Publications
328 results found
Leinster DA, Colom B, Whiteford JR, et al., 2013, Endothelial cell junctional adhesion molecule C plays a key role in the development of tumors in a murine model of ovarian cancer, FASEB JOURNAL, Vol: 27, Pages: 4244-4253, ISSN: 0892-6638
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- Citations: 16
Rockall AG, Avril NE, Lam R, et al., 2013, [18F]Fluorodeoxyglucose PET and Volumetric CT analysis are early biomarkers of survival in platinum-sensitive relapsed ovarian cancer - a multicentre trial, European Cancer Congress 2013 - 17th ECCO / 38th ESMO / 32nd ESTRO, Publisher: ELSEVIER SCI LTD, Pages: S735-S735, ISSN: 0959-8049
McNeish I, Anthoney A, Loadman P, et al., 2013, A phase I pharmacokinetic (PK) and pharmacodynamic (PD) study of the selective aurora kinase inhibitor GSK1070916A., 49th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0732-183X
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- Citations: 7
McNeish IA, Ledermann JA, Webber LC, et al., 2013, A randomized placebo-controlled trial of saracatinib (AZD0530) plus weekly paclitaxel in platinum-resistant ovarian, fallopian-tube, or primary peritoneal cancer (SaPPrOC), 49th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0732-183X
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- Citations: 4
Hall M, Gourley C, McNeish I, et al., 2013, Targeted anti-vascular therapies for ovarian cancer: current evidence, BRITISH JOURNAL OF CANCER, Vol: 108, Pages: 250-258, ISSN: 0007-0920
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- Citations: 69
Archibald KM, Kulbe H, Kwong J, et al., 2012, Sequential genetic change at the TP53 and chemokine receptor CXCR4 locus during transformation of human ovarian surface epithelium, ONCOGENE, Vol: 31, Pages: 4987-4995, ISSN: 0950-9232
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- Citations: 14
Young A-M, Archibald KM, Tookman LA, et al., 2012, Failure of Translation of Human Adenovirus mRNA in Murine Cancer Cells Can be Partially Overcome by L4-100K Expression <i>In Vitro</i> and <i>In Vivo</i>, MOLECULAR THERAPY, Vol: 20, Pages: 1676-1688, ISSN: 1525-0016
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- Citations: 29
Leinster DA, Kulbe H, Everitt G, et al., 2012, The peritoneal tumour microenvironment of high-grade serous ovarian cancer, JOURNAL OF PATHOLOGY, Vol: 227, Pages: 136-145, ISSN: 0022-3417
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- Citations: 48
Saha A, Varughese M, Gallagher CJ, et al., 2012, Primary Chemotherapy for Inoperable Ovarian, Fallopian Tube, or Primary Peritoneal Cancer With or Without Delayed Debulking Surgery, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 22, Pages: 566-572, ISSN: 1048-891X
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- Citations: 14
Emeagi PU, Van Lint S, Goyvaerts C, et al., 2012, Proinflammatory Characteristics of SMAC/DIABLO-Induced Cell Death in Antitumor Therapy, CANCER RESEARCH, Vol: 72, Pages: 1342-1352, ISSN: 0008-5472
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- Citations: 29
Stone RL, Nick AM, McNeish IA, et al., 2012, Paraneoplastic Thrombocytosis in Ovarian Cancer, NEW ENGLAND JOURNAL OF MEDICINE, Vol: 366, Pages: 610-618, ISSN: 0028-4793
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- Citations: 561
Syed N, 2012, Polo Like Kinase 2 Tumour Suppressor and cancer biomarker: new perspectives on drug sensitivity/resistance in ovarian cancer, Oncotarget, Vol: 3, Pages: 78-83, ISSN: 1949-2553
The polo-like kinase PLK2 has recently been identified as a potential theranostic marker in the management of chemotherapy sensitive cancers. The methylation status of the PLK2 CpG island varies with sensitivity to paclitaxel and platinum in ovarian cancer cell lines. Importantly, extrapolation of these in vitro data to the clinical setting confirms that the methylation status of the PLK2 CpG island predicts outcomes in patients treated with carboplatin & paclitaxel chemotherapy. A second cell cycle regulator, p57Kip2, is also subject to epigenetic silencing in carboplatin resistance in vitro and in vivo, emphasising that cell cycle regulators are important determinants of sensitivity to chemotherapeutic agents and providing insights into the phenomenon of collateral drug sensitivity in oncology. Understanding the mechanistic basis and identification of robust biomarkers to predict collateral sensitivity may inform optimal use of chemotherapy in patients receiving multiple lines of treatment.
