Day1

  • University of Rochester Medical Center ,USA
  • Title:Biomarker and Multigene Assay Testing in ER Positive, HER-2 Negative Breast Carcinomas: An International Guidelines-Based Approach
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Abstract
Multigene genomic profiling has become the standard of care in the clinical risk-assessment and risk-stratification of ER positive, HER2 negative breast cancer patients, with Oncotype DX® (ODX) emerging as the genomic profile test with the most support from the international community. Cost-efficiency and geographic availability must be considered when evaluating the clinical utility of multigene profile tests such as ODX. ODX is an expensive test, and may not be the most cost-efficient option in certain subsets of breast cancer patients. Access to multigene testing for breast cancer is not readily available in less developed geographies of the world. Breast cancer patients in these areas of the world should have opportunities for evidence-based clinical risk-assessment and risk-stratification, even when multigene testing is not available. Several studies have suggested that certain lower risk patients can be identified in a more cost-efficient manner than simply reflexing all ER positive, HER2 negative breast cancer patients to ODX testing. The Magee equations use several histopathologic variables, including four highly weighted variable used by ODX (ER, PR, HER-2, and Ki-67), to calculate a recurrence score which correlates well with ODX. Outcome data in patients we have studied with at least five years of follow-up or a breast cancer recurrence strongly suggests that breast cancer patients can be confidently stratified using an algorithmic approach into lower and higher risk recurrence groups using a modification of the Magee score. We will present data further reinforcing that breast cancer patients can be confidently stratified into low and high-risk recurrence groups using an algorithmic approach, with comparable outcomes to similar risk-stratification categories defined by ODX.

Biography
Dr .Bradley M Turner he completed a combined medical degree and Master of Public Health at Robert Wood Johnson Medical School/School of Public Health – Rutgers University, and a Master in Health Administration at the University of South Florida College of Public Health. After completeing a residency in Family Medicine at Duke University/Southern Regional AHEC, he praticed family medicine for five years. He then returned back to training, completing a second residency in Pathology at the University of Florida, with subsequent fellowships in General Surgical Pathology at the University of Texas Heatlh Science Center in San Antonio, Oncologic Surgical Pathology at Roswell Park Cancer Institute, and Breast/GYN Pathology at the Yale School of Medicine). He is an Associate Professor of Pathology and co-director of the Breast/GYN Pathology fellowship at the University of Rochester Medical Center, with interests in how the breast microenvironement, breast biomarkers, and histologic variables may provide cost-efficient and cost-effective prognostic and predictive outcome data for breast cancer patients.

  • Ageo Central General Hospital, Japan                  
  • Title:Pembrolizumab for Fanconi Anemia with Advanced Tongue Cancer~Our Approaches to Head and Neck Cancer Treatment
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Abstract
Immune Checkpoint Inhibitors(ICIs)for recurrent or metastatic head and neck cancer have significantly prolonged survival compared with conventional anticancertherapy.Treatment with ICIs can result in a variety of immune-related adverse events (irAEs), sometimes even fatal. In terms of actual therapeutic efficacy, tail plateau, which indicates long-term progression-free survival, and other phenomena such as pseudoprogression and hyperprogression are also characteristic of immunotherapy. In Japan, ICIs have been used for head and neck cancer for more than five years, and actual clinical practice has been providing more evidence regarding their efficacy, adverse effects and possible interactions with other anticancer drugs.We have experienced the use of pembrolizumab in a patient with Fanconi anemia, an autosomal recessive genetic disorder characterized by juvenile onset of solid tumors, pancytopenia, transformation to leukemia, and physical malformations.28% of the 1-9 cases per million people annually reported worldwide are associated with head and neck squamous cell carcinoma by the age of 40. Although the prevalence rate is low, it is not rare for specialized head and neck cancer facilities to encounter this disease. Because of the early age of the onset, the risk of carcinogenesis is not fully recognized by both patients and health care providers, and patients are often diagnosed with advanced cancer.Due to repair disorders of DNA double-stranded crosslinking, cytotoxic chemotherapy and radiotherapy are often not applicable and treatment options are limited because of high risk of severe side effects.Although immunotherapy is expected to play an important role in the treatment of Fanconi anemia patients, we could not find any reports of pembrolizumab monotherapy for Fanconi anemia.In this session, we report our experience with pembrolizumab administration to a Fanconi anemia patient with advanced tongue cancer, and discuss certain important observations we made regarding immunotherapy. I would also like to briefly introduce a few specific approaches to head and neck cancer treatment in our department.
Biography
Dr. Keitaro Nagano 2009 Graduated from Kyushu University,2009-2011 Kumamoto University department of maxillofacial oral surgery,2011-2016 Oita university, Nagano dental clinic oral surgery ,2016-2019 Teine Keijinkai hospital department of otolaryngology, head and neck surgery,2019-present Ageo Central General Hospital otolaryngology, head and neck surgery, He is the Member of the Japanese Society of otorhinolaryngology-Head and neck surgery ,the Japanese Society of Head and Neck Cancer the Japan society for head and neck surgery ,Japanese Society of Oral and Maxillofacial Surgeons.

  • Department of Nuclear Medicine, South Africa
  • Title:Nuclear Medicine Therapy of Prostate Cancer: State of the Art and Future Perspectives.
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Abstract
The incidence and prevalence of prostate carcinoma (PCa) is universally increasing and causing significant morbidity and mortality in males. Worldwide, the incidence, prevalence and aggressiveness of Pca varies across different race groups in the US and Africa is significantly greater in Blacks; this may be due to social and other epigenetic factors.Various pathogenetic aberrations have been proposed leading to a better comprehension of tumourogenesis however the translation to these findings into therapeutic modalities that impact survival has not been realised fully.It is anticipated that comprehension of the pathogenesis may lead to better outcomes. Thus far, there are various therapeutic modalities available based of the Gleason staging however none has proven to be fully effective for all patients in the various staging. This chapter will mainly focus on the therapy of PCa. Despite the availability of various therapeutic modalities i.e. surgery, chemotherapy, endotherapy and androgen deprivation therapy, systematic reviews have shown that the side-effect profiles of these interventions invariably affects the physical activity (PA) and quality of life (QoL). Novel and efficacious agents should then demonstrate safety i.e. less toxicity, overall survival and a better health-related quality of life (HRQoL).
Biography
Dr.Tebatso M.G. Boshomane is a Nuclear Medicine Physician who is currently active in both private and academic practice.He completed his undergraduate medical studies at the University of the Witwatersrand (Wits) in 2006, after which he underwent internship training and medical officer training at the hospital in which he was born i.e. Pietersburg Hospital in South Africa.

  • Inha University, Korea
  • Title:The DDR1 Targeting Increased the Anticancer Effect of Gemcitabine by Inhibition of ECM Accumulation in Pancreatic Cancer
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Abstract
Pancreatic cancer is an extracellular matrix (ECM)-rich carcinoma, which promotes chemoresistance by inhibiting drug diffusion into the tumor. Discoidin domain receptor 1 (DDR1) binds to collagen which is major component of tumor ECM. Therefore, inhibition of DDR1 can behelpful target of cancer therapeutics by enhancing drug delivery efficiency. In this study, we developed a novel DDR1 inhibitor, KI-301690 and investigated whether it could improve the anticancer activity of gemcitabine, a cytotoxic agent widely used for the treatment of pancreatic cancer. KI-301690 synergized with gemcitabine to suppress the growth of pancreatic cancercells. Importantly, its combination with gemcitabine significantly attenuated the expression of major ECM components including collagen, fibronectin, and vimentin in tumor spheroids compared with gemcitabine alone. Also, this combination effectively decreased mitochondrial membrane potential, thereby inducing apoptosis. Additionally, the combination synergistically inhibitedthe cell migration and invasion. The enhanced anticancer efficacy by the co-treatment could be explained by the inhibition of DDR1/FAK signaling. Our results demonstrate that KI-301690 can inhibit expression of aberrant ECM by blockade of DDR1/FAK signaling and attenuate the ECM-induced chemoresistance observed in desmoplastic pancreatic tumor, resulting in apotent antitumor effect through effective induction of apoptosis.
Biography
Dr. Soyeon ko graduated from CHA University, Korea in 2019. She has worked as a Ms-Ph.D course since 2019 in department of Medicine, College of Medicine, and Program in Biomedical Science & Engineering, Inha University, Korea. Her research interests are finding a novel oncogene, discovery of biomarkers for carcinogenesis, cancer immunotherapy, and drug development.

