Day2

  • Center for Biomedical Research, USA
  • Title:Randomized Trial of Topical Ascorbic Acid in DMSO versus Imiquimod for the Treatment of Basal Cell Carcinoma
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Abstract:
Skin cancer is the most common cancer in the United States and among Caucasians worldwide, with more people diagnosed each year than all other cancers combined. Basal cell cancer is the most common form with an estimated 4.3 million cases diagnosed annually, and treatment costs estimated at $4.8 billion. The objective of this study was to compare efficacy of a topical solution consisting of 30% ascorbic acid in 95% dimethylsulfoxide with topical imiquimod in the treatment of basal cell carcinoma. Twenty-five patients with 29 biopsy confirmed basal cell carcinomas were randomly assigned to receive either the topically applied ascorbic acid treatment twice daily for 8 weeks or topical imiquimod, a standard and well characterized topical treatment. After 8 weeks, post-treatment biopsy of lesions showed complete resolution of 13/15 (86.7%) in the ascorbic acid group, while 8/14 (57.1%) lesions in the IMQ group were resolved (p<0.05 Chi Square). Topical ascorbic acid was superior at 8 weeks, and non-inferior at 12 weeks to topical imiquimod in the treatment of low risk nodular and superficial lesions. In addition, ascorbic acid was associated with fewer adverse effects than imiquimod. 70% of patients in theimiquimod group showed residual hypopigmentation at 30mo follow up versus 0% in the ascorbate group. Biography:
Dr. Burke is currently Medical Director for the Center for Biomedical Research, Inc., a non-profit research institute in Boise, Idaho USA. He received his Medical Degree from the University of Connecticut School of Medicine where he was elected to the Sigma Chi Scientific Research Society. His graduate degree was awarded in molecular biology from Yale University. He has practiced clinical medicine for 25 years in addition to research activities. Previous appointments include Adjunct Professor of Chemistry, Boise State University; Boise Veterans Administration Medical Center Research Service investigating molecular mechanisms of cardiotoxicity of anthracyclines; multiple grant awards from the Mountain States Tumor Institute in Idaho. He holds 3 US patents and has published in a variety of research areas over the decades.

  • University of Texas ,USA
  • Title:Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis.
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Abstract
There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which melatonin reportedly restrains cancer development and growth. These diverse actions suggest that what is being observed are merely epiphenomena of an underlying more fundamental action of melatonin that remains to be disclosed. Some of the arresting actions of melatonin on cancer are clearly membrane receptor-mediated while others are membrane receptor-independent and involve direct intracellular actions of this ubiquitously-distributed molecule. While the emphasis of melatonin/cancer research has been on the role of the indoleamine in restraining breast cancer, this is changing quickly with many cancer types having been shown to be susceptible to inhibition by melatonin. There are several facets of this research which could have immediate applications at the clinical level. Many studies have shown that melatonin’s co-administration improves the sensitivity of cancers to inhibition by conventional drugs. Even more important are the findings that melatonin renders cancers previously totally resistant to treatment sensitive to these same therapies. Melatonin also inhibits molecular processes associated with metastasis by limiting the entrance of cancer cells into the vascular system and preventing them from establishing secondary growths at distant sites. This is of particular importance since cancer metastasis often significantly contributes to death of the patient. Another area that deserves additional consideration is related to the capacity of melatonin in reducing the toxic consequences of anti-cancer drugs while increasing their efficacy. Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level. Even if the only beneficial actions of melatonin in cancer patients are its ability to attenuate acute and long-term drug toxicity, melatonin should be used to improve the physical wellbeing of the patients. The experimental findings, however, suggest that the advantages of using melatonin as a co-treatment with conventional cancer therapies would far exceed improvements in the wellbeing of the patients.

Biography:
Dr. Russel J. Reiter is Professor of Cell Biology in the Department of Cell Systems and Anatomy at the UT Health, San Antonio, Texas, USA, In addition to his Ph.D. degree, Dr. Reiter has received three honorary M.D. degrees and one honorary D.Sc. degree from international universities. His research relates to the multiple receptor-independent and receptor-dependent actions of melatonin in humans, animals and plants. He has trained 25 Ph.D. students and 144 postdoctoral fellows. Dr. Reiter has received numerous awards for his research including the A. Ross McIntyre Gold Metal (USA), US Senior Scientist Award (Germany), Lizoni Lincee Award (Italy), Inaugural Aaron B. Lerner Pioneer Award (USA), Chulabhorn Royal Academy Medal (Thailand), etc. He has published numerous research papers, reviews and chapters and he has written or edited 25 books. Based on Google Scholar, his papers have been cited in the scientific literature more than 130,000 times and his h-index is 175. Thomson Reuters/ Clarivate Analytics have identified Dr. Reiter as a Highly Cited Scientist (top 1%) and listed him as one of the World’s Most Influential Scientific Minds in 2014. Dr. Reiter has been an invited speaker at more than 300 international meetings and symposia. He is the Co-Editor of Melatonin Research and he is the Founder and past Editor of the Journal of Pineal Research.