Perren TJ, Swart AM, Pfisterer J, et al., 2011, A Phase 3 Trial of Bevacizumab in Ovarian Cancer, NEW ENGLAND JOURNAL OF MEDICINE, Vol: 365, Pages: 2484-2496, ISSN: 0028-4793
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- Citations: 1568
Balkwill FR, Coward J, Kulbe H, et al., 2011, IL-6 and Ovarian Cancer-Response, CLINICAL CANCER RESEARCH, Vol: 17, Pages: 7838-7838, ISSN: 1078-0432
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- Citations: 2
Ateh DD, Leinster VH, Lambert SR, et al., 2011, The intracellular uptake of CD95 modified paclitaxel-loaded poly(lactic-co-glycolic acid) microparticles, BIOMATERIALS, Vol: 32, Pages: 8538-8547, ISSN: 0142-9612
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- Citations: 15
Ledermann JA, Hackshaw A, Kaye S, et al., 2011, Randomized Phase II Placebo-Controlled Trial of Maintenance Therapy Using the Oral Triple Angiokinase Inhibitor BIBF 1120 After Chemotherapy for Relapsed Ovarian Cancer, JOURNAL OF CLINICAL ONCOLOGY, Vol: 29, Pages: 3798-3804, ISSN: 0732-183X
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- Citations: 168
Connell CM, Shibata A, Tookman L, et al., 2011, Genomic DNA damage and ATR-Chk1 signalling determine adenovirus oncolytic efficacy in ovarian cancer, Publisher: MARY ANN LIEBERT INC, Pages: A113-A113, ISSN: 1043-0342
Vaughan S, Coward JI, Bast RC, et al., 2011, Rethinking ovarian cancer: recommendations for improving outcomes, NATURE REVIEWS CANCER, Vol: 11, Pages: 719-725, ISSN: 1474-175X
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- Citations: 942
Coward J, Kulbe H, Chakravarty P, et al., 2011, Interleukin-6 as a Therapeutic Target in Human Ovarian Cancer, CLINICAL CANCER RESEARCH, Vol: 17, Pages: 6083-6096, ISSN: 1078-0432
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- Citations: 296
Syed N, Crook T, 2011, Polo-like kinase Plk2 is an epigenetic determinant of chemosensitivity and clinical outcomes in ovarian cancer, Cancer Research
Ledermann JA, Marth C, Carey MS, et al., 2011, Role of Molecular Agents and Targeted Therapy in Clinical Trials for Women With Ovarian Cancer, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 21, Pages: 763-770, ISSN: 1048-891X
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- Citations: 25
Connell CM, Shibata A, Tookman LA, et al., 2011, Genomic DNA damage and ATR-Chk1 signaling determine oncolytic adenoviral efficacy in human ovarian cancer cells, JOURNAL OF CLINICAL INVESTIGATION, Vol: 121, Pages: 1283-1297, ISSN: 0021-9738
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- Citations: 24
Salako MA, Kulbe H, Ingemarsdotter CK, et al., 2011, Inhibition of the Inflammatory Cytokine TNF-α Increases Adenovirus Activity in Ovarian Cancer via Modulation of cIAP1/2 Expression, MOLECULAR THERAPY, Vol: 19, Pages: 490-499, ISSN: 1525-0016
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- Citations: 12
Kehoe S, Edmondson RJ, Gore M, et al., 2011, Consensus views arising from the 60th study group: Gynaecological cancers: Biology and therapeutics, Gynaecological Cancers: Biology and Therapeutics, Pages: 245-248, ISBN: 9781906985448
There is a pressing need to reclassify gynaecological cancers. Through recent work we have begun to realise that the most common type of ‘ovarian cancer’, high-grade serous cancer, is characterised by mutation of the p53 (TP53) gene. This has allowed the identification of precursor lesions in the fallopian tube and the realisation that in fact much, if not all, of this type of cancer probably originates in the tube itself. Thus serous cancer of the corpus, tube, ovary and peritoneum are almost certainly variants of the same disease. Similarly, clear-cell