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Author Patch, A.M.; Christie, E.L.; Etemadmoghadam, D.; Garsed, D.W.; George, J.; Fereday, S.; Nones, K.; Cowin, P.; Alsop, K.; Bailey, P.J.; Kassahn, K.S.; Newell, F.; Quinn, M.C.; Kazakoff, S.; Quek, K.; Wilhelm-Benartzi, C.; Curry, E.; Leong, H.S.; Australian, O.C.S.G.; Hamilton, A.; Mileshkin, L.; Au-Yeung, G.; Kennedy, C.; Hung, J.; Chiew, Y.E.; Harnett, P.; Friedlander, M.; Quinn, M.; Pyman, J.; Cordner, S.; O’Brien, P.; Leditschke, J.; Young, G.; Strachan, K.; Waring, P.; Azar, W.; Mitchell, C.; Traficante, N.; Hendley, J.; Thorne, H.; Shackleton, M.; Miller, D.K.; Arnau, G.M.; Tothill, R.W.; Holloway, T.P.; Semple, T.; Harliwong, I.; Nourse, C.; Nourbakhsh, E.; Manning, S.; Idrisoglu, S.; Bruxner, T.J.; Christ, A.N.; Poudel, B.; Holmes, O.; Anderson, M.; Leonard, C.; Lonie, A.; Hall, N.; Wood, S.; Taylor, D.F.; Xu, Q.; Fink, J.L.; Waddell, N.; Drapkin, R.; Stronach, E.; Gabra, H.; Brown, R.; Jewell, A.; Nagaraj, S.H.; Markham, E.; Wilson, P.J.; Ellul, J.; McNally, O.; Doyle, M.A.; Vedururu, R.; Stewart, C.; Lengyel, E.; Pearson, J.V.; Waddell, N.; deFazio, A.; Grimmond, S.M.; Bowtell, D.D. url  openurl
  Title Whole-genome characterization of chemoresistant ovarian cancer Type Journal Article
  Year 2015 Publication Abbreviated Journal Nature  
  Volume 521 Issue 7553 Pages 489-494  
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  Abstract Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1.  
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  Call Number UofT @ ankit.sinha @ Serial 45069  
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Author Drerup, J.M.; Liu, Y.; Padron, A.S.; Murthy, K.; Hurez, V.; Zhang, B.; Curiel, T.J. url  openurl
  Title Immunotherapy for ovarian cancer Type Journal Article
  Year 2015 Publication Abbreviated Journal Curr Treat Options Oncol  
  Volume 16 Issue 1 Pages 317  
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  Abstract OPINION STATEMENT: All work referenced herein relates to treatment of epithelial ovarian carcinomas, as their treatment differs from ovarian germ cell cancers and other rare ovarian cancers, the treatments of which are addressed elsewhere. Fallopian tube cancers and primary peritoneal adenocarcinomatosis are also generally treated as epithelial ovarian cancers. The standard of care initial treatment of advanced stage epithelial ovarian cancer is optimal debulking surgery as feasible plus chemotherapy with a platinum plus a taxane agent. If this front-line approach fails, as it too often the case, several FDA-approved agents are available for salvage therapy. However, because no second-line therapy for advanced-stage epithelial ovarian cancer is typically curative, we prefer referral to clinical trials as logistically feasible, even if it means referring patients outside our system. Immune therapy has a sound theoretical basis for treating carcinomas generally, and for treating ovarian cancer in particular. Advances in understanding the immunopathogenic basis of ovarian cancer, and the immunopathologic basis for prior failures of immunotherapy for it and other carcinomas promises to afford novel treatment approaches with potential for significant efficacy, and reduced toxicities compared with cytotoxic agents. Thus, referral to early phase immunotherapy trials for ovarian cancer patients that fail conventional treatment merits consideration.  
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  Call Number UofT @ ankit.sinha @ Serial 45091  
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Author Sharma, P.; Allison, J.P. url  openurl
  Title Immune checkpoint targeting in cancer therapy: toward combination strategies with curative potential Type Journal Article
  Year 2015 Publication Abbreviated Journal Cell  
  Volume 161 Issue 2 Pages 205-214  
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  Abstract Research in two fronts has enabled the development of therapies that provide significant benefit to cancer patients. One area stems from a detailed knowledge of mutations that activate or inactivate signaling pathways that drive cancer development. This work triggered the development of targeted therapies that lead to clinical responses in the majority of patients bearing the targeted mutation, although responses are often of limited duration. In the second front are the advances in molecular immunology that unveiled the complexity of the mechanisms regulating cellular immune responses. These developments led to the successful targeting of immune checkpoints to unleash anti-tumor T cell responses, resulting in durable long-lasting responses but only in a fraction of patients. In this Review, we discuss the evolution of research in these two areas and propose that intercrossing them and increasing funding to guide research of combination of agents represent a path forward for the development of curative therapies for the majority of cancer patients.  
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  Call Number UofT @ ankit.sinha @ Serial 45097  
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Author Butterfield, L.H. url  openurl
  Title Cancer vaccines Type Journal Article
  Year 2015 Publication Abbreviated Journal Bmj  
  Volume 350 Issue Pages h988  
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  Abstract Cancer vaccines are designed to promote tumor specific immune responses, particularly cytotoxic CD8 positive T cells that are specific to tumor antigens. The earliest vaccines, which were developed in 1994-95, tested non-mutated, shared tumor associated antigens that had been shown to be immunogenic and capable of inducing clinical responses in a minority of people with late stage cancer. Technological developments in the past few years have enabled the investigation of vaccines that target mutated antigens that are patient specific. Several platforms for cancer vaccination are being tested, including peptides, proteins, antigen presenting cells, tumor cells, and viral vectors. Standard of care treatments, such as surgery and ablation, chemotherapy, and radiotherapy, can also induce antitumor immunity, thereby having cancer vaccine effects. The monitoring of patients’ immune responses at baseline and after standard of care treatment is shedding light on immune biomarkers. Combination therapies are being tested in clinical trials and are likely to be the best approach to improving patient outcomes.  
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  Call Number UofT @ ankit.sinha @ Serial 45100  
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Author Urbanska, K.; Powell, D.J. url  openurl
  Title Advances and prospects in adoptive cell transfer therapy for ovarian cancer Type Journal Article
  Year 2015 Publication Abbreviated Journal Immunotherapy  
  Volume 7 Issue 5 Pages 473-476  
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  Call Number UofT @ ankit.sinha @ Serial 45106  
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Author Hasan, N.; Ohman, A.W.; Dinulescu, D.M. url  openurl
  Title The promise and challenge of ovarian cancer models Type Journal Article
  Year 2015 Publication Abbreviated Journal Transl Cancer Res  
  Volume 4 Issue 1 Pages 14-28  
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  Abstract The complexity and heterogeneity of ovarian cancer cases are difficult to reproduce in in vitro studies, which cannot adequately elucidate the molecular events involved in tumor initiation and disease metastasis. It has now become clear that, although the multiple histological subtypes of ovarian cancer are being treated with similar surgical and therapeutic approaches, they are in fact characterized by distinct phenotypes, cell of origin, and underlying key genetic and genomic alterations. Consequently, the development of more personalized treatment methodologies, which are aimed at improving patient care and prognosis, will greatly benefit from a better understanding of the key differences between various subtypes. To accomplish this, animal models of all histotypes need to be generated in order to provide accurate in vivo platforms for research and the testing of targeted treatments and immune therapies. Both genetically engineered mouse models (GEMMs) and xenograft models have the ability to further our understanding of key mechanisms facilitating tumorigenesis, and at the same time offer insight into enhanced imaging and treatment modalities. While genetic models may be better suited to examine oncogenic functions and interactions during tumorigenesis, patient-derived xenografts (PDXs) are likely a superior model to assess drug efficacy, especially in concurrent clinical trials, due to their similarity to the tumors from which they are derived. Genetic and avatar models possess great clinical utility and have both benefits and limitations. Additionally, the laying hen model, which spontaneously develops ovarian tumors, has inherent advantages for the study of epithelial ovarian cancer (EOC) and recent work champions this model especially when assessing chemoprevention strategies. While high-grade ovarian serous tumors are the most prevalent form of EOC, rarer ovarian cancer variants, such as small cell ovarian carcinoma of the hypercalcemic type and transitional cell carcinoma, or non-epithelial tumors, including germ cell tumors, will also benefit from the generation of improved models to advance our understanding of tumorigenic mechanisms and the development of selective therapeutic options.  
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  Call Number UofT @ ankit.sinha @ Serial 45119  
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Author Bobbs, A.S.; Cole, J.M.; Cowden Dahl, K.D. url  openurl
  Title Emerging and Evolving Ovarian Cancer Animal Models Type Journal Article
  Year 2015 Publication Abbreviated Journal Cancer Growth Metastasis  
  Volume 8 Issue Suppl 1 Pages 29-36  
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  Abstract Ovarian cancer (OC) is the leading cause of death from a gynecological malignancy in the United States. By the time a woman is diagnosed with OC, the tumor has usually metastasized. Mouse models that are used to recapitulate different aspects of human OC have been evolving for nearly 40 years. Xenograft studies in immunocompromised and immunocompetent mice have enhanced our knowledge of metastasis and immune cell involvement in cancer. Patient-derived xenografts (PDXs) can accurately reflect metastasis, response to therapy, and diverse genetics found in patients. Additionally, multiple genetically engineered mouse models have increased our understanding of possible tissues of origin for OC and what role individual mutations play in establishing ovarian tumors. Many of these models are used to test novel therapeutics. As no single model perfectly copies the human disease, we can use a variety of OC animal models in hypothesis testing that will lead to novel treatment options. The goal of this review is to provide an overview of the utility of different mouse models in the study of OC and their suitability for cancer research.  