  • Medical University of Vienna ,Austria
  • Title:Influence of Adjunctive Classical Homeopathy on Global Health Status and Subjective Wellbeing in Cancer Patients - A Pragmatic Randomized Controlled Trial.
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Abstract:
Background:
The use of complementary and alternative medicine has increased worldwide over the past decade. The aim of this study was to evaluate a possible influence of homeopathy on global health status and subjective wellbeing when used as an add-on to conventional cancer therapy.
Design:
In this pragmatic randomized controlled trial, 410 patients, who were treated by standard anti-cancer therapy, were randomized to receive or not receive classical homeopathic add-on therapy. The study was performed at the Medical University Vienna, Department of Medicine I, Clinical Division of Oncology.
Main outcome measures: The main outcome measures were global health status and subjective wellbeing as assessed by the patients. At each of three visits (one baseline, two follow-up visits), patients completed two different questionnaires.
Results:
373 patients yielded at least one of three measurements. The improvement of global health status between visits 1 and 3 was significantly stronger in the homeopathy group (p=0.005) when compared with the control group. A significant group difference was also observed with respect to subjective wellbeing (p<0.001) in favor of the homeopathic as compared with the control group. Control patients showed a significant improvement only in subjective wellbeing between their first and third visits. Conclusion: Results suggest that the global health status and subjective wellbeing of cancer patients improve significantly when add-on classical homeopathic treatment is administered.                                                                                            Biography:
Dr.Michael Frass, MD, Professor of Medicine, Specialist in Internal Medicine, Homeopathy, Senior Intensivist. Head, Outpatient Unit 2014 to 2019: Homeopathy in malignant Diseases, Division of Clinical Oncology, Department of Internal Medicine I, Medical University Vienna, Austria. Vice President ”Doctors Association for Classical Homeopathy”, President “Austrian Umbrella Association for Medical Holistic Medicine”, Chairperson of WissHom: Scientific Society for Homeopathy. Invention, development, and evaluation of the Esophageal Tracheal Combitube (CombitubeTM, produced by Covidien, Mansfield, Massachusetts, USA). The Combitube is included as a Class IIa device in the Guidelines of the American Heart Association (AHA).

  • National Cancer Institute/NIH, USA
  • Title:The Landscape of Genomic Copy Number Alterations in Carcinomas and their Consequences on Gene Expression Levels and Disease Outcome
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Abstract
Aneuploidy, the unbalanced state of the chromosome content, represents a hallmark of most solid tumors. Such aneuploidies result in tumor specific genomic imbalances, which emerge in premalignant precursor lesions. Moreover, increasing levels of chromosomal instability have been observed in adenocarcinomas and are maintained in distant metastases. A number of studies have systematically integrated copy number alterations with gene expression changes in primary carcinomas, cell lines, and experimental models of aneuploidy. In fact, chromosomal aneuploidies target a number of genes conferring a selective advantage for the metabolism of the cancer cell. Copy number alterations not only have a positive correlation with expression changes of the majority of genes on the altered genomic segment, but also have effects on the transcriptional levels of genes genome-wide. Finally, copy number alterations have been associated with disease outcome; nevertheless, the translational applicability in clinical practice requires further studies. Here we review (i) the spectrum of genetic alterations that lead to solid tumors, (ii) the most frequent copy number alterations at different stages of cancer, (iii) exemplify their positive correlation with gene expression levels, and (iv) discuss copy number alterations that are potentially involved in disease outcome of individual patients.

Biography
Dr.Ried received his M.D. from the Max Planck Institute for Medical Research in Heidelberg, Germany. After having completed his postdoctoral training at the University of Leiden and at Yale University, he joined the faculty of the National Human Genome Research Institute in 1994. Dr. Ried became an investigator at the NCI in 1998 and a senior investigator and Chief of the Cancer Genomic Section in 2002. Since 1998 he has co-directed the Cancer Chromosome Aberration Project. In 2000, Dr. Ried received the AMGEN award of the American Society of Biochemistry and Molecular Biology. Dr. Ried serves as a member of the editorial board for numerous scientific journals.

  • Ross University School of Medicine, USA
  • Title:Repair of Iatrogenic Injury Secondary to Breast Cancer Metastasis
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Abstract:
We present a case of unforeseen ureteral metastasis from a primary breast cancer. A ureteral injury leak was postoperatively recognized after a hysterectomy and bilateral oophorectomy were performed. Subsequent repair with a psoas hitch ureteral re-implant was performed and breast cancer metastasis was discovered in the ureteral stump specimen.

  • University of Florence Medical School , Italy
  • Title:Insufficiency of Today’s Cancer Modeling in Pediatric Tumors. Alternative Molecular Mechanisms are Suggested for Progression and Therapy
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Abstract:
In a review published in April 2021 in Cancer Letters (Rovigatti, U.: “The glycosphingolipid GD2 as an effective but enigmatic target of passive immunotherapy in children with aggressive neuroblastoma (HR-NBL) ”CL, 503: pp 220-230), I suggested that the present understanding of the pediatric tumor neuroblastoma (NBL) is insufficient for disease onset and progression, despite approximately four decades of molecular discoveries and characterization of genetic and genomic aberrations. In this sense, NBL epitomizes the genetic landscape of the majority of human cancers, where the appearance of genetic alterations was often considered independent from direct causality. An extreme version of such modeling was presented a few years ago by Tomasetti and Vogelstein and has been often recognized as the “bad luck” model (Science Vol. 355, pp. 1330-1334). In this type of modeling, causation appears to be irrelevant and the emphasis is placed upon therapeutic interventions. In NBL however, amplification of the MYCN oncogene (MNA) is a recurrent event in 20%-25% of cases and this dramatic genomic aberration is difficult to reconcile with a normal-rate mutation accrual. Furthermore, NMA patients have a “different disease” in terms of prognosis and excellent sensitivity to passive immunotherapy with anti-GD2 monoclonal antibodies (Kushner et al. 2017, Oncotarget, 8: 95.293- 302). Similar recurring aberrations are present in lung, breast, colon cancer etc. (Vogelstein et al. Cancer Genome Landscapes: Science Vol. 339, pp. 1546-1558). From the study of a cancer-cluster of NBL cases, we have isolated a dsRNA virus capable of inducing MNA in previously diploid cells (called Micro-Foci inducing Virus or MFV). Therefore, the excellent sensitivity of these patients to anti-GD2 monoclonals therapy –which is not otherwise explainable with the plethora of NBL genomic aberrations- could be explained by the chemical nature of GD2, which appears to be a receptor for this family of viruses (Reoviridae). In the concluding general discussion, I will present new data against a unique or dominating model for cancer onset and progression (such as Hallmarks of Cancer, 2000 and 2011) and encourage alternative explicatory mechanisms which are more capable of resolving the different puzzles of cancer genetic and genomics (Rovigatti, U.: Cancer Modeling in the NGS Era: CROH 2015, 96: 274-307 ).

  • University of Kentucky, USA
  • Title:Homophilic CD44 interactions mediate tumor cell aggregation and metastasis
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Abstract:

Circulating tumor cells (CTC) seed cancer metastases; however, the underlying cellular and molecular mechanisms remain unclear. CTC clusters were less frequently detected but more metastatic than single CTCs. Using intravital multiphoton microscopic imaging, we found that clustered tumor cells in migration and circulation resulted from aggregation of individual tumor cells rather than collective migration and cohesive shedding. Aggregated tumor cells exhibited enriched expression of the breast cancer stem cell marker CD44 and promoted tumorigenesis and polyclonal metastasis. Depletion of CD44 effectively prevented tumor cell aggregation and decreased PAK2 levels. We further demonstrated that CD44 directly mediated cell aggregation through CD44 homophilic interactions. Machine learning-based computational modeling combined with experimental mutagenesis tests revealed that the extracellular domains I and II of CD44 are essential for its trans-dimerization and predicted high-score residues to be required for dimerization. Substitutions of 10 these residues in domain I (Ser-45, Glu-48, Phe-74, Cys-77, Arg-78, Tyr-79, Ile-88, Arg-90, Asn-94, and Cys-97) or 5 residues in domain II (Ile-106, Tyr-155, Val-156, Gln-157, and Lys-158) abolished CD44 dimerization and reduced tumor cell aggregation in vitro. Importantly, the substitutions in domain II dramatically inhibited lung colonization in mice. The CD44 dimer-disrupting substitutions decreased downstream PAK2 activation without affecting the interaction between CD44 and PAK2, suggesting that PAK2 activation in tumor cell clusters is CD44 trans-dimer-dependent. These results shed critical light on the biochemical mechanisms of CD44-mediated tumor cell cluster formation and may help inform the development of therapeutic strategies to prevent tumor cluster formation and block cluster-mediated metastases.

Biography:

Dr. Xia liu received her PhD degree from Peking Union Medical College, China. Then I pursued her postdoctoral training at Case Western Reserve University and NOrthwestern University. In 2020, she became an Assistant Professor at the Department of Toxicology and Cancer Biology, University of Kentucky, USA. Currently, the research in her laboratory is focused on the mechanisms of breast cancer metastasis, cancer liquid biomarkers discovery, the role of innate immunity in cancer, and development of novel therapeutic strategies to treat metastatic cancers, .

  • 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.

  • 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
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:
Dr. Anthony Nicolaysen was born in Salem, Oregon in 1990. Attended New York University where he double-majored in biochemistry and anthropology, graduating cum laude in 2012. He attended medical school at Oregon Health & Science University, graduating in 2018. He currently an internal medicine resident at Mount Sinai Beth Israel Hospital in New York City with plans of pursuing a fellowship in nephrology. He enjoys 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:
Jaspriya Bal , born and brought up in a town in the state of Punjab, India, after completion of my high school she was selected into one of the prestigious medical institutes of India- Maulana Azad Medical College, New Delhi where she did her graduation. She did her 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 her post graduation when the modality of PET-CT was still in the stage of infancy in India, she started developing a great interest in this field and role it played in oncology. That interest turned into passion for this branch when she 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 she love playing the part ,she entrusted with day in and day out as a Consultant in the Department of Nuclear Medicine.

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