  • Inha University, Korea
  • Title:Discovery of a Novel KRAS-Specific Antibody to Enhance Chemotherapy for Pancreatic Cancer
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Abstract
KRAS mutation is associated with the progression and growth of pancreatic cancer and contributes to chemo-resistance to drugs such as gemcitabine. Here, we developedaRT22-ep59 antibody that directly targets the intracellularly activated GTP-bound formof oncogenic KRAS mutants after is internalized into cytosol by endocytosis through tumor-associated receptor of EpCAM and investigated its synergistic anticancer effectsin the presence of gemcitabine in pancreatic cancer. We first observed that RT22-ep59specifically recognized tumor-associated EpCAM and reached the cytosol by endosomal escape. In addition, the anticancer effect of RT22-ep59 was observed in the high-EpCAM-expressing cancer cells and gemcitabine-resistant cancer cells, but it had little effect on the low-EpCAM-expressing cells. Additionally, co-treatment with RT22-ep59 and gemcitabine synergistically inhibited cell viability, migration, and invasion and exhibited synergistic anticancer activity by inhibiting the RAF/ERK or PI3K/AKT pathways in cells with high-EpCAM expression. In an orthotopic mouse model, the co-administration significantly inhibited tumor growth. Furthermore, the co-treatment suppressed cancer metastasis by blocking EMT signaling. Our results demonstrated that RT22-ep59 synergistically increased the antitumor activity of gemcitabine by specifically targeting KRAS. This indicates that co-treatment with RT22-ep59 and gemcitabine mightbeconsidered a potential therapeutic strategy for pancreatic cancer patients harboring KRAS mutation.
Biography
Dr. Soon-Sun Hong graduated from Seoul National University, Korea in 1996, and got the Master degree in 1998 and Ph.D. degree in 2001. He worked as a post-doctoral fellow for College of Medicine, Yale University, USA in 2001 ~2003. He has worked as a professor since 2007 in department of Medicine, College of Medicine, and Program in Biomedical Science & Engineering, Inha University, Korea. His research interests are finding a novel oncogene, and the discovery of biomarkers for carcinogenesis, especially in liver and pancreatic cancers.

  • University of Health Sciences ,Turkey
  • Title:Effects of Melatonin on Uterine Hypertrophy/Hyperplasia: An Experimental Preliminary Rat Study
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Abstract
Endometrial hyperplasia is a process of endometrial proliferation that results in a thickening of the endometrial tissue. Melatonin might be able to change the pathophysiological process and prognosis into a positive way that might prevent and heal endometrial hyperplasia, which is the first stage of endometrial cancer. For this perspective, we tried to investigate the effect of melatonin on uterine hypertrophy/hyperplasia in an experimental rat model. Forty Wistar-albino rats were undergone bilateral oophorectomy and randomized to four groups. To create a model of endometrial hypertrophy/hyperplasia all groups, except the control group [C], were given 4 mg/kg/day estradiol hemihydrate for 14 days. The uterine hypertrophy/hyperplasia was evaluated histopathologically in the left uterine horns, then the groups were treated for 14 days as follows: melatonin (10 mg/kg/day/po) [M], melatonin+estradiol hemihydrate (10 mg/kg/day/po and 4 mg/kg/day/po) [M+E], and dark environment [D]. Finally, the effects of the melatonin were examined histopathologically in the right uterine horns. A uterine hypertrophy/hyperplasia model was established in all groups compared to the control group (p<0.05). In the [M] and [M+E] groups, epithelial cell height and luminal epithelial cell height significantly decreased (41µm vs 12µm, p=0.005; 14µm vs 10µm, p=0.005, respectively for [M] group) and (32µm vs 14µm, p=0.012; 17µm vs 10µm, p=0.017, respectively for [M+E] group). The [D] group exhibited a significant decrease in epithelial cell height (33µm vs 20µm, p=0.017).Whether or not there was exposure to estrogen, melatonin-treated and –released physiologically rats experienced a significant uterine hypertrophy/hyperplasia recovery. Melatonin may have protective effects on endometrial hyperplasia. Biography
Dr. Mustafa Can Sivas completed his medical education at Istanbul University Cerahpaşa Faculty of Medicine in 2012. Afterwards, he started to specialize in cardiovascular surgery. During his education, he transferred to the obstetrics and gynecology department and graduated from the department of obstetrics and gynecology, University of Health Sciences, Etlik Zubeyde Hanim Women’s Health Training and Research Hospital/Ankara/Turkey in 2018. In 2018, he won the first place in Turkey in the hypothesis competition of the gynecology and obstetrics department. Currently, he continues his scientific work in University of Health Sciences, Başakşehir Çam and Sakura City Hospital. His areas of interest are minimally invasive gynecological surgery, gynecological and obstetric diseases and their treatments, animal experiments. In daily life, her favorite hobbies are playing piano, guitar, sports and watching the Bosphorus of Istanbul.

  • Inha University, Korea
  • Title:Novel TGF-β Receptor I Inhibitor, EW-7197 Increases Sensitivity of Gemcitabine in Pancreatic Cancer
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) produces an excessive amount of transforming growth factor β (TGFβ), which promotes tumor progression and metastasis. Also, TGFβ signaling contributes to rapidly acquired resistance and incomplete responses of gemcitabine. Recently, selective inhibitors of the TGFβ signaling pathway have shown early promise in PDAC treatment, particularly as an option of augmenting responses to chemotherapy. Here, we investigated synergistic anticancer effects of EW-7197 in the presence of gemcitabine together with its mechanism in pancreatic cancer. EW-7197sensitized pancreatic cancer cells to gemcitabine by synergistically inhibiting the viability. The apoptotic effect of combination of EW-7197 and gemcitabine was observed by increased cleaved caspase and TUNEL-positive cells via loss of mitochondrial membrane potential. Additionally, combination of EW-7197 and gemcitabine decreased metastasis by inhibition of migration and invasion, and exhibited synergistic anticancer activity by inhibiting the TGF/Smad pathways in pancreatic cancer cells. Importantly, co-treatment significantly suppressed tumor growth in orthotopic models. Taken together, our findings show that EW-7197 synergistically increased the antitumor activity of gemcitabine by inhibiting TGF/Smad, suggesting that combination of EW-7197 and gemcitabine might be considered a potential treatment option for pancreatic cancer patients.
Biography
Dr.Kyung Hee Jung graduated from Dongduk Womens University, Korea in 1997 andgot the Master degree in 2004. Also, she got the Ph.D. degree from Kyung Hee University in 2007. She has worked as a research professor since 2008 in department of Medicine, College of Medicine, Inha University, Korea. Her research interests are finding a novel oncogene, and the discovery of biomarkers for carcinogenesis.

  • Inha University, Korea
  • Title:Lidocaine Enhances the Anticancer Efficacy of Pabociclib in Breast Cancer via AKT/GSK3β Signal
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Abstract
The use of anesthetics in the surgical resection of tumors may influence the prognosis of cancer patients. Lidocaine, a local anesthetic, is known to act as a chemosensitizer and relieve pain in some cancers. In addition, palbociclib, a potent cyclin-dependent kinase (CDK) 4/6 inhibitor, has been approved for chemotherapy of advanced breast cancer. However, recent studies have revealed the acquired resistance of breast cancer cells to palbociclib. Therefore, the development of combination therapies that can extend the efficacy of palbociclib or delay resistance is crucial. This study investigated whether lidocaine would enhance the efficacy of palbociclib in breast cancer. Lidocaine synergistically suppressed the growth and proliferation of breast cancer cells by palbociclib. The combination treatment showed an increased cell cycle arrest in the G0/G1 phase by decreasing retinoblastoma protein (Rb) and E2F1 expression. In addition, it increased apoptosis by loss of mitochondrial membrane potential as observed by increases in cytochrome c release and inhibition of mitochondria-mediated protein expression. Additionally, it significantly reduced epithelial-mesenchymal transition and PI3K/AKT/GSK3β signaling. In orthotopic breast cancer models, this combination treatment significantly inhibited tumor growth and increased tumor cell apoptosis compared to those treated with a single drug. Taken together, this study demonstrates that the combination of palbociclib and lidocaine has a synergistic anti-cancer effect on breast cancer cells by the inhibition of the PI3K/AKT/GSK3β pathway, suggesting that this combination could potentially be an effective therapy for breast cancer.

Biography
Dr.Beomseok Han graduated from Chungbuk National University, Korea in 2019. He has worked as a Ms-Ph.D course since 2019 in department of Medicine, College of Medicine, and Program in Biomedical Science & Engineering, Inha University, Korea. His research interests are finding a novel oncogene, discovery of biomarkers for carcinogenesis, cancer immunotherapy.

  • King’s College London, United Kingdom
  • Title:A Simple and High‐Accuracy PID‐Based Temperature Control System for Magnetic Hyperthermia Using Fiber Optic Thermometer
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Abstract
In the antibody-mediated oncotherapy, IgG monoclonal antibodies have been the class of choice to the treatment of different types of cancer. However, IgG antibodies present limitations such as, relatively low affinity for cognate Fc receptors and the disadvantage of interaction with inhibitory Fcγ receptors, abundant in the tumour microenvironment. The IgE class antibodies are emerging as a new option for cancer therapy, due to its high affinity for cognate Fcε receptors expressed on different immune effector cells such as macrophages and mast cells, and lack of inhibitory. Studies on IgE antibodies recognizing the tumour‐ associated antigen folate receptor α (FRα) and the cell surface proteoglycan, chondroitin sulfate proteoglycan 4 (CSPG4) induced superior immune responses in FRα‐expressing ovarian carcinomas and human melanoma, respectively. In breast cancer, in vitro studies of trastuzumab (IgG1) and an engineered trastuzumab IgE recognizing the tumour‐associated antigen HER2/neu indicated that IgE could act as a coadjutant by improving the clinical performance of trastuzumab. In this work, a multi‐gene cloning, enzyme‐free assembly system for rapid expression of functionally active antibody was established (within 7‐9 days from transfection to purification in serum‐free cultures) with improved expression efficiency, speed (7‐9 days vs 4‐6 weeks) and yields (70‐80 mg/mL vs <20‐25 mg/mL), compared to previous platforms. Anti‐HER2 IgE recognized HER2/neu‐overexpressing and moderately expressing breast cancer cells, comparable to trastuzumab. Anti‐HER2 IgE and trastuzumab similarly restricted breast cancer cell viability and epidermal growth factor signalling, while addition of antibodies together did not improve HER2 signalling inhibition. Anti‐HER2 IgE recognized RBL SX‐38 rat basophilic leukaemia cells, expressing the human tetrameric FcεR I(αβγ2 ), and human U937 monocytes expressing the low‐affinity IgE receptor FcεRII/CD23. Compared with isotype controls, anti‐HER2 IgE induced >2‐fold higher antibody-dependent cell-mediated cytotoxicity (ADCC) of HER2‐ overexpressing breast cancer cells by unstimulated and IL‐4 stimulated U937 effector cells and, by peripheral blood mononuclear cells from human volunteers. Anti‐HER2 IgE induced degranulation of RBL SX‐38 cells when cross‐linked by polyclonal anti‐IgE on the cell surface HER2‐expressing tumour cells. In basophil activation tests (BAT) conducted in unfractionated human blood, anti‐HER2 IgE did not induce basophil activation. Mast cell and basophil tests therefore confirm lack of activation with IgE in the absence of cross‐linking stimuli, supporting potential safe administration in human circulation. Altogether, these results suggest anti-HER2 IgE as a safe and efficient antitumor effector with significant potential in cancer immunotherapy

Biography
Lais Cristina initiated scientific training at the Bioactive glycoconjugates laboratory of the Federal University of Rio Grande do Norte in Brazil, when she was a first-year undergrad in Biomedical Science, and following my graduation she has obtained Master’s degree and my PhD in Biochemistry. During this time, she worked with the structural characterization of glycosaminoglycans obtained from marine sources and evaluated their interaction with proteins involved in different biological process, including coagulation, inflammation and cancer. she’s main area of interest is Immuno-oncology and currently, she researched associate at the Cancer Antibody Discovery & Immunotherapy Group at St. John’s Institute of Dermatology – King’s College London.

  • Yonsei University College of Medicine, Seoul, Korea
  • Title:Cancer‐Associated Fibroblasts Secret Interleukin-8 which Induces S100A8 Upregulation, Promoting the Aggressive Phenotypic Shift in Non‐Malignant Breast Epithelial Cells
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Abstract
Cancer‐associated fibroblasts (CAFs) in the tumor microenvironment have been associated with tumor progression in breast cancer. Although crosstalk between breast cancer cells and CAFs has been studied, the effect of CAFs on non‐neoplastic breast epithelial cells is not fully understood to date. Here, we investigated the effect of CAFs on aggressive phenotypes in non‐neoplastic MCF10A breast epithelial cells. CAFs induced epithelial‐to‐mesenchymal transition (EMT) and invasive phenotype in MCF10A cells. S100A8, a potential prognostic marker in several cancers, was markedly increased in MCF10A cells by CAFs. S100A8 was crucial for CAFs‐induced invasive phenotype of MCF10A cells. Among cytokines increased by CAFs, interleukin (IL)‐8 induced S100A8 through transcription factors p65 NF‐κB and C/EBPβ. In a xenograft mouse model with MCF10A cells and CAFs, tumor was not developed, suggesting that coinjection with CAFs may not be sufficient for in vivo tumorigenicity of MCF10A cells. Xenograft mouse tumor models with MDAMB‐231 breast carcinoma cells provided an in vivo evidence for the effect of CAFs on breast cancer progression as well as a crucial role of IL‐8 in tumor growth and S100A8 expression in vivo. Using a tissue microarray of human breast cancer, we showed that S100A8 expression was correlated with poor outcomes. S100A8 expression was more frequently detected in cancer‐adjacent normal human breast tissues than in normal breast tissues. Together, this study elucidated a novel mechanism for the acquisition of invasive phenotype of non‐neoplastic breast cells induced by CAFs, suggesting that targeting IL‐8 and S100A8 may be an effective strategy against breast cancer.

Biography
Aree Moon is a professor at College of Pharmacy, Duksung Women’s University, Seoul, Korea. She is currently in dispatch service as the Director General at Directorate for National Strategic R&D Programs, NRF, Korea. She received her B.S. degree at College of Pharmacy, Seoul National University in 1983. She moved to the USA and continued to study in Biochemistry. She got her Ph.D. degree at Department of Biochemistry and Biophysics, Iowa State University, USA in 1989. Since 1995, she has been a professor at College of Pharmacy, Duksung Women’s University. She has received a number of awards including ‘Presidential Award’, ‘Order of Science and Technology Merit’, and ‘Korea L’Oreal-UNESCO Award for Woman in Science’.

  • J. W. Goethe University, Frankfurt am Main, Germany
  • Title:Caspase-8: Do we really know it well enough?
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Abstract
Caspase-8 has been synonymous with triggering apoptosis, either by itself, in the death- receptor mediated pathway, or in cahoots with the DNA damage response pathway, apart from being involved in anoikis, autophagy and pyroptosis. The long-held notion, therefore, has been that Caspase-8 activity/expression is lost in cancer cells, enabling them to evade apoptosis, thereby resisting anti-cancer therapeutics. However, in recent years, a number of non-apoptotic functions of Caspase-8 has come to the fore. In our latest work, we have identified a novel non-apoptotic function of pro-Caspase-8 in inhibiting the migration and invasion of cervical, breast and ovarian cancer cell lines, by negatively regulating the transcriptions of metastasis associated genes. Caspase-8 performed these functions by negatively regulating the activation of a transcription-associated kinase, which in-turn, inhibited the latter’s activity on a transcription-associated RNA polymerase. Cementing our cellular findings, analysis of patient derived materials and TCGA data showed that Caspase-8 was frequently down-regulated in these cancer entities, resulting in significantly poorer prognosis with reduced distant metastasis-free survival, cancer-specific survival and relapse-free survival. The loss of Caspase-8 expression also led to significantly enhanced resistance to standard platin-based chemotherapeutics, which could be synergistically overcome when combined with small-molecule inhibitors against the aforementioned kinase, in 2D as well as in 3D spheroid models. Presently, we are working on generating ovarian and cervical cancer patient derived 3D organoids, and ovarian cancer orthotopic mouse models, to further validate these results. We are also working on the development of better combination therapies, which would also be tested on the above-mentioned 3D organoid and in vivo models. In summary, our work has identified a novel mechanism of Caspase-8 which could result in it being used as a biomarker for stratifying cervical, breast and ovarian cancer patients for targeted anti-cancer therapeutics.

Biography
Ranadip Mandal a junior group leader, presently working at the Department of Gynaecology of the University Hospital of J. W. Goethe University, Germany. He has completed my Bachelors in Microbiology in 2003, from the University of Pune, India, he had completed my second Masters in Research (M.Res.) in Molecular Medicine in 2010, from the University of Glasgow, UK. He had obtained my Doctorate in Molecular Biology in 2015, from the J. W. Goethe University, under the aegis of Prof. Dr. Klaus Strebhardt. From 2016 to 2018, he had worked as a post- doctoral scientist at the German Cancer Research Centre (DKFZ), Heidelberg, Germany, in the group of Prof. Dr. Claudia Scholl, before re-joining my alma mater, in Prof. Strebhardt’s group. Recently, my work has been awarded a 3-year research grant by the prestigious Deutsche Forschungsgemeinschaft (DFG).

  • Sir Ganga Ram Hospital, New Delhi, India
  • Title:Case series of Non -Ampullary Duodenal Adenomas
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Abstract
Duodenal adenomas are benign tumours of the duodenum which carry a malignant potential. They present either sporadically or with familial syndromes. Majority of the cases are treated endoscopically but in select cases, surgical resection is a better alternative to endotherapy. Endotherapy is associated with higher chances of local recurrence and require frequent check endoscopies in the follow up period, while surgery offers a one-time treatment option. Identification and a local duodenal resection sparing ampulla becomes difficult in large lesions of the 2nd part of duodenum. Passage of a catheter from the cystic duct, through common bile duct to the duodenum aids in identification of the ampullary area and is helpful in performing a local/wedge resection of the duodenum containing adenoma without injuring ampullary orifice.

Biography
Dr Amitabh Yadav is a senior consultant in the Department of Surgical Gastroenterology and Liver Transplantation at Sir Ganga Ram Hospital, New Delhi, India. He also serves as the academic supervisor and teaching coordinator in his department. In addition to that, he is an examiner at the National Board of Examinations in India and has various publications in the national and international peer reviewed journals to his credit. His interest lies particularly in pancreatic, cyto-reductive, and advanced laparoscopic surgeries.

  • University Hospital of Getafe, Madrid, Spain
  • Title:What if it´s not a Pulmonary Thromboembolism?
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Abstract
Pulmonary artery intimal sarcoma is an extremely rare type of malignant tumor, which mimics pulmonary thromboembolism. A misdiagnosis of pulmonary thromboembolism is usually made because both pathologies have a similar clinical presentation, and a repletion defect in the pulmonary arteries is identified in the chest computed tomography.
Despite its low incidence, it is essential to suspect this entity, since therapeutic management is different from pulmonary thromboembolism and early diagnosis can increase the life expectancy of these patients.
We present the case of a 58-year-old woman, with no personal history of interest who consults for left pleuritic pain, dyspnea and dry cough of one month of evolution. A CT pulmonary angiogram is performed, which is interpreted as a pulmonary thromboembolism, so anticoagulant treatment is scheduled. Two months later, she comes again for worsening dyspnea and pleuritic pain. The chest X- ray shows a newly appeared left pleural effusion. After this, a diagnostic thoracocentesis is performed with a result compatible with exudate of lymphocytic predominance without complication data. A new chest CT without intravenous contrast is requested in which the occupation of the light of the left main pulmonary artery persists. On this occasion, it can be seen that the material is calcium density, which may correspond to an endovascular involvement by an intimal sarcoma.Given these findings, the study is extended with a positron emission tomography (PET-CT), which reinforces the suspicion and also shows an increase in metabolism in the pleura in relation to pleural implants.
An ultrasound-guided thick needle biopsy (BAG) of the left pleural calcified lesion was performed with anatomopathological result of osteoforming fusocellular sarcoma with endothelial phenotype (osteogenic variant) and immunohistochemical study. After confirming the diagnosis of suspicion and in the presence of disseminated lymph node and pleuropulmonary disease, the patient is referred to the Oncology service to assess the option of participating in a clinical trial given the impossibility of surgical option.
The case that is exposed is a rare entity, which only in half of the cases progresses locally and that exceptionally metastasizes, being the extension to pleura and lymph nodes of our patient, unusual.
Biography
Dra. Beatriz Raboso Moreno. Pulmonology Resident doctor. Department of Respiratory Medicine. University Hospital of Getafe, Madrid, Spain. In addition, I am a Member of the Residents of the National Commission on Pulmonology.
In the field of research, I am actively working in various areas, including Oncology. With regard to the publications to be highlighted: “What if it´s not a Pulmonary Thromboembolism”, in Open Respiratory Archives and “High-flow nasal cannula for acute respiratory distress syndrome due to Covid-19 in Multidisciplinary Respiratory Medicine.
In relation to scientific societies, I actively participate in regional societies (Neumomadrid) and national societies such as SEPAR.
In addition, I have won an award for my scientific activity, “The case” in 2020 and special mention for my work and dedication in the COVID pandemic by Neumomadrid.
Finally, I have many concerns and desire to continue training

  • University of Uyo Teaching Hospital
  • Title:Giant Hydronephrosis Associated with Angiomyo-Lipoma in an Adult Male : A Case Report
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Abstract
Giant Hydronephrosis (GH) in the adult can reach elephantoid proportions, containing several liters of fluid. It can be associated with rare renal neoplasms. We present a 27 year old man with progressive painless abdominal distention whose imaging investigations (ultrasound and CT scan) disclosed a left GH. This was successfully removed en-bloc by simple nephrectomy via a midline laparotomy. Obstruction was at the UPJ, the mass contained 13.5L of fluid and histopathologic examination revealed Angiomyolipoma of the kidney and pelvis. This is a rare discovery in a rare pathology.

Biography
Dr Albert E Ukpong, MBBS, FWACS, FICS, PgD (MGT); Senior Lecturer / Honorary Chief Consultant Urologist, Department of Surgery, University of Uyo Teaching Hospital, Uyo is a clinician, surgeon, teacher, researcher and author with interest in Uro-Oncology and reconstruction Urology. He joined the service of his institution in 2006 and has been involved in training of medical students and residents in the past 15years. “He lectures as a preacher,” as fondly described by his colleagues. He currently coordinates research activities in the urology division of his department. He’s a fellow of the West African and International Colleges of Surgeons. Obtained his MBBS degree from University of Jos Medical School in 1988. He’s presently involved with studies related to etiology, management and prevention of Prostate cancer-the commonest male cancer in his environment.

  • University of Crete, Heraklion, Crete, Greece
  • Title:The SMYD5 Protein Promotes the Development of Heptocellular Carcinoma in mice
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Abstract
Background: SMYD5 is a Su(Var)3-9, Enhancer-of-zeste and Trithorax (SET) and Myeloid, Nervy, and DEAF-1 (MYND) domain-containing histone methyltransferase, which was originally described as a component of the nuclear receptor corepressor (NCoR) complex catalyzing histone 4 lysine 20 trimethylation (H4K20me3).
Rationale: Based on its domain composition and on previously published data indicating its role as a methyltransferase, we sought to identify putative methylation substrates of SMYD5 in vitro. In addition, given that other members of the SMYD family, such as SMYD2 and SMYD3, have shown to play important roles in cancer promotion, including liver and colon cancer, we investigated the potential implication of SMYD5 in carcinogenesis using murine models and human samples.
Approach: We performed an in vitro methylation assay using the recombinant human SMYD5 protein with histone and non-histone substrates. In addition, we generated Smyd5-deficient mice, in which the Smyd5 gene was inactivated either in all tissues (Smyd5flox/MX-Cre) or specifically in the liver (Smyd5flox/Alfp-Cre and Smyd5flox/Alb-Cre). Moreover, we produced intestine-specific Smyd5-deficient mice (Smyd5flox/Villin-Cre). Analysis of SMYD5 expression in human hepatocellular carcinoma (HCC) and colon cancer was conducted using The Human Cancer Genome Atlas (TCGA) datasets.
Results: We show that purified, baculovirus-expressed SMYD5 preferentially methylates histones 2A and 2B (H2A and H2B) in vitro.
All four SMYD5 mouse knockout (KO) strains generated developed normally and did not display any visible phenotype. However, when subjected to a protocol of chemically induced carcinogenesis by diethylnitrosamine (DEN) injection, whole-tissue and liver Smyd5-deficient mice exhibited delayed liver tumor growth compared to wild-type (WT) mice exposed to the same treatment. The mice were subjected to macroscopic and histological analysis, including stainings to evaluate hepatic DNA damage and proliferation, as well as expression profiling by RNA-sequencing (RNA-seq) and by quantitative polymerase chain reaction (qPCR). A number of cancer- and proliferation-related genes showed reduced expression in the liver of Smyd5-deficient mice compared to WT mice.

Biography
Teresa Rubio-Tomás completed a BSc in Biology and then a MSc in Biomedical Research, both of them in Pompeu Fabra University (UPF) in Barcelona, Spain. She moved to Greece to do a PhD in the study of the epigenetic regulation of liver cancer. She’s PhD was part of a Marie Skłodowska-Curie Initial Training Network, she had the opportunity to travel to Sweden, Switzerland and Hungary to meet our collaborators and share our work with them. After that she have been working in IDIBAPS research centre in Barcelona, leading my own projects related to liver diseases, cell plasticity, aging and cellular senescence.

  • Free University of Brussels, Belgium
  • Title:Urachal Mucinous Cystadenoma in Infant : First Case Report and Review of Literature
  • Time :

Abstract
Background: As only ten cases have been described in current literature, urachal mucinous cystadenoma seems to be a rare disease. All reported cases concerned adults, except for a fifteen-year-old girl. We report the first case of urachal mucinous cystadenoma affecting an infant.
Case description: We report the case of a seven-month-old male infant presenting persistent umbilical purulent liquid discharge. No others pathological symptoms nor signs were detected. Abdominal ultrasound showed a nodular structure with liquid content, evoking urachal cyst. Surgical radical excision was then performed. Histopathologic examination proved diagnosis of urachal mucinous cystadenoma. There were no post-operative complications. In a one year postoperative follow-up, no local recurrence and excellent scar healing were observed.
Conclusions: Urachal mucinous cystadenoma in infants seems to be very rare. In case of suspicion of mucinous cystadenoma, prophylactic radical surgical excision is recommended, since its potential malignant transformation. Prognosis depends on radicalness of surgical excision. No long-term follow-up of this pathology is available in current literature. We suggest annual ultrasound follow up in childhood.

  • University of São Paulo, Brazil
  • Title:Action of Differente Photobiomodulation Parameters on Cell Proliferation and Cell Death in Multipotent Adipose Tissue Cells in Vitro.
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Abstract:
Aim: To investigate the effect of different parameters of photobiomodulation (PBMT) with low power LASER in multipotent mesenchymal stem cells (MSCs), derived from adipose tissue, on cell proliferation and death. Methods: mesenchymal stem cells derived from adipose tissue, at a concentration of 2×104 maintained in αMEM medium (minimum essential medium) with 15% FBS (Fetal Bovine Serum), were seeded in 24-well plates and subjected to FBM applications with the parameters physical: 660 nm and 830 nm wavelength; the energy of 0.5 J, 2 J and 4 J, powers of 40 mW and 100 mW. The analysis of the plates with MSCs was carried out with the MetaXpress® software at 24, 48, and 72 hours, and the statistical analyzes were carried out with the GraphPad Prism® 7.0 software. Results: The results obtained in the experiments showed that irradiation promoted a significant increase in cell proliferation, especially using the variables 830 nm, 100 mW, 2.0 and 4.0 J, and 830 nm, 40 mW, and 0.5 and 4.0 J compared with the other parameters used. PBMT with 660 nm and power of 40 mW was the one that produced more significant cell death compared to the other irradiation parameters. Conclusion: The results found show that both wavelengths were effective in cell proliferation. The 660 nm wavelength produced more cell death.

Biography
Ana Paula Ferro graduated in Physiotherapy from the Faculty of Medicine of Ribeirão Preto, University of São Paulo. Participated in a research project with women who underwent mastectomy with a FAPESP grant at the Center for Teaching, Research and Assistance in Rehabilitation of Mastectomized Women at EERP-USP; She is currently a direct doctoral student in the Postgraduate Program in Rehabilitation and Functional Performance at the Faculty of Medicine of Ribeirão Preto, University of São Paulo. Member of the Dermatofunctional Assessment and Intervention Laboratory.
Specialization in Specialization in Dermatofunctional Physiotherapy. by the Faculty of Health Technology, Brazil (2021)

  • Medical University of Lodz, Poland
  • Title: Inflammatory Stimuli in HER-2 Dependent Evolution of Ductal Carcinoma in Situ (DCIS).
  • Time :

Abstract:
Ductal carcinoma in situ (DCIS), the nonobligate precursor of invasive ductal
breast carcinoma (IDC), is characterized by proliferation of neoplastic cells within the duct lumen. Molecular profiles of synchronous DCIS and IDC breast cancers (BC) are remarkably similar suggesting that the invasive potential of the lesion is not dependent solely on specific genomic alterations in preinvasive cells, but stimuli derived from the tumour microenvironment (TME) may be playing a substantial role. In particular, immune cells present in TME as either subtle infiltration or gross inflammation may be involved in disease progression. As DCIS → IDC evolution is associated with loss of HER2 expression (approximately 50% of DCIS HER2(+) vs 20% of IDC HER2(+)), it can be postulated that the HER2 status determines cell sensitivity and response to inflammatory stimuli. Proliferative dominance of the HER2-negative tumour subclones would comply with the evolutionary bottleneck model of DCIS evolution as well as point to a hitherto unknown aspect of HER2 role in BC biology. Results of combined mechanistic and clinical analyses verifying the above hypothesis i.e.: i) a functional role of HER2 in proliferative response of mammary epithelial cells to inflammatory stimuli (Il1- beta, TNF-alfa) explored in a culture system representative of human DCIS, based on two human mammary non-invasive epithelial cell lines (MCF10A and HB2) and their HER2-overespressing variants and b) evaluation of the clinical value of the extent and type of the inflammatory infiltration by tumour-infiltrating lymphocytes / tumour-associated macrophages (TILs/TAMs) in surgical specimens from DCIS patients, using a panel of specific markers selected on the basis of available clinical follow-up database, will be presented and discussed.
Biography:
Dr. Hanna Maria Romanska, Associate Professor in the Department of Pathology of the Medical University of Lodz, Poland, graduated from the Medical University of Katowice, Poland in 1985. Having received her PhD degree in Pathology from the Imperial College London in 1997, she joint The Tissue Engineering and Regenerative Medicine Centre (TERM) l Professor Dame Julia Polak, Faculty of Medicine and Professor Larry Hench, Department of Materials, Imperial College London. In 2002 she was appointed non-clinical Lecturer at the University of Birmingham, UK, where she began her investigation into Biology of Cancer, with special emphasis on hormone-dependent human malignancies. A collaboration with Dr. Fedor Berditchevsky (University of Birmingham, UK) in Tetraspanins in breast cancer resulted in several publications in renowned scientific journals. In 2011 she returned to Poland, where in the Medical University of Lodz, she continues her research into mechanisms of breast cancer progression, particularly those activated by stimuli derived from tumour microenvironment. She received various awards, with the most prestigious being Award for Teaching Excellence in Medical Education, Imperial College London 2002; the Rector Awards for academic achievements, Medical University of Lodz, 2013, 2014, 2016, 2019 and 2020.

  • King Abdulaziz Medical City, Saudi Arabia
  • Title:Defining radiologic complete response using a correlation of presurgical ultrasound and mammographic localization findings with pathological complete response following neoadjuvant chemotherapy in breast cancer
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Abstract:
The study is stimulated by the increasing number of pathological complete response (PCR) to neoadjuvant chemotherapy, which promotes breast conservation treatment. Also, surgical reports indicated that the time has come for nonsurgical management in selected cases of breast cancer. Radiological contribution for these improving cancer care is therefore evolving to identify radiological complete response (RCR), from using simple, reproducible and widely available ways of imaging. Ninety-three cases for presurgical localization for excision have been used for the retrospective study. The findings suggested that a combined application of ultrasound and mammography identified that no mass with postbiopsy clip on normal tissue (clip sign) identified RCR with 93% accuracy as against mammography alone or ultrasound alone.
The clip sign is therefore used to define RCR and a new BI-RADS category (e.g. 6nil or 6 -ve) is suggested to herald surgical excision or vacuum biopsy in selected cases. Examples will be presented.
Biography:
Prof. Dorothy Ibifuro Makanjuola

• Trained in University of Edinburgh with DMRD Edinburgh and FRCR London
• Currently section head in Women’s Imaging of King Abdulaziz Medical City, Riyadh, Saudi Arabia
• Main interest is mammography and body imaging
• Over 60 scientific publications
• Peer reviewer for journals/articles
• Several invitations as guest speaker
• Several biographic awards including “2000 Outstanding Scientists of the 20th Century” from Cambridge, England

  • University of Blida 1, Algeria.
  • Title:Epidemiology Of Breast Cancer In Women Based On Diagnosis Data From Oncologists And Senologists In Algeria
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Abstract:
Breast cancer (BC) is a major health issue threatening women’s life. No reliable epidemiological data on BC diagnosed by oncologists/senologists are available in Algeria.
The BreCaReAl study, a non-interventional prospective cohort study, included adult women with confirmed BC in Algeria. Disease incidence, patients and disease characteristics, treatment patterns, and mortality rate were recorded up to 12 months of follow-up.
Overall, 1,437 patients were analysed: median age was 48 [41;57] years and 337 (23.5%) women had a family history of BC. BC incidence was 22.3 (95% CI: 21.5; 23.2) cases per 100,000 inhabitants over 8 months. Delayed diagnosis was reported in 400 (29.2%) patients. First line of treatments were mainly chemotherapy and surgery. Twenty-eight serious adverse events were reported including 10 (37.0%) events which led to death. Mortality rate reached 3.2% at 12 months.
A delayed diagnosis highlights the importance of implementing more effective screening strategies

Biography:
Pr Abdelkader El Hakim Boudjella is a practising full-time medical Oncologist at the Cancer Center in Blida Algeria since 2005. This is a 170 bedded tertiary care centre and educational institution including medical oncology, cancer surgery and radiotherapy. It is the prime centre in the Wilaya of Blida for the management of all malignant tumours.
He has completed his residency at Faculty of Medicine at University of Algiers in the capital in 2003. He graduated as Professor in 2019; held the position of head of the female hospitalization unit, head of the day hospital and interim head of the Blida cancer center. Currently; he also holds the position of vice president of the Blida oncology society (SOB)
Incidentally, he has benefited throughout his career from several training courses given in renowned centers such as practical courses in oncology at the Saint Louis hospital in Paris France and breast cancer training with Prof. Martine Piccart at the Jules Bordet Institute Brussels.
He was solicited several times to participate in advisory boards, in his quality of experts to share and benefit from his expertise in pathology, he also participated as an investigator in several national clinical projects in Algeria such as: EPIONCO, observational study on quality of life and BreCaReal (Breast Cancer Register in Algeria) of which he is the coordinating investigator and the co-author correspondent on the publication of the interim results.
Apart from work, he is passionate about football and jogging; a spiritual person, participating in the support of associations to help cancer patients care.

  • Morehouse School of Medicine ,USA
  • Title:Fertility Sparing Treatment in Cervical Cancer: Abdominal Trachelectomy.
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Abstract:
In the last two decades, great strides have been made to treat cancer while sparing fertility for young women. This is at least partly in response to changing demographics including delayed childbearing and fewer historically traditional couples. The trachelectomy has become emblematic in this endeavor. With comparable outcomes to hysterectomy and successful conceptions, trachelectomy utilization has increased over time. It is now a standard of care for many situations. While there are several approaches, (vaginal, laparoscopic, robotic) the abdominal trachelectomy allows surgeons to overcome several limitations such as patient anatomy, surgical experience and resources (i.e. no robot) to provide women everywhere with this revolutionary operation. This overview will outline surgical techniques, outcomes and other considerations of the abdominal trachelectomy.
Biography:
Dr. Cyra Cottrell is a second year Obstetrics and Gynecology resident at Morehouse School of Medicine located in Atlanta, GA, USA. Her interests include fertility preservation and health care disparity, specifically regarding access to reproductive assistance. She aims to complete a Reproductive Endocrinology and Infertility fellowship after finishing residency.

  • University of Granada, Spain
  • Title:Estrone and HSD17B enzymes involved in its synthesis drive Epithelial to Mesenchymal transition and Metastasis in Estrogen Receptor Positive Breast Cancer .
  • Time :

Abstract:
Breast cancer is one of the most frequently diagnosed neoplastic diseases among women worldwide and the leading cause of cancer death in women in the developed world. Recent studies highlight the close relationship between circulating estrogen levels, obesity, and menopausal status in the outcome of estrogen receptor-positive (ER +) breast cancer patients. One of the known molecular mechanisms by which obesity drives cancer development is through the activation of the NF-κB pathway in obese adipose tissue, which establishes a chronic inflammatory environment. Estradiol (E2), the main serum estrogen before menopause, linked to ER is known to inhibit the NF-κB pathway; but the role of Estrone (E1), the main estrogen after menopause and whose levels increase with obesity, in the regulation of NF-κB and in tumorigenesis is unknown. In our experiments, we studied the role of overexpression of HSD17B14, an enzyme that synthesizes E1 from E2, in the progression of ER + breast cancer in MCF7 cells and tested the roles of E1 and E2, in the context of inflammation, in the regulation of the NF-κB pathway and tumorigenesis in HeLa cells. Our results demonstrate that the overexpression of HSD17B14 in the ER+ breast cancer cell line MCF7 induces a higher expression of pro-inflammatory cytokines, EMT markers, increased ALDH activity, and increased mammalian formation capacity. Furthermore, we found that E1, unlike E2, contributes to increasing NF-κB-mediated inflammation. We verified how E1 induces EMT and increases the expression of ES-TF in ER + HeLa cells, suggesting a different role for E1 and E2 in the regulation of the NF-κB signaling pathway and tumorigenesis. In addition, an analysis of public databases showed that changes in the expression of different isoforms of the HSD17B enzyme family are associated with the risk of distant metastasis, demonstrating that increased intracellular E1 levels correlates with higher risk of metastasis. For decades, it has been assumed that E2 and E1 had identical biological functions, only differentiating in their ability to bind ER, greater for E2. For that, almost all previous works have focused in studying E2. However, this work demonstrates for the first time a key role of E1, nor E2, and the HSD17B enzymes involved in E1-synthesis in EMT and metastasis in ER+ breast cancer and potentially other ER dependent cancer types.

Biography:
Manuel Picón Ruiz conducted his PhD at the University of Granada (UGR) in Spain, successfully defending his thesis work in November 2012. After that, Dr. Picón moved to the Sylvester Comprehensive Cancer Center of the UM (USA), first as Postdoctoral Associate Researcher and then as Assistant Scientist. During his postdoctoral stage, Dr. Picón obtained the prestigious Susan G. Komen award, a grant intended to form outstanding postdoctoral researchers to become the next generation leaders in the field of breast cancer, in the role of Principal Investigator (PI) for his project entitled “ESTROGENS, INFLAMMATION AND THE AGGRESSIVE BEHAVIOR OF BREAST CANCER IN OBESITY”.
As PI, Dr. Picón participated in the publication of a Review article as first author in the top ranked journal in oncology (IF=244.585), which served as cover page and was classified as “Continuing Medical Education” and “Continuing Nursing Education” by the American Cancer Society. Furthermore, he co-directed a group of 15 researchers for the elaboration of a research article recently published in the prestigious journal Cell Metabolism.
Until date, Dr. Picón has conducted his research career in a total of 5 international research centers from three different countries (Spain, UK and USA), has obtained 7 competitive fellowships and has participated in 12 national and international research projects (2 as PI). He has authored 15 papers in scientific journals, 12 of them included in first quartile journals; and 6 as first, last or corresponding author. He has an H-index of 11 and an i-10 index of 13, with a total of over 800 citations. Furthermore, has published 3 book chapters in prestigious publishers; has participated in a considerable number of congress/symposium with more than 30 communications and 3 first prizes; and has also participated in the development of an international patent. Furthermore, he has served as reviewer for five different Q1 journals.
In September 2019, Dr. Picón moved back to the UGR as Marie Curie fellow. Actually, he is leading a research group to continue his investigations to clarify the role of different estrogens and obesity in Estrogen Receptor positive breast cancer. In addition, he is Professor at the Department of Human Anatomy and Embryology at the UGR, and supervises several Master degree and PhD students.

  • Hospital Ruber Juan Bravo, Spain
  • Title:Pancreatic metastasis from infiltrating lobular breast carcinoma: Difficulties in diagnosis and review of medical literature .
  • Time :

Abstract:
Context: Neoplasms that secondarily affect the pancreas are extremely rare, occur in less than 3% of cases and make differential diagnosis with a primary adenocarcinoma of the pancreas difficult, due to clinical and nonspecific radiological and cytological characteristics. Surgical treatment has been considered the first-choice option in selected patients with single metastases. However, the required surgical procedures are characterized by significant mortality and significant morbidity and each case must be assessed by a multidisciplinary committee.
Case report: We report the case of a 47-year-old woman who presented a lesion in the pancreatic head, 4 years after radical mastectomy modified by an infiltrating lobular carcinoma of the right breast. Suspecting a primary tumour, a cephalic duodenopancreatectomy was performed. Immunohistochemical analysis of the surgical specimen suggested the metastatic nature of the described lesion.
Conclusion: We think that when a pancreatic lesion develops in a patient with previous neoplasia, the hypothesis of a solitary metastasis in the pancreas should always be considered. The medical history should be carefully analysed, and all assumptions should be included in the diagnostic process.

Biography:
1. Tsitouridis I, Diamantopoulou A, Michaelides M, Arvanity M, Papaioannou S.Pancreatic metastases: CT and MRI findings. Diagn Interv Radiol 2010;16:45–51.
2. Rumancik WM, Megibow AJ, Bosniak MA. Metastatic disease to the pancreas:Evaluation by computed tomography. J Comput Assist Tomogr 1984;8:829–34.
3. Lee Y-TM. Breast carcinoma: Pattern of metastasis at autopsy. J Surg Oncol1983;23:175–80.
4. Crippa S, Bonardi C, Bovo G, Mussi C, Angelini C, Franco U. Pancreaticoduode-nectomy for pancreatic metastases from breast carcinoma. JO. Pancreas (online)2004;5:377–83.
5. Apodaca-Rueda M, Henrique Mendonc ̧ a Chaim F, da Silva Garcia M, Paes deAlmeida de Saito H, Antonio Gestic M, Pimentel Utrini M, et al. Solitary pancreatic metastasis from breast cancer: Case report review of literature. Sao Paulo Med J2019:137.
6. Z’graggen K, Fernandez-del Castillo C, Rattner DW, Sigala H, Warshaw AL. Metastases to the pancreas and their surgical extirpation. Arch Surg 1998;133:413–7.
7. Hiotis S, Klimstra DS, Conlon KC, Brennan MF. Results after pancreatic resection for metastatic lesions. Ann Surg Oncol 2002;9:675–9.
8. Asch MJ, Wiedel PD, Habif DV. Gastrointestinal metastases from carcinoma ofthe breast. Arch Surg 1968;96:840–3.
9. Cifuentes N, Pickren JW. Metastases from carcinoma of mammary gland: An autopsy study. J Surg Oncol 1979;11:193–205.
10. Page DL, Anderson TJ. Diagnostic histopathology of the breast. Edimburgo: Chur-chill Livingstone. 1987.
11. Merino MJ, Livolsi VS. Signet ring carcinoma of the female breast: A clinicopathologic analysis of 24 cases. Cancer 1981;48:1830–7.
12. Pappo I, Feigin E, Uziely B, Amir G. Biliary and pancreatic metastases of breastcarcinoma: Is surgical palliation indicated? J Surg Oncol 1991;46:211–4.
13. Le Borgne J, Partensky C, Glemain P, Dupas B, de Kerville B. Pancreaticoduodenec-tomy for metastatic ampullary and pancreatic tumours. Hepatogastroenterology2000;47:540–4.
14. Hiotis S, Klimstra DS, Conlon KC, Brennan MF. Results after pancreatic resection for metastatic lesions. Ann Surg Oncol 2002;9:675–9.
15. Muranaka T, Teshima K, Honda H, Nanjo T, Hanada K, Oshiumi Y. Computed tomography and histologic appearance of pancreatic metastases from distant sources. Acta Radiol 1989;30:615–9.
16. Klein KA, Stephens DH, Wech TJ. CT characteristics of metastatic disease of the pancreas. Radiographics 1998;18:369–78.
17. Kitamura N, Murata S, Abe H, Hanasawa K, Tsukashita S, Tani T. Obstructive jaundice in a metastatic tumour of the pancreas from breast cancer: a case report.Jpn J Clin Oncol 2003;33:93–7.
18. Kidney DD, Cohen AJ, Butler J. Abdominal metastases of infiltrating lobular breastcarcinoma: CT and fluoroscopic imaging findings. Abd Imaging 1997;22:156–9.
19. Ferrozzi F, Bova D, Campodonico F, Chiara FD, Passari A, Bassi P. Pancreaticmetastases: CT assessment. Eur Radiol 1997;7:241–5.
20. Duffy MJ. Serum tumour markers in breast cancer: Are they of clinical value? Clin Chem 2006;52:345–51.
21. Roland CF, van Heerden JA. Non pancreatic primary tumours with metastasis to the pancreas. Surg Gynecol Obstet 1989;168:245–347.
22. Buzdar AU. Endocrine therapy in the treatment of metastatic breast cancer.Semin Oncol 2001;28:291–304.
23. Sperti C, Pasquali C, Liessi G, Pinciroli L, Decet G, Pedrazzoli S. Pancreatic resection for metastatic tumours to the pancreas. J Surg Oncol 2003;83:161–6.

  • Sawanpracharak Hospital, Thailand
  • Title:Operative outcome of laparoscopic colorectal cancer surgery in a regional hospital in a developing country: a propensity score-matched comparative analysis .
  • Time :

Abstract
Objective: Laparoscopic surgery is an alternative procedure for colorectal cancers. However, high-level supporting evidence has been derived from high-volume centers in developed countries. During the early phase of applying the laparoscopic approach, we evaluated the procedure’s short-term outcomes in our regional middle- volume hospital in a developing country.
Methods: We retrospectively analyzed data for a cohort of 223 colorectal cancer patients who underwent elective surgery from October 2017 to September 2019. We compared 165 patients undergoing open surgery (OS group) with 58 undergoing laparoscopic surgery (LS group) using a propensity score-matched analysis.
Results: After matching, each group contained 58 patients for evaluating outcomes. The LS group had more harvested mesenteric lymph nodes (5.0 nodes, 95% confidence interval (CI): 1.8–8.1; p-value: <0.01) with comparable blood loss (p- value: 0.54) and margin status (p-value: 0.66). However, LS was more time- consuming (68.8 minutes longer; 95% CI: 53.0–84.7; p-value: <0.01). Morbidity and mortality rates were equivalent (odds ratio (OR): 1.3, 95% CI: 0.25–2.73, p-value: 0.74, and OR: 2, 95% CI: 0.18–22.1, p-value: 0.57, respectively). The LS group experienced fewer days to begin normal eating (−0.5 days, 95% CI: −0.9 to −0.1, p- value: 0.04) and shorter hospital stay (−1.5 days, 95% CI: −2.7 to −0.4, p-value:<0.01). The conversion rate was 3.5%. Conclusion: The laparoscopic approach was applicable even in a regional middle- volume hospital in a developing country. However, longer surgical time was a drawback. Biography
Dr. Tunruttanakul is a general surgeon, graduated his surgical training on 2010. Since finished training, he’s been working in a regional hospital of Thailand. He is interested in the field of laparoscopic surgery, therapeutic endoscopy and oncology. In 2015, He was awarded Dunlop-Bonpong scholarship and went to learn in his interested fields in Nepean Hospital Penrith NSW, Australia. He’s been trying to improve quality of the surgical service in his regional hospital by developing and introducing the minimally invasive surgery until this day.

  • Azerbaijan Medical University, Azerbaijan
  • Title:Quality of Life in patients with Oral Cancer .
  • Time :

Abstract:
Treatment and surgery for head and neck cancers often causes anatomical changes that can lead to severe dysfunction in oral cavity such as difficulties in speech, chewing, and swallowing. In addition, such treatments might interfere with patients’ appearance, pain, and suffering that all could influence quality of life in these patients. These undesirable conditions are mostly occurring due to postoperative radiotherapy, which is often needed. Until recently, neither restoration nor reconstruction, or the usual prosthetic techniques were able to resolve these problems successfully. Therefore, choosing an appropriate reconstruction technique seems to be an important parameter when treating these patients. However, regardless of different treatment regimens and reconstruction procedures, improving health-related quality of life remains essential for these patients. A study of patients with head and neck cancer showed that even greater than treatment modality, baseline quality of life and comorbidity influenced post treatment quality of life. Also, a long-term multicenter study of quality of life and psychosocial outcomes after oropharyngeal cancer surgery and radial forearm free-flap reconstruction reported that psychosocial distress was the main determinant of long-term quality of life and suggested that the multidisciplinary management of these patients is of prime importance.

Biography:
1996-2001 – Azerbaijan Medical University, Baku, Azerbaijan Republic D.D.S
2001-2002 – Azerbaijan Medical University, Baku, Azerbaijan Republic, oral&maxillofacial surgery/internship
2004-2008 – Azerbaijan Medical University, Baku, Azerbaijan Republic, PhD degree in oral&maxillofacial surgery
2010-2011 -Tehran University of Medical Scienses, Cancer Institute. Tehran, I.R. of Iran clinical fellowship in head&neck surgery
2016-2020 – research fellow of Cancer Institute. Tehran, I.R. of Iran.
Oral& maxillofacial, head and neck surgeon DDS,MD, PhD assistant professor. The department of Oral&maxillofacial surgery, Azerbaijan Medical University Department .

  • Michigan State University, USA
  • Title:Gap junctional intercellular communication, a biomarker to determine chemopreventive activity of natural products.
  • Time :

Abstract:
Natural products are chemical compounds produced by living organisms with potential pharmacological properties that can benefit human health, particularly cancer and cardiovascular diseases. Selection of an appropriate biological endpoint for in vitro screening is critical in maximizing the identification of a compound(s) that can contribute to cancer prevention. Gap junctional intercellular communication (GJIC) is one such biomarker that has been used in screening for tumorigenic and antitumorigenic properties of compounds. GJIC plays a central role in maintaining tissue homeostasis through the coordination of intercellular signaling with that of intracellular signal transduction pathways controlling gene expression. The homeostasis of a tissue requires gap junction channels to be in the open state, and chronic closures of channels result in pathological states. GJIC has been implicated in cancer in which all early stage cancer cells have no or reduced GJIC, oncogenes and toxicants that contribute to the cancer process dysregulates GJIC. Restoration of GJIC in cancer cells by the transfection of gap junction genes results in cells reverting back to normal epithelial morphologies, reduced anchorage independent growth in soft agar, and lack of tumor formation in nude mice injected with these re-communicating cancer cells. The screening strategy we use involve experiments that (1) treat cancer cells with a natural product and determine if it increase GJIC, (2) treat cell lines transfected with specific oncogenes with a natural product, and determine if it increase GJIC, (3) pretreat normal cells with a natural product and determine if it reverses the GJIC-inhibitory effects of known tumor promoters. Using this screening method, we have identified natural products that can restore GJIC or prevent the dysregulation of GJIC by cancer causing compounds or oncogenes.

Biography:
Brad L. Upham, Ph.D., is an Associate Professor in the Department of Pediatrics & Human Development, and the Center of Integrative Toxicology at Michigan State University MSU). Dr. Upham conducts innovative research in cell biology determining the underlying signaling mechanisms involved in epigenetic responses of mammalian cells to environmental contaminants, oxidative stress and oncogenes, and determines how chemopreventive agents from natural products interact with these signaling pathways in preventing or reversing the tumor promoting effects of environmental toxicants and oncogenes. He has established an international reputation in the field of toxicology relevant to gap junctional intercellular communication and signal transduction. His research has been published in numerous highly cited publications with relevance to human health and risk assessment, and has received federal grants from the U.S. National Institute of Health (NIH) to support his research program at MSU, and has mentored a number of post-doctoral fellows and undergraduate students, and trained numerous international scholars. Professional activities included serving as president and councilor of the Michigan Society of Toxicology (MISOT), has served in numerous elected officer position for the Society of In Vitro Biology (SIVB), received several distinguished service awards for outstanding contributions to the SIVB and is currently the chair of the SIVB Education committee. He has served on numerous study sections for NIH, and serves on the editorial boards of the “Journal of Toxicology”, “BioMed Research International”, and “Biomedicines”.