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  Call Number UofT @ ankit.sinha @ Serial 45127  
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Author Kadiyska, T.; Nossikoff, A. url  openurl
  Title Stool DNA methylation assays in colorectal cancer screening Type Journal Article
  Year 2015 Publication Abbreviated Journal World J Gastroenterol  
  Volume 21 Issue 35 Pages 10057-10061  
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  Abstract Colorectal cancer (CRC) is fourth most common cancer in men and third in women worldwide. Developing a diagnostic panel of sensitive and specific biomarkers for the early detection of CRC is recognised as to be crucial for early initial diagnosis, which in turn leads to better long term survival. Most of the research on novel potential CRC biomarkers in the last 2 decades has been focussed on stool DNA analysis. In this paper, we describe the recent advances in non-invasive CRC screening and more specifically in molecular assays for aberrantly methylated BMP3 and NDRG4 promoter regions. In several research papers these markers showed superior rates for sensitivity and specificity in comparison to previously described assays. These tests detected the majority of adenomas ≥ 1 cm in size and the detection rates progressively increased with larger adenomas. The methylation status of the BMP3 and NDRG4 promoters demonstrated effective detection of neoplasms at all sites throughout the colon and was not affected by common clinical variables. Recently, a multitarget stool DNA test consisting of molecular assays for aberrantly methylated BMP3 and NDRG4 promoter regions, mutant KRAS and immunochemical assay for human haemoglobin has been made commercially available and is currently reimbursed in the United States. Although this is the most sensitive non-invasive CRC screening test, there is the need for further research in several areas – establishment of the best timeframe for repeated DNA stool testing; validation of the results in populations outside of North America; usefulness for surveillance and prognosis of patients; cost-effectiveness of DNA stool testing in real-life populations.  
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  Call Number UofT @ ankit.sinha @ Serial 45144  
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Author Das, S.; Batra, S.K. url  openurl
  Title Understanding the Unique Attributes of MUC16 (CA125): Potential Implications in Targeted Therapy Type Journal Article
  Year 2015 Publication Abbreviated Journal Cancer Res  
  Volume 75 Issue 22 Pages 4669-4674  
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  Abstract CA125, the most widely used ovarian cancer biomarker, was first identified approximately 35 years ago in an antibody screen against ovarian cancer antigen. Two decades later, it was cloned and characterized to be a transmembrane mucin, MUC16. Since then, several studies have investigated its expression, functional, and mechanistic involvement in multiple cancer types. Antibody-based therapeutic approaches primarily using antibodies against the tandem repeat domains of MUC16 (e.g., oregovomab and abagovomab) have been the modus operandi for MUC16-targeted therapy, but have met with very limited success. In addition, efforts have been also made to disrupt the functional cooperation of MUC16 and its interacting partners; for example, use of a novel immunoadhesin HN125 to interfere MUC16 binding to mesothelin. Since the identification of CA125 to be MUC16, it is hypothesized to undergo proteolytic cleavage, a process that is considered to be critical in determining the kinetics of MUC16 shedding as well as generation of a cell-associated carboxyl-terminal fragment with potential oncogenic functions. In addition to our experimental demonstration of MUC16 cleavage, recent studies have demonstrated the functional importance of carboxyl terminal fragments of MUC16 in multiple tumor types. Here, we provide how our understanding of the basic biologic processes involving MUC16 influences our approach toward MUC16-targeted therapy.  
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  Call Number UofT @ ankit.sinha @ Serial 45164  
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Author Lannoo, N.; Van Damme, E.J. url  openurl
  Title Review/N-glycans: The making of a varied toolbox Type Journal Article
  Year 2015 Publication Abbreviated Journal Plant Sci  
  Volume 239 Issue Pages 67-83  
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  Abstract Asparagine (N)-linked protein glycosylation is one of the most crucial, prevalent, and complex co- and post-translational protein modifications. It plays a pivotal role in protein folding, quality control, and endoplasmic reticulum (ER)-associated degradation (ERAD) as well as in protein sorting, protein function, and in signal transduction. Furthermore, glycosylation modulates many important biological processes including growth, development, morphogenesis, and stress signaling processes. As a consequence, aberrant or altered N-glycosylation is often associated with reduced fitness, diseases, and disorders. The initial steps of N-glycan synthesis at the cytosolic side of the ER membrane and in the lumen of the ER are highly conserved. In contrast, the final N-glycan processing in the Golgi apparatus is organism-specific giving rise to a wide variety of carbohydrate structures. Despite our vast knowledge on N-glycans in yeast and mammals, the modus operandi of N-glycan signaling in plants is still largely unknown. This review will elaborate on the N-glycosylation biosynthesis pathway in plants but will also critically assess how N-glycans are involved in different signaling cascades, either active during normal development or upon abiotic and biotic stresses.  
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  Call Number UofT @ ankit.sinha @ Serial 45205  
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