and endometrioid cancers also share many molecular characteristics, including driver mutations of PTEN, and this is irrespective of whether they appear to originate in the ovary or the uterine corpus. Changing the taxonomy and nomenclature of gynaecological cancers is not just an academic exercise. If we are to make serious inroads into improving the management of these diseases then we need to think about these cancers as distinct entities, types not sub-types of cancer, and initially design our clinical trials to reflect this. Ultimately, based on the results of these trials, we would envisage the development of different management strategies for each type.
Kehoe S, Edmondson RJ, Gore M, et al., 2011, Gynaecological cancers: Biology and therapeutics, ISBN: 9781906985448
Gynaecological cancers are categorised as 'rare' diseases, although collectively they affect over 16,000 women each year in the UK alone. There is a lack of real understanding of these conditions compared with other malignancies, possibly owing to their relative rarity when viewed as individual diseases. The 60th RCOG Study Group brought together a range of experts to examine as many biological aspects of gynaecological cancers as possible, including both surgical and non-surgical therapies. This book presents the findings of the Study Group, with contents including: current understanding of the biology of gynaecological cancers translation of biology to the clinic state of the art in imaging and therapy current clinical trials advances in multimodal therapy individualised treatment.
McNeish IA, 2011, Oncolytic viral gene therapy in ovarian cancer, Gynaecological Cancers: Biology and Therapeutics, Pages: 139-152, ISBN: 9781906985448
Oncolytic viruses are a novel treatment for cancer. These agents infect cancer cells and replicate selectively within them, causing death with release of mature virions that can subsequently infect neighbouring cells. A series of viruses have been developed and are being taken towards clinical trials in women with relapsed ovarian cancer. However, the majority of data derive from research on adenoviruses. In this chapter, I review the biology of adenoviruses, clinical trials of oncolytic viral gene therapy in ovarian cancer and recent developments that may give cause for cautious optimism.Successful completion ofany DNA virus life cycle requires the virus to overcome many cellular pathways and checkpoints in order to permit replication of the viral DNA and generation of new virions. Many of the pathways targeted by DNA viruses are the same as those deregulated in cancer and it is this overlap between virus and cancer biology that makes replicating viruses potential treatments for human malignancy.The first description of viruses as anti-cancer agents came over 100 years ago and, in 1953, a clinical trial to investigate the therapeutic potential of adenoviruses was conducted in women with cervical cancer and some short-lived responses were seen. More recently, there have been anecdotal descriptions of lymphoma regressing following measles infection.
Ingemarsdotter CK, Baird SK, Connell CM, et al., 2010, Low-dose paclitaxel synergizes with oncolytic adenoviruses via mitotic slippage and apoptosis in ovarian cancer, ONCOGENE, Vol: 29, Pages: 6051-6063, ISSN: 0950-9232
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- Citations: 45
Coughlan L, Alba R, Parker AL, et al., 2010, Tropism-Modification Strategies for Targeted Gene Delivery Using Adenoviral Vectors, VIRUSES-BASEL, Vol: 2, Pages: 2290-2355, ISSN: 1999-4915
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- Citations: 84
Trimble EL, Birrer MJ, Hoskins WJ, et al., