanisms having key role in cell cycle regulation, metabolism. The decrease of D concentration can intervene in the signal transduction pathways. Deuterium depletion opens new perspectives in drug development offering a completely safe and non-invasive treatment modality.

Keynote Forum

J C Hahne

The Institute of Cancer Research, UK

Keynote: Translational research and cancer patient stratification based on modern molecular biological methods

Time : 12:20-13:10

Conference Series Euro Cancer 2019 International Conference Keynote Speaker J C Hahne photo
Biography:

C Hahne has obtained his PhD in Biochemistry at the Albert-Ludwigs-University Freiburg i.Br. Germany. During his PhD work he was trained in virology, cell and molecular-biology. During several postdoc positions, he received broad training and knowledge in molecular pathology and cancer research. Currently, he is working in the Department of Molecular Pathology at the ICR, London, UK. He has published more than 60 papers in reputed journals and has been serving as an Editorial Board Member of reputed journals.

Abstract:

The use of molecular biological methods especially droplet-digital PCR and NanoString technology offer several possibilities for translational research and cancer patient stratification. In this workshop some examples based on RNA or microRNA expression in solid tumors will be discussed. MicroRNAs are pivotal regulators for RNA silencing and post-transcriptional regulation of gene expression under physiological as well as pathological conditions. MicroRNAs can be detected in tissues and in most biologic fluids including serum, plasma and urines. Secreted microRNAs are either incorporated into micro-vesicles or circulate bound to proteins. In both cases microRNAs are protected from RNase degradation so that they may remain intact for long periods of time. Therefore they might represent potential new biomarkers. We analyzed expression of 800 miRNA’s using nCounter NanoString technology in cancer cell lines, formalin fixed paraffin embedded tissues and plasma from cancer patients. Potential clinical applications of microRNA detection for cancer patients’ management will be discussed.

  • Poster Presentations
Location: Foyer
Speaker

Chair

Emmanouil Karteris

Brunel University, UK

Speaker
Biography:

Araceli Cue has her expertise in Whole Body Computed Tomography and has worked in this specific field for the past nine years, implementing new protocols and scanning methods to improve the diagnosis and wellbeing of her patients. She has experience as General Radiologist as well, with good experience in Fluoroscopic studies, urology diagnostic radiology and gyneco-obtetric ultrasound. In her hospital setting, teaching and administration are a daily basis activity. She is actively involved in the Mexican Board of Radiology, currently working with the Evaluation committee. Her background includes Radiology Specialty and Whole Body Computed Tomography subspecialty, Radiation Protection Diploma, Health administration diploma.

 

Abstract:

Colon cancer is an important cause of death among the general population, although it is highly preventable and treatable when early detection occurs. The main problem is the lack of patient adhesion to screening methods and some limitations in its performance due to particular patients’ features (video colonoscopy). Computed Tomography Colonography (CTC) has shown high sensitivity, low cost, less exploration time and is less invasive to the patient. In Mexico the colorectal cancer has the 1st place in incidence among digestive tube cancer. Video colonoscopy is the most sensitive and specific method for the detection of polyps and colorectal cancers. Many international organizations including the World Health Organization (WHO), the United States Agency for Health Care Policy and Research (USAHCPR), and the United States Preventive Service Task Force (USMSTF), have developed guides for colorectal cancer screening which includes CTC. Th e CTC allows the exploration of intra and extra colonic findings, thou the gathering of more information is possible. In this study all the patients having video colonoscopy had CTC in a one year period. 95% of the studied cases had positive intra and extra colorectal findings that included polyps, malignant tumor, peri colonic/perirectal fat stranding, metastatic lymph nodes and extra colorectal metastasis. Some of the malignant lesions were deeper and larger than prior stated in the video colonoscopy. Th e CTC can be used as a screening method in general population not willing to have a video colonoscopy and should be used as an obligatory complement for those patients with video colonoscopy positive  findings instead of just an Abdominal CT for staging. The information obtained from CTC helps the clinician to plan a better treatment and have a better panorama for each case.

Speaker
Biography:

Qing Zhou: Attending physician of Sichuan Provincials People’s Hospital, Master of Imaging Medicine and Nuclear Medicine. She has been engaged in ultrasound and contrast-enhanced ultrasound of abdominal and superficial organs for 9 years. She has published several publications and participated in two monographs on ultrasound.

 

Abstract:

Statement of the Problem: Orbital cavernous venous malformation (used to be known as "orbital cavernous hemangioma") is one of the common orbital occupancies; it is not a neoplasm but a venous malformation. Vision and appearance may be affected by the mass effect masses, such as blurred vision and exophthalmos may be caused by eyeball pushing. Orbital cavernous venous malformation usually present as a mass solitary, with well-defined margin, sometimes it is difficult to be identified with some tumors, such as schwannoma, solitary fibrous, and pleomorphic adenoma. The application of contrast-enhanced ultrasound imaging technology has become more and more extensive and mature recently, but there were few studies on orbital cavernous venous malformation. This study aims to help improve the diagnostic accuracy by analyzing the enhanced manifestations of orbital cavernous vascular malformation. Th e purpose of this study is to improve the ultrasound diagnostic accuracy of orbital cavernous vascular malformations by analyzing the enhanced features of contrast-enhanced ultrasound. Methodology & Theoretical Orientation: Th e contrast-enhanced ultrasound findings of orbital cavernous venous malformation cases were reviewed and analyzed to find the characteristics.

Findings: All cases showed nodular contrast enhancement after injection of contrast agent, and these nodules grew larger progressively over time. Compared with surrounding tissues, the enhancement of cavernous venous malformations were usually later or synchronous.

Conclusion & Significance: Contrast-enhanced ultrasound of orbital cavernous venous malformation has typical characteristics, and it is helpful for qualitative diagnosis.

Speaker
Biography:

Zih-Yin Lai is a Postdoctoral Fellow of the Institute of Bioinformatics and Structural Biology at National Tsing Hua University in Taiwan. She is the manager of Dr. Yung-Jen Chuang’s lab with excellent ability to guide other lab members. Her work focuses specifically on precision cancer medicine and drug combination strategy. She has established a special primary neuroendocrine tumor cultured model from the patient’s ex vivo biopsy after years of experience. Moreover, she is also responsible for two projects: boron neutron capture therapy for melanoma and EGFR/MDM2 combined inhibition therapy for ovarian cancer. Her recent publication can be found in Archives of Biochemistry and Biophysics, Oncotarget and Journal of Biomedical Science.

Abstract:

Precision cancer medicine is an evolving treatment approach that aims to associate the tumor’s unique genomic characters and histological changes to first determine the cancer subtype, and use the information to select targeted therapy for enhanced efficacy. In this study, we focus on neuroendocrine cervical carcinoma (NECC), which is a rare and aggressive subtype of cervical cancer. A NECC specimen obtained from a consented 44-year-old female patient was first analyzed by RNA sequencing. Interestingly, we found the transcription profile of the tumor case highly correlated with metabolic disease. Meanwhile, we processed and established a novel NECC cell line (annotated as Hsinchu Mackay-4, HM-4) from the patient’s ex vivo biopsy, and used it to explore novel drug combination for enhanced cytotoxic response. Drug screening revealed that, when etoposide (a known genotoxic drug for NECC) was used in combination with agent X (an FDA-approved metabolic disease drug), the proliferation of HM-4 cells was significantly inhibited as compared to etoposide or agent X treatment alone. Immunoblot assay revealed the expression level of pAKT was remarkably reduced, while p21 was upregulated when HM-4 cells were treated with a combination of etoposide and agent X. These results suggested that the drug combination of etoposide and agent X might become a novel synergistic treatment option for NECC.

Speaker
Biography:

Kuan-Hao Chen is pursuing his Master’s degree. He worked as an Intern at Academia Sinica for two months, where he studied heme oxygenase 2 protein-protein interactions with cytochrome P450 reductase. He was awarded for poster competition at 2018 Taiwan Zebrafish Symposium. He is now investigating the BNCT-induced biological effects in hepatocellular carcinoma (HCC), especially the DNA damage responses.

 

Abstract:

Background: Boron neutron capture therapy (BNCT) is a two-step radiation treatment modality, which kills tumor cells and leaves normal cells undamaged. In previous studies, boric acid (BA)-mediated BNCT has demonstrated its therapeutic efficacy in treating hepatocellular carcinoma (HCC) in rat and rabbit models. However, the DNA damage responses and repair mechanisms induced by BA-BNCT in HCC remain unclear.

Aim: This study thus aims to investigate whether the BA-BNCT induced DNA double-strand break (DSB) and to explore which DSB repair pathways, homologous recombination (HR) and non-homologous end joining (NHEJ), would be the primary pathway.

Methods: Huh7 (human HCC cell line) was pre-treated with BA 30 minutes before exposing to neutron irradiation at Tsing Hua open pool reactor in National Tsing Hua University, Taiwan. Afterwards, cells were harvested for immunocytochemistry and immunoblotting analysis.

Results: The expression of γH2AX, a marker of DSB damages, was observed to peak at 4 h and diminished by 24h after BA-BNCT. The protein expression of BRCA1 and Rad51, both involving the HR pathway, were activated at 4 h. Surprisingly, BRCA1 sustained its activation to 48 h, while NHEJ-related proteins Ku70/Ku80 did not show significant changes after BA-BNCT.

Conclusion: These results suggested that DSB damages induced by BA-BNCT were primarily repaired through the HR pathway in HCC. Our findings could enable the identification of radio-sensitizer or adjuvant treatment by targeting the HR pathway, which could help to address treatment resistance and potentiate the efficacy of BA-BNCT for HCC.

Speaker
Biography:

Kai-Yun Tsai is pursuing her Master’s degree. She has experience with two research labs in applying professional knowledge to study unresolved medical challenges. Her recent work sheds light on the importance of p53 R248Q mutation in HGSOC with different drug responses. She was selected to be a valedictorian of National Tsing Hua University.

 

Abstract:

The dysfunction of tumor suppressor p53 and its regulators is a common feature of human cancer, including ovarian cancer. Specifically, the genetic alteration of p53 mutation is detected in up to 96% of high-grade serous ovarian carcinoma (HGSOC). Moreover, mutant p53 may cause oncogenic gain-of-function phenotypes under sustained activation of EGFR signaling. Thus, we aimed to investigate whether p53 mutation could affect combined inhibition of EGFR and the p53-specific ubiquitin ligase MDM2 in ovarian cancer. We selected p53 R248Q mutant, which has the highest mutation frequency in cancer, for this study. We found that, when p53 R248Q was transiently overexpressed, the p-AKT protein expression would increase significantly. Immunocytochemistry analysis further showed that, upon EGF stimulation or p53 R248Q mutant overexpression, several EGFR pathway and cross-talking mediators would translocate in unique patterns within the cell. Previously, we have demonstrated that combined inhibition of EGFR and MDM2 pathways by Gefitinib and JNJ exerts strong synergistic inhibition on p53-mutated HGSOC cells. Our immunofluorescence analysis revealed that, under such combined inhibition, the cytonuclear trafficking of these mediators would be disrupted. Moreover, when we compared the drug responses in different p53 status, we observed the sensitivity to single- or combined-inhibition treatments would be altered in p53 R248Q overexpressed cells. In summary, our findings suggest that p53 R248Q mutation might cause differential responses in signal transduction, molecular trafficking, and drug efficacy, which helps to advance our understanding in p53 signaling and cancer biology and to improve future therapeutic strategies on HGSOC.

Speaker
Biography:

Itzíar González is Dr. in Physics. She belongs to the scientif staff of the Research Council of Spain CSIC. She has her expertise in the development of new technologies based on strategic application of ultrasounds. She and her group RESULT of ultrasonic resonators for manipulation in the National have developed low-cot polymeric chips to perform particle and cell sorting based on their whole structure resonance, with application in early detection of circulating tumor cells in peripheral blood samples. She leads various competitive research projects involving cancer solutions.

 

Abstract:

Study of cancer involving cell behaviors in different conditions is a current tending topic in scientific investigations. Blood samples can be used as liquid biopsy for early diagnosis and monitoring of chemotherapy in cancer patients. Separation of rare cells from blood samples by acoustic waves “acoustophoresis” repesentss a new label-free and biocompatible technique. Acoustic sorting works on the basis of the different physical cell properties and works at power intensities and frequencies similar to the ultrasonic imaging, with a little impact on the cell viability (high biocompatibility). It presents clinical advantages such as the fact the media in which cells are cultured and separated does not need to be modified, thus no labeling is required. Our recent microfluidic device: “THINUS-Chip”, actuated by ultrasounds flow-through separation approach, provides an efficient separation of tumor cells (TCs) from white blood cells (WBCs) in. With this microfluidic device we have introduced for the first time the concept of plate acoustic waves (PAW) applied to acoustophoresis as a new strategy in low-cost devices for clinical applications. We have also explored the effects of low intensity continuous ultrasound (LICU) on the inflammatory response of mouse pancreatic tumor explants. We found a significant upregulation of IFN-γ, IL-1β, and TNF-α on the tumor explants exposed to LICU. Meanwhile, no detectable effects were observed on tumor vasculature or collagen I deposition. This paper showed for the first time the ability of our technology based on the application of low intensity ultrasounds as a noninvasive actuator in cancer processes associated to tumor growth, enhancing some anti-tumor markers and inhibiting others related to a tumor progression. Herein, we describe our studies to remark the relevance of the LICUS as future medical solutions involving blood or tissue cell manipulation.

Speaker
Biography:

Ewa L Gregoraszczuk is specialized in reproductive endocrinology as well as hormone dependent cancer. She has graduated from Jagiellonian University in Krakow, Poland. She is a Professor of endocrinology, Head of Department of Physiology and Toxicology of Reproduction from 1998. She has authored 173 peer-reviewed articles in leading journals such as Biology of Reproduction, Reproduction, Reproductive Toxicology, Toxicology, Cancer Chemotherapy and Pharmacology. She is a Member of Polish Endocrinology Society, International Society of Endocrinology (ISE), The New York Academy of Sciences, and The European Tissue Culture Society. Her research topics focusing on the effects of metabolic hormones produced by adipose tissue in light of the increasing incidence of obesity and related problems in reproduction and hormone dependent cancer; reprotox and canceriogenic action of endocrine disruptors, testing antiepileptic drugs as a potent anticancer drug in combination with chemotherapy; testing leptin receptor blockers as a novel treatment for ovarian cancer.

Abstract:

Introduction: Despite rapid progress in understanding the ethology of epithelial ovarian cancer it is still the most lethal form of cancers. In Poland, ovarian cancer is the sixth most common women’s cancer. Vitamin C (L-ascorbic acid) has been widely used in the treatment and prevention of cancer; nevertheless, the clinical results are still inconclusive. Still there are many controversies regarding the role of vitamin C in the prevention and treatment of cancer.

Study Design: In the present data we estimated dose dependent effect of VitC on SVCT1, involved in whole body vitamin C homeostasis, SVCT2, protects metabolically active cells from oxidative stress and GLUT hexose transporters protein expression. Additionally action of Vitamin C on cell membrane permeability, measured by LDH release, lysosomal activity measured by acid phosphate assay (AP), mitochondrial activity measured by Alamar Blue assay and caspase3 activity as an indicator of apoptosis in non-cancer epithelial cells HOSEpiC and cancer chemoresistant OVCAR-3 cells

Results: Vitamin C at doses of 10 and 100 µM increased SVCT1, had no effect on SVCT2 and in dose of 100 µM increased GLUT expression in cancer cells. In dose 0.1-10 μM had no effect on cell membrane permeability mitochondrial activity, lysosomal activity and caspase-3 activity in non-cancer epithelial cells HOSEpiC, however in this doses increased LDH realize, decreased mitochondrial activity, had no effect on lysosomal activity while increased casapase-3 activity in epithelial cancer cells OVCAR-3.

Conclusion: The results of the presented data will provide new and unique information on the merits of Vitamin C as preventive and supportive for the treatment of ovarian cancer. Our study is the first concerning potential action of Vit C not only on cancer but also non-cancer ovarian cells. We suggesting that its nontoxic effects on non-cancer cells may be an indicator of its prophylactic use. This is an extremely important knowledge for biologists, doctors and most importantly for high-risk women. 

 

Speaker
Biography:

Dr Shafatujjahan, passed my MBBS on January, 2007 from Chittagong medical college and started my post graduate training on 2010 and passed my fellowship in radiation oncology on July, 2015, since then I am working as Assistant professor and head of department of medical oncology and radiotherapy of Chattogram maa o shishu hospital medical college .This is a 800 bed tertiary hospital located in the center of port city Chittagong of Bangladesh. I am teaching the undergraduate and post graduate students. I am attached with some research project in this hospital .I am attached with the project for establishing our own cancer institute with all modern chemotherapy and radiotherapy facilities.

Abstract:

Introduction: Breast cancer is increasing in Bangladesh among both young and adult woman group. Long term oral contraceptive consumption is believed to be associated with breast cancer.

Aim: This study was aimed to provide a descriptive statistics of breast cancer situation and explore the association of OCP with breast cancer in a single center located in one of the major cities in Bangladesh.

Methods & Materials: This study was carried out in Chattogram Ma O Shishu Hospital in Chittagong from July 2017 to April 2019. Patients were enrolled after histopathologically confirmed breast cancer and aged 20 and above. Patients were screened for ER, PR and HER status. Descriptive and regression analysis was done by using SPSS (v. 20).

Result: Total 40 histopathologically confirmed breast cancer patient aged from 27 to 67 years were enrolled in this study. Median age was found 46.50 with a mean BSA of 1.673. Out of 40 breast cancer patient highest number of patient were found to have stage II A followed by stage IV, IIIA, IIIB and IB. It was also found that, 60% patient were ER positive whereas 47.5% were PR positive. In HER 2+ status 52.5% were found to be negative where 17.5% were HER2 2+ positive and 20% were HER2 3+Positive. 57.5% patients were on Oral contraceptive pill (OCP) during their lifetime and 42.5% patients were not on OCP. No significant relationship was observed among OCP consumption and Hormone receptor status (P>0.05).

Conclusion: It is evident from this study is the prevalence of HER 2 positive breast cancer is increasing in daily practice without any significant association with OCP. Further studies with large sample size are required to explore the relationship in local context.

 

Speaker
Biography:

Hayaa Alhuthali is a haematology scientist at university of Nottingham (CSB, City Hospital). She is in last year of her PhD, which focuses on studying response of AML to novel therapeutic drug and explores mechanisms of drug action. She has Skills in cell culture, molecular biology, immunoblotting, flow cytometry, cell cycle analysis and cell signaling

 

Abstract:

Statement of the Problem: Acute myeloid leukaemia (AML) is a complex malignancy associated with genetic, epigenetic, and phenotypic heterogeneity. Chemoresistance and relapse are the major challenges in AML treatment. Activation of JNK pathway was demonstrated to be a vital step for the chemotherapy agent, anthracycline, to induce apoptosis in AML cells and defects in JNK-activation contributes to AML chemoresistance. Jerantinine B is a novel aspidosperma alkaloid isolated from the leaf extract of Tabernaemontana corymbosa. Preliminary screens established that JB possess in vitro anticancer activities against various human derived solid cancer cell lines but, the effect on AML was unknown.

Aim: The purpose of this study was to demonstrate whether this novel agent provide potential effective targeting of AML cells.

Methodology: Following determination of JB cytotoxicity in AML cell lines and patient samples, flow cytometry and immunoblotting was used for further experiments to explore the mechanism of action of JB.

Findings: JB exhibited significant inhibition of growth and colony formation of AML cell lines accompanied by an induction of apoptosis in a time and dose-dependent manner. JB IC50 dose at early time point (4 hrs) resulted in strong expression of both total and phosphorylated c-Jun (S63) protein and significant increases in reactive oxygen species (ROS) level (P≤0.01.) Co-treatment with a ROS scavenger, N-acetylcysteine (NAC), in JB-treated HL60 cells significantly reduced JB-induced ROS (P=0.031) and reversed JB-mediated c-Jun/JNK activation and subsequent cell apoptosis. This suggests that JB-mediated intracellular oxidative stress acts as signal for c-Jun/JNK-induced death in HL60 cells. Furthermore, JB caused cell cycle perturbation, Polo-like kinase 1 (PLK1) inhibition (evidenced by phosphorylation of phospho-histone H3 (pHH3)) and up-regulation of apoptotic markers including active caspase 3 and cleaved PARP (p≤0.02). These findings indicate that JB appears to be a potential chemotherapeutic agent in AML and its continued development is recommended. 

  • Cancer | Cancer Drugs | Cancer Science | Clinical Oncology | Cancer Case Reports | Cancer Vaccines
Location: Bleriot 1
Speaker

Chair

Olivier E Pardo

Imperial College London, UK

Speaker

Co-Chair

Qingyong Ma

First Affiliated Hospital-Xi’an Jiaotong University, China

Session Introduction

Jiguang Ma

First Affiliated Hospital of Xi’an Jiaotong University, China

Title: Sonic hedgehog signaling pathway promotes pancreatic cancer pain via nerve growth factor

Time : 15:10-15:30

Speaker
Biography:

Jiguang Ma has completed her PhD from Xi’an Jiaotong University. She has published more than 30 papers in reputed journals. Currently, she works in the Department of Anesthesia, First Affiliated Hospital, Xi'an Jiaotong University, Xi’an, and China.

 

Abstract:

Many pancreatic cancer (PC) patients suffer from abdominal pain and back pain. However, the cause of pain associated with PC is largely unclear. In this study, we tested the potential influence of the sonic hedgehog (sHH) signaling pathway on PC pain. Substance P (SP) and calcitonin gene-related peptide (CGRP) expression was measured in cultured PC cells and dorsal root ganglions (DRGs) by real-time PCR, western blotting analysis and ELISA. Small interfering RNA transfection and plasmid constructs were used to regulate the expression of sHH in the AsPc-1 and Panc-1 cell lines. Pain-related behavior was observed in an orthotopic tumor model in nude mice. In this study, the results showed that sHH increased the expression of SP and CGRP in DRGs in a concentration and time-dependent manner. Additionally, sHH secretion from PC cells could activate sHH signaling pathway and in turn, increase the expression of nerve growth factor (NGF), P75 and TrkA in DRGs. Furthermore, sHH signaling pathway and NGF/NGF receptor contributed to pain factors and pain behavior. Our results demonstrate that PC pain originates from sHH signaling pathway, and NGF mediates the pain mechanism via regulating SP and CGRP.

 

Speaker
Biography:

Jehad Zweiri is a Lecturer in Cancer studies at the University of Liverpool Medical School. He has received his Bachelor’s degree from the University of Jordan in 1990; Master’s degree from London School of Hygiene and Tropical Medicine/University of London, and PhD degree from Kings College Medical School/University of London, in the field of Immune Gene Therapy of Cancer under the supervision of Professor Farzin Farzaneh in 2000. He then started his work as a Postdoctoral Associate in the Department of Immunology and Medicine at the University of Liverpool in 2002. He was appointed as a Lecturer in the University of Liverpool Medical School in 2010 and he is currently a Fellow of the British Higher Education Academy since 2012.

 

 

Abstract:

It is well established that GCV causes bone-marrow toxicity in CMV-infected patients, particularly on the neutrophil lineage. Therefore it may also induce T cell immunosuppression, although this does not appear to have been directly investigated. If GCV does have such a side-effect it may reduce the efficiency of the immunological component of the bystander effect induced by HSV-TK/GCV. The rationale for the studies described here was to devise a strategy whereby the TK+ve tumour cells would be exposed to GCV in vitro, in order to pre-load the tumour cells with GCV, wash the excess GCV away and then inject the cells for study of their in vivo bystander effect. It is also possible that the intravenous administration of GCV does not allow the achievement of a therapeutically high enough dose at the site of injection of TK+ve cells (e.g. in the peritoneum). By contrast, the pre-loading of the TK+ve tumour cells with GCV may ensure that the cells have received the required dose of GCV. This may reduce the possible immuno toxic effects of GCV. This in turn may enhance the systemic immune mediated anti-tumour efficacy of treatment with HSV-TK expressing tumour cells.

 

Speaker
Biography:

Ramida Watanapokasin has her expertise in Cancer Biology and Molecular Biology. Her research focuses on identification of drug-lead for cancer by bioactive compounds from medicinal plants and microorganisms.

 

Abstract:

Statement of the Problem: Chondrosarcoma is the second most common malignant tumor of bone. The cancer originates from chondrocytes with abnormal proliferation and usually grows within a bone or on its surface. As 90% of human cancer death is due to metastasis process, in this study the anti-metastasis activity of Senna alata extract was studied in the highly metastasis SW1353 cell line. Senna alata is a medicinal plant which has been used in traditional folk medicine especially antimicrobial activity.

Methodology & Theoretical Orientation: S. alata extract was dissolved and diluted in DMSO at the desired concentrations. MTT assay was used to investigate the effects of S. alata extract on cell proliferation and cell growth. To study the effects of S. alata extract on cell migration and invasion, wound healing assay and transwell migration assay were performed, respectively. Signaling proteins were observed using Western blot analysis.

Findings: Our study found that at sub-toxic dose of S. alata extract inhibited cell migration and cell invasion in SW1353 treated cells. Moreover, Western blot analysis indicated that S. alata extract down-regulated p-ERK1/2 and p-Akt (S473) that involved in cell growth and proliferation.

Conclusion & Significance: S. alata extract showed the effect on metastasis inhibition in SW1353 treated-cells. In addition, S. alata extract could inhibit cell growth and proliferation via mediator proteins, ERK1/2 and Akt. These finding could be useful in the development of S. alata extract to be a metastasis inhibition agent.

Break: Networking & Refreshments 16:10-16:30 @ Foyer
Speaker
Biography:

Yan Zhu has her expertise in pre-clinically reproductive pharmacology research and devoted to improve application of contraceptives for ameliorating gynecological diseases. She has received her PhD degree at Fudan University, China and studied as a Visiting Scholar at University of British Columbia, Canada. She is the PI of Lab of Reproductive Pharmacology and National Health Commission Key Lab of Reproduction Regulation, Shanghai Institute of Planned Parenthood Research, and she is the current Council Member of Chinese Pharmacological Society and the Director of the professional committee of Reproductive Pharmacology. She has published more than 90 scientific papers in Chinese journals and international journals indexed by SCI. She has received several grants from Shanghai Municipal Science and Technology Commission, and two of research projects were awarded 3rd prize by the Nation National Health Commission of China.

 

Abstract:

Endometrial cancer (EC) has been one of most common gynecological malignancies in western countries, and in China as well. Hysterectomy is a primary treatment but not suitable for patients who desire to preserve fertility and with advanced or recurrent disease. Several clinically used progestins showed different response rates for patients with different pathological types and stages and varied greatly (11-56%), especially in recurrent or advanced patients. Here, we investigated the inhibitory effect of several progestins, including nomegestrol acetate (NOMAC), medroxyprogesterone acetate (MPA), levonorgestrel, cyproterone and drospirenone on various types of EC cells. NOMAC, a highly selective 19-nor progestogen derivative, equally suppressed the growth of RL95-2, Hec1A and AN3CA cells and showed stronger activity than the other progestins in Hec 1A cells. In vivo, NOMAC decreased the growth of ectopic endometria in a rat model and produced a stronger inhibition on the growth of xenograft tumor of nude mice borne RL95-2 cell lines than MPA did, and the inhibition rates for 50,100, and 200 mg/kg NOMAC were 24.74%, 47.04% and 58.06%, respectively, and for 100 and 200 mg/kg MPA were 41.06% and 27.01%, respectively. When equal dose of NOMAC and metformin were combined (100mg/kg, respectively), the tumor volume inhibitory rate were increased by approximately 8% and 10% compared with metformin used alone in Hec1A and RL95-2 cells, respectively. Additionally, NOMAC induced apoptosis of RL95-2 and Hec 1A EC cells and arrested cell cycle at phase of Go/G1 and impeded the protein expression and the activity of mTOR and its downstream genes, such as 4EBP1 and eIF4G, but not influence the activity of Akt. Furthermore, when combining NOMAC and metformin, the activities of mTOR, 4EBP1 and eIF4G were more strongly suppressed, comparing with metformin used alone in Hec1A and RL95-2 cells. It suggests that NOMAC may have a potential ability against the growth of EC, which effect may associate with suppressing mTOR signaling, and metformin could enhance the effect in some degree.

Speaker
Biography:

Magda Mohamed Sultan has completed her MD in Clinical Pathology and Laboratory Oncology in the National Cancer Institute at Cairo University in 1992. She was the Head of the Hematology Department of Medical Research Institute, Alexandria University, Egypt for eight years from 2007-2015. She is an Emeritus Professor in the institute, teaching for doctors and master degrees students and she is the Head of Hematology Department at Alborg Lab in Alexandria since 1996. She has published more than 25 papers and she is Arbitrator for many thesis and many published papers.

 

Abstract:

The development of myelodysplastic syndrome (MDS) secondary to treatment of non-Hodgkin lymphoma is a common finding. In the literature we found some cases diagnosed with MDS and NHL simultaneously, other cases were first diagnosed as MDS with low risk IPSS and were managed only with an observational program and then they developed NHL later on with interval ranging from 5 month to 4 years. T-cell lymphoma has a higher incidence of coexistence with MDS compared to B-NHL. We are presenting a case of co-existing de novo myelodysplastic syndrome (MDS) and non-Hodgkin lymphoma (NHL) prior to therapy diagnosed by bone marrow aspiration, bone marrow trephine biopsy, immunophenotyping and immunohistochemistry.