Day2

  • National Center for Radiation Research in Oncology, Germany
  • Title:DDR1 in Glioblastoma: Resistance Mechanisms and Therapeutic Targeting
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Abstract:
Enhancing therapy sensitivity is a big challenge in oncology. Based on genetic and epigenetic modifications altering intra- and extracellular processes, glioblastoma (GBM) belongs to the group of tumor entities with unmet need, is highly refractory to therapy and associated with poor clinical outcome. Novel effective treatment approaches are urgently required. Here, we found the collagen type-I receptors discoidin domain receptor 1 (DDR1) and beta1 integrin overexpressed in GBM. We identified a critical function of the promitotic and adhesion-mediating DDR1 in altering GBM treatment resistance. In a large number of GBM cultures and clinical samples, we show a DDR1 and GBM stem cell marker co-expression that correlates with patient outcome. We exhibit DDR1 inhibition in combination with radiochemotherapy using temozolomide in GBM models to enhance sensitivity and prolong survival to a degree superior to conventional therapy. We further identify a 14-3-3-Beclin-1-Akt1 protein complex assembling with DDR1. This protein complex is required for prosurvival Akt and mTOR signaling and the regulation of autophagy-associated therapy sensitivity. Our results uncover a mechanism driven by DDR1 that controls GBM therapy resistance via autophagy and suggest DDR1 as a rationale target for the development of therapy-sensitizing agents.

Biography:
Dr. Nils Cordes graduated from Medical School of the University Erlangen-Nürnberg, Germany, in 1998. Subsequently, he worked as resident in radiation oncology at the Universities Erlangen-Nürnberg and Tübingen before he took on a position as radiobiologist at the Institute of Radiobiology of the German Army. His studies on cell-matrix interactions pioneered the field by untangling the role of the cancer cell adhesion resistome. In 2010, he became Full Professor of Radiobiology at the Technische Universität Dresden, and Head of Radiobiology of OncoRay and the Department of Radiobiology, Institute of Radiooncology, Helmholtz Center Dresden-Rossendorf. Based on Dr. Cordes´ research, our understanding of how cancer cells resist therapy by adhesion to extracellular matrix or neighboring cells has essentially increased. By using more physiological, matrix-based 3D cell cultures, it become obvious that the physiological environment mediates a tremendous impact on signal transduction, gene expression, chromatin organization and adaptation mechanisms induced by therapy.

  • Genentech Inc ,USA
  • Title:MHC class I presented antigens from malignancies: A perspective on analytical characterization & immunogenicity
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Abstract:
The field of cancer immunotherapy has expanded rapidly in the past few years, with many new approaches entering the clinic for T cell mediated killing of tumors. Several of these clinical approaches involve the exploitation of a CD8 + T cell response against MHC I presented tumor antigens. Here, we describe the types of tumor antigens which are considered as targets in the design of T cell based therapeutic approaches, the rationale for targeting MHC I antigens and the analytical tools commonly employed for the discovery of MHC I presented peptides. The advantages and disadvantages of each approach are discussed and a perspective on the future directions of the MHC I peptide exploration field and biotherapeutic strategies is given.

  • ABL Bio, Inc. R&D center ,Korea
  • Title:Development of an Anti-Cancer Bispecific Antibody Targeting VEGF and DLL4 (ABL001) for Phase 1 Clinical Study
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Abstract:
Emerging reports suggest Delta-like-ligand 4 (DLL4) is a promising target to augment the effects of VEGF inhibitors. Simultaneous blockade of VEGF/VEGFR and DLL4/Notch signaling pathways leads to more potent inhibition of tumor progression by a synergic anti-angiogenic activity in various mouse xenograft models. We have developed a bispecific antibody targeting VEGF and DLL4 (ABL001, TR009) with similar in vitro biological and biochemical activities compared to each monoclonal antibody, e.g., binding affinities on each target, competitive inhibition abilities on ligand-receptor interactions, and inhibition effects on endothelial cell proliferation and DLL4-induced Notch1-dependent activation. In addition, ABL001 more efficiently inhibited the tumor progression of several cancer cell line derived xenograft models as well as patient-derived xenograft models than an anti-VEGF antibody or anti-DLL4 antibody alone. Currently the safety and tolerability of ABL001 are evaluating in clinical phase 1 trial (ClinicalTrials.gov Identifier: NCT03292783). In conclusion, ABL001 is being developed as a promising therapeutic bispecific antibody for cancer treatment.

Biography:
Weon-Kyoo You received his PhD majored in Biochemistry at Yonsei University in 2004. Then, he worked as a postdoctoral fellow at UC San Francisco, and as a researcher at Sanford-Burnham Prebys Medical Discovery Institute from 2004 to 2012. He successfully performed several research projects and published many peer-reviewed papers in the field of tumor-induced angiogenesis and tumor microenvironments. After he came back to Korea, he joined at the Hanwha Chemical, R&D center as a principal research scientist to discover and develop a novel bispecific antibody until March, 2016. Currently he is working as the R&D Head at a startup biotech company, ABL Bio, Inc. and leading new antibody-based drug development projects.

  • Regeneron Pharmaceuticals, Inc. NY, USA
  • Title:A Mucin 16 Bispecific T cell–engaging Antibody for the Treatment of Ovarian Cancer
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Abstract:
Bispecific antibodies that interact with tumor antigens on cancer cells and activating receptors on immune cells offer an innovative immunotherapy approach. REGN4018 is a bispecific antibody that binds both Mucin 16 (MUC16), a glycoprotein that is highly expressed on ovarian cancer cells, and CD3, thus bridging MUC16-expressing cells with CD3+ T cells. REGN4018 induced T cell activation and killing of MUC16-expressing tumor cells in vitro. In preclinical studies with human ovarian cancer cells and human T cells in immunodeficient mice, REGN4018 potently inhibited growth of intraperitoneal ovarian tumors. Moreover, in a genetically engineered immunocompetent mouse expressing human CD3 and human MUC16 [humanized target (HuT) mice], REGN4018 inhibited growth of murine tumors expressing human MUC16, and combination with an anti– PD-1 antibody enhanced this efficacy. Immuno-PET imaging demonstrated localization of REGN4018 in MUC16-expressing tumors and in T cell–rich organs such as the spleen and lymph nodes. Toxicology studies in cynomolgus monkeys showed minimal and transient increases in serum cytokines and C-reactive protein after REGN4018 administration, with no overt toxicity. Collectively, these data demonstrate potent antitumor activity and good tolerability of REGN4018, supporting clinical evaluation of REGN4018 in patients with MUC16-expressing advanced ovarian cancer.

Biography:
Dr. Alison Crawford is a Senior Staff Scientist in the department of Oncology and Angiogenesis at Regeneron Pharmaceuticals, Inc. She completed her BSc in Immunology from Glasgow University before being admitted to the Wellcome Trust Ph.D. program at Edinburgh University where she focused on T cell memory. Her post-doctoral work at the University of Pennsylvania examined T cell exhaustion during chronic viral infection and the role of checkpoint inhibition in alleviating T cell exhaustion. This piqued her interest in immunotherapies and she made the transition into industry at Regeneron Pharmaceuticals where her group uses pre-clinical models to examine bispecific antibodies targeting solid tumors. She led the in vivo pre-clinical research efforts on REGN4018 (MUC16xCD3) to advance the antibody through to IND submission.

  • Cardiff University, UK
  • Title:Targeting Her Family kinases in Metastatic Diseases in Solid Human Cancers and Therapeutic Considerations
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Abstract:
The Her receptor tyrosine kinase family has four members, namely Her-1 (EGFR or ErB1), Her-2 (Neu or ErbB2), Her-3 (ErB3) and Her-4 (ErB4). Activation of the kinases results in intracellular signalling events leading to some oncogenic and aggressive behaviour of cancer cells including those involved in cell growth, apoptosis and cellular migration and invasiveness. Known downstream signalling events include activation of the Ras, PI3K, MAPK pathways. Clinically, the levels of the Her family members have been shown to be aberrantly expressed in various tumour types including breast cancer and lung cancer. Mutations of the coding genes for the family members have also been found in solid cancers and have been key indicators for the choice and success of anti-Her treatments. Our team has been investigating the relationship between the Her family gene expression levels and the clinical outcomes of patients with breast, gastric, pancreatic and lung cancers and exploring the prospects and potential mechanisms of targeting Her kinases in the intervention of metastatic diseases from these cancers in particular in their bone and brain metastases. Significant correlations were found between the expression levels of selective members of the Her family and the overall as well as disease free survivals in these cancer types. Using cancer cell models, brain endothelial cell models and in vitro ‘metastasis’ models, combined with protein kinase platform technologies, we further explored the prospect of specific and broad spectrum inhibitors to the Her kinases on the invasive and metastatic behaviour of cancer cells. We have identified that certain broad spectrum Her kinase inhibitors, for example Nerlynx, have some profound effects on the bone and brain metastatic properties of cancer cells and also impact on the permeability of brain endothelial cells. Together with the clinical cohort results, our protein kinase platform assays have also identified patterns of responsive signalling events that may contribute to the anti-metastatic properties of the Her kinase inhibitors. In summary, our studies on the expression of the Her family kinases in clinical cancer cohorts together with laboratory investigation have shown that targeting certain Her family kinases are highly useful when treating metastatic cancers including those metastasised to bone and brain. We have also identified patterns of responsive signalling events that may allow prediction of the likelihood in patient’s response to the anti-Her treatment.

Biography:
Professor Wen G. Jiang is a Professor of Surgery and Tumour Biology at Cardiff Medical School of Cardiff University. He is currently the Director of Cardiff’s China Medical Research Collaborative (CCMRC) and Cardiff University Dean of International. Professor Jiang’s research interest is the molecular and cellular basis of cancer invasion and metastasis and development of anti-metastasis treatment.

  • Brigham and Women's Hospital, USA
  • Title:New Evidence supporting Lung Cancer Screening with Low Dose CT & Surgical Implications; is The Controversy Over?
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Abstract:
Lung cancer is the leading cause of cancer-death worldwide. In the United States, The U.S. Preventative Services Task Force (USPTSF) approved screening for current or former smokers aged 55- 80 based on the results of the National Lung Screening trial (NLST). This decision has been criticized for lack of corroborative trials. Following the NLST, new evidence has emerged to support lung cancer screening with low dose computed tomography (LDCT) and the surgical implications.
Multiple new prospective randomized control trials on lung cancer screening support LDCT including the Multicentric Italian Lung Detection (MILD), the German Lung Cancer Screening Intervention trial (LUSI), the UK Lung Screening pilot study (UKLS), and the Nederlands-Leuvens Longkanker Screening Onderzoek (NELSON) trials. Furthermore, the extended results of the NLST trial has provided further insight into the benefits to lung cancer screening with LDCT, especially for women. The use of standardized nodule classifications (lung-RADS and volumetric analysis) reduce harm and lower false positive rates. The use of the emerging field of risk-prediction models can identify individuals that are appropriate for screening with lower tobacco exposures. The downstream effect of screening will require an increase in the thoracic workforce to accommodate the amount of surgically operable cancers.

Biography:
Dr. Aaron R. Dezube is a general surgery resident in the Department of Surgery at St. Elizabeth’s Medical Center, Boston, USA an affiliate of Tufts University School of Medicine. In addition he is the Jack Mitchell Thoracic Surgery Oncology research fellow in the Division of Thoracic Surgery at Brigham and Women’s Hospital/Harvard Medical School in the Michael T Jaklitsch lab . He is the author and co-author of multiple peer-reviewed publications, as well as contributes as a co-author for multiple articles on UptoDate. His research interests include clinical outcomes in thoracic surgery and lung cancer screening.

  • Tanta University, Egypt
  • Title:Dexamethasone Simulates the Anticancer Effect of Nano-Formulated Paclitaxel in Breast Cancer Cells
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Abstract:
Although the chemosensitizing effect of Dexamethasone (DEX) was previously reported, this study aimed to explore how far cotreatment of breast cancer cells with paclitaxel (PTX) and DEX mimics the anticancer effect of nanoformulated PTX. To establish this goal, PTX was nanoformulated with PLGA and physically authenticated. Breast cancer cells (MCF-7) were treated with PTX or PTX-NPs in presence or absence of low concentration (10 nM) of DEX. Cells viability, apoptosis and the expression of PTX resistance gene (TRX1) and PTX metabolizing genes (CYP2C8 and CYP3A4) were investigated. The nanoformulated PTX was validated by nano-size assessment, increased the anionic surface charge and prober conjugation with the biodegradable carrier (PLGA), as indicated by the FTIR spectroscopy. Initially, the IC50 value of PTX was 19.3 μg/ml and cotreatment with DEX minimized it to 5.22 μg/ml, whereas PTX-NPs alone inhibited cell proliferation with IC50 6.67 μg/ml. Also, in presence of DEX, PTX-NPs further decreased the IC50 to5 μg/ml. In parallel, DEX has increased the cell responsiveness to PTX without potentiating its apoptotic effect. Moreover, the glucocorticoid (with PTX or PTX-NPs) downregulated TXR1 gene by 26% (P<0.01) and 28.4% (P < 0.05), respectively. Similarly, the mRNA level of CYP3A4 significantly decreased in presence of DEX. The main PTX metabolizing gene CYP2C8, in contrast, was upregulated, especially in cells cotreated with PTX/DEX (P<0.001). Conclusively, the study reports that cotreatment of breast cancer cells with submolar concentration of DEX acts as similar as the nanoformulated PTX, possibly through its modulatory effects on the expression of the main PTX metabolizing gene (CYP2C8) and downregulating Taxol resistance gene. Biography
Professor Hessien received his B.S., M.Sc. in biochemistry from Ain-Shams University, Egypt and his Ph.D. from Ain-Shams and Albert Einstein College of Medicine, NY, USA (channel program) in Molecular Biology of hepatitis B virus in 2000. After receiving his degree, he was awarded Fulbright fellowship to Lombardi Cancer Center, Georgetown University, Washington, D.C. with Professor Richard Pestell in 2003. In his leave to KSA he was the head of The Department of Medical Laboratory Technology in the International Academy of Health Sciences and Community College, KKU. Also, he was an associate professor of Medical Biochemistry in the Collage of Medicine, KKU. Now he is a full professor in the Division of Biochemistry, faculty of Science Tanta University, Egypt, where he established his lab and crew members working on cancer cell biology. Prof Hessien published more than 40 research articles, 5 books and received many grants.

  • University of Nebraska Medical Center, USA
  • Title:p66Shc Enhances Oxidant Species Production to Support Advanced Cancer Progression and Metastasis
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Abstract:
Oxidant species including Reactive oxygen species (ROS) play a vital role in mediating diverse cellular signalling and apoptosis in normal cells. Excess oxidant species can oxidize numerous vital molecules to promote the development and progression of many cancers. While there are numerous studies on the correlative influence of oxidant species on cancer progression, the effect of oxidant species and its molecular mechanism by a specific oxidase/pro-oxidant protein of clinical relevance on cancer progression remains investigation.
Using prostate cancer (PCa) as a model system, we investigate p66Shc protein’s role in the progression of advanced castration-resistant (CR) phenotype, a lethal PCa. p66Shc, a member of Src homologue and collagen homologue family, can interact with Cytochrome C in mitochondria and via Rac 1 with NAD(P)H oxidases (NOXs) in cytosol for enhancing oxidant species production. In clinical archival specimens, p66Shc protein is significantly elevated in cancerous cells. Upon cDNA transfection, increased expression of the wild type p66Shc protein, but not inactive mutant, via oxidant species production supports PCa cells to obtain the CR phenotype in androgen-deprived conditions and metastasis in xenograft tumors. Hence, p66Shc and its downstream signaling molecules can serve as effective therapeutic targets for treating the patient sub-population with cancers of prostate, colon, breast, ovarian, thyroid and other types.

Biography:
Dr. Lin is Professor and Vice-Chair for Research in the Department of Biochemistry and Molecular Biology, UNMC, USA. Dr. Lin is a veteran in prostate cancer (PCa) biology research with over 30 years’ experience and performed initial biochemical characterizations of PCa biomarkers, prostate-specific antigen and prostatic acid phosphatase, under Dr. T. Ming Chu’s guidance. The ultimate goal of Dr. Lin’s research is to reduce cancer-related death.
Over his career, Dr. Lin is recognized by peers as a leading expert in investigating the integration of signaling pathways involved in castration-resistant (CR) PCa. Dr. Lin made the first seminal observation on the cross-talk between androgens and tyrosine phosphorylation signaling. Dr. Lin further discovered that cellular prostatic acid phosphatase (cPAcP) functions as a PTEN-functional homologue with tumor suppressor activity and is involved in regulating androgen sensitivity, a hallmark of PCa. By knockdown cPAcP, androgen-sensitive cells obtain the CR phenotype, corroborating the loss of cPAcP expression in clinical carcinomas. Dr. Lin then discovered that elevated p66Shc protein as seen in clinical specimens enhances oxidant species production, PCa progression and tumorigenecity, in part by inhibiting cPAcP under androgen-deprived conditions. His lab is currently elucidating the novel, dynamic integration via androgen, p66Shc/ROS and tyrosine phosphorylation in CR PCa progression. In parallel, Dr. Lin is a leading expert in investigating neuroendocrine transdifferentiation.

  • Eskisehir Osmangazi University, Turkey
  • Title:Hepatocelllular Cancer Epidemiology and Risk Factors
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Abstract:
Hepatocellular cancer (HCC) is the 5th common cancer in man and 7th cancer in women overall in the world. Although HCC is not in the most frequent cancers in the majority of the world, its high mortality and short survival time causes a serious worldwide health burden. Incidence to mortality rate is 0.95 for HCC and five years survival is only 6.9 %. HCC is not distributed evenly throughout the world. More cases of HCC occur in Asia and Africa than in Western countries. China by itself has half of the world’s HCC amount, 395.00 annual cases with the incidence of 35 in 100 000. High incidence of HCC also occurs in the Sub-Saharan Africa, particularly the western region of Africa. Mediterranean countries have intermediate incidence rates while North and South America have a relatively low. The most important risk factors for HCC are hepatitis B virus (HBV), hepatitis C virus (HCV), consumption of aflatoxin contaminated food stuffs, excessive consumption of alcohol, and non-alcoholic fatty liver disease (NAFLD). Risk factors for HCC vary by region. Geographical variability in the incidence of HCC has mainly been attributed to the distribution of HBV and HCV infection. Eighty percent of HCC are associated with either of two viruses. HBV infection is the predominant HCC risk factor worldwide and accounts for 75 to 80 percent of virus-associated HCCs. In the Western world, chronic alcoholic liver disease has become one of the leading risk factors of HCC. Aflatoxin is produced by a fungus in Asia and sub-Saharan Africa in which climatic factors and storage techniques favour the fungus to be a common contaminant of foods, and make it a serious risk factor for HCC in those regions. HCC incidence is higher in NAFLD patients than that observed in general population. This association is alarming due to the globally rising incidence of NAFLD in many countries, which means HCC will present itself as a major health burden in the near future.

Biography:
Prof. Dr. Ayşegul Ozakyol attended, in the years 1979-1985, Eskisehir Osmangazi University Medical School in Eskisehir, Turkey and earned her degre of medicine. She completed her residency in internal medicine at the same faculty in 1991. Her interest in gastroenterology lead her to earn a subspecialty degree in gastroenterology in 1996. She pursued an academic career, becoming an associate professor in 2001, and a professor in 2007. She is currently working as a faculty member in the department of gastroenterology at Eskisehir Osmangazi University. Her current acedemic interest is the area of hepatocellular cancer. She has had many scientific papers and presentations in peer-reviewed international publicatıons.

  • Bahrain Defence Force Hospital ,Kingdom of Bahrain
  • Title:Osteoid Osteoma of the Base of the Coracoid Process – A Case Report
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Abstract:
Introduction: Osteoid osteomas (OO) are small, well-defined, benign bone tumors of the young that are commonly found in long bones. In rare circumstances, when present elsewhere, they can mimic the symptoms of other pathologies pertaining to that area.
Presentation of case: We present such case in which an “OO” of the coracoid process led to a 2-year delay in diagnosis and management of a young male due to the presenting symptoms resembling those of other shoulder pathologies. Ultimately, the use of advanced imaging modalities proved to be useful in detecting the “OO”, which was consequently arthroscopically excised.
Discussion: Appropriate imaging modalities such as CT or MRI often visualize the characteristic nidus more clearly as opposed to an X-ray and should therefore be used early when conservative management of shoulder pain has not been proven to be useful.
Conclusion: A long history of shoulder pain that is not responsive to conservative management in young patients should raise the suspicion of an “OO”, and physicians should be encouraged to use early advanced imaging modalities in order to confirm it.

Biography:
Dr. Dalal AlGhoozi’s journey in medicine commenced in 2019, earning a Bachelors of Medicine, Surgery, and Obstetrics with distinction from the Royal College of Surgeons in Ireland.
Driven by her interest in oncology and realising the sharp increase of cancer cases in the gulf, Dr. AlGhoozi conducted further research in this field utilizing the extensive knowledge gained during her studies and practice.
Following graduation, she is currently pursuing her passion for oncological research (medicine?) at the Bahrain Defence Force Hospital – Royal Medical Services where Dr. AlGhoozi published her case report “Osteoid Osteoma of the Base of the Coracoid Process”.

  • Nyon’s Hospital, Switzerland
  • Title:Caecal Dermoid Cyst Presenting as an Appendicular Mucocele on Abdominal Imaging
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Abstract:
Dermoid cysts are benign tumors rarely arising from the cecum. Also, including this report, 10 cases have been described in the literature, to our knowledge. Dermoid cysts are benign tumors rarely found in the cecum. A literature research has found only 9 other cases. Case: We describe the case of a healthy 44-year-old man with no surgical history, in whom a well-defined cystic-mass was incidentally found on abdominal computed tomography, presenting as an appendicular mucocele. An hemicolectomy was performed and pathological analysis revealed a dermoid cyst of the cecum. This paper describes the case of a healthy 44-year-old male with no prior surgical history, with a well-defined cystic mass found incidentally on abdominal computed tomography, thought to be an appendicular mucocele. After hemicolectomy and pathological analysis, this was revealed to be a dermoid cyst of the cecum. Conclusion: Although dermoid cysts are a rare tumor of the cecum, they should be considered in the differential diagnosis of a nontender palpate mass in right lower quadrant (RLQ) or cecal mass on imaging. Although rarely found in the cecum, a dermoid cyst should be included in the differential diagnosis of nontender palpable masses of the RLQ, or if revealed by imagery.

Biography
Benedikta Kamdem, DDM., MSc., MD.
Dr Benedikta Kamdem qualified in Dental Medecine (2003) and got a Master’s in Biological and Medical Sciences (2004) at the University of Lyon (France). After working as a Dental Surgeon during ten years, she returned to university where she received a Bachelor‘s and a Master’s in Medecine, followed by a Swiss Medical degree in 2017(University of Lausanne, Switzerland). Her aim is to qualify in maxillo-facial surgery. In this context, she obtained a Diploma of Head and Neck Plastic Surgery in 2019 (Lyon) and is currently a resident at a Plastic and Hand Surgery Center in Nyon, Switzerland. She will complete her Internship at the University Hospital of Lausanne in the Department of Oral and Maxillofacial Surgery. The present work was carried out during her residency in the Department of Visceral Surgery in Nyon’s Hospital.

  • Mount Sinai Beth Israel, USA
  • Title:Nephrotoxic Chemotherapy Agents: Old and New
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Abstract:
In the last several decades, advancements in chemotherapy have improved the overall survival of cancer patients. These agents, however, are associated with adverse effects, including various kidney lesions. This review summarizes the nephrotoxic potential of chemotherapy agents, old and new, as well as the different factors that contribute to kidney injury. Provided for each class of chemotherapy agent is the associated kidney lesion and a brief discussion of clinical manifestation, mechanism of action, and possible treatment when available. Understanding the nephrotoxic potential these agents have on the kidneys is imperative for both the oncologist and the nephrologist to properly care for cancer patients and ensure their best outcomes.

Biography:
Born in Salem, Oregon in 1990. Attended New York University where I double-majored in biochemistry and anthropology, graduating cum laude in 2012. I attended medical school at Oregon Health & Science University, graduating in 2018. I am currently an internal medicine resident at Mount Sinai Beth Israel Hospital in New York City with plans of pursuing a fellowship in nephrology. I enjoy traveling, cooking, music, films, golfing, and skiing.

  • Henry Ford Cancer Institute ,USA
  • Title:The Role of a Low Erythropoietin Level for the Polycythemia Vera Diagnosis
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Abstract:
A low erythropoietin (EPO) level is a minor diagnostic criterion for polycythemia vera (PV). Controversies exist regarding the diagnostic value of a low EPO level when considering increasing availability of advanced molecular testing. We assessed the role of low EPO level for PV diagnosis in the context of positive JAK2 mutation status as well as other diagnostic parameters. Of 138 patients, 75 patients had PV and 63 had secondary erythrocytosis. Of the 75 patients with PV, 32% had EPO levels within the normal range. EPO level positively correlated with obesity and smoking status, making it an unreliable diagnostic marker in those patients. Although EPO level below normal as a standalone diagnostic modality was significantly associated with PV (odds ratio [OR] 0.857; p < 0.001), when JAK2V617F mutation status was included in the prediction model, the association of low EPO was not statistically significant (OR 0.962, p = 0.269). Positive JAK2V617F demonstrated a strong predictive value for PV (OR 670.5, p = 0.006) either alone or in combination with other variables. Results show that EPO level is not a reliable diagnostic marker due to physiologic variation in association with obesity and smoking.

  • Max Superspeciality Hospital ,India
  • Title:Primary Hyperparathyroidism with Brown Tumors Masquerading Skeletal Metastases – Role of Functional Imaging in Diagnosis and Management.
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Abstract:
Brown tumors of bone are highly vascular, lytic bone lesions representing a reparative cellular process rather than a neoplastic process seen in patients with hyperparathyroidism. These tumors may behave aggressively and can be destructive. We present a case of 33 year old male who presented with progressively increasing swelling in right leg region. A lytic lesion involving right tibia was seen in regional CT which was suspicious for malignancy. Whole body F18-FDG PET-CT was done for further evaluation. PET-CT showed multiple sites of skeletal lesions with a large mass in right lobe of thyroid gland. Biopsy from tibial lesion revealed it to be osteoclast rich tumor raising a possibility of parathyroid mass with multiple brown tumors. Biochemical parameters revealed high Serum Calcium, Serum Total Alkaline Phosphatase and Serum parathyroid hormone (S. PTH). 99mTehnitium Sestamibi (99m Tc MIBI) imaging was done which localized a right superior parathyroid adenoma with a suspicious right inferior parathyroid adenoma. The patient underwent right superior and inferior parathyroidectomy along with right hemithyroidectomy. Intra-operative fresh S.PTH sample was sent which dropped down to 73.4 ng/ml from 1500 ng/ml. Brown tumor is a potential cause of false-positive result in evaluation of a patient for unknown primary tumor or skeletal metastases with F18-FDG PET-CT imaging.

Biography:
Born and brought up in a town in the state of Punjab, India, after completion of my high school I was selected into one of the prestigious medical institutes of India- Maulana Azad Medical College, New Delhi where I did my graduation. I did my post graduation in Nuclear Medicine from one of the first institutes for Nuclear Medicine, in India- The Institute of Nuclear Medicine and Allied Sciences, Delhi University. During my post graduation when the modality of PET-CT was still in the stage of infancy in India, I started developing a great interest in this field and role it played in oncology. That interest turned into passion for this branch when I started working with the topmost people in the field of oncology at Max Superspeciality Hospital, New Delhi where there is a dedicated Max Institute of Cancer Care. Today PET-CT has become an integral part of the patient treatment and management in oncology and I love playing the part I am entrusted with day in and day out as a Consultant in the Department of Nuclear Medicine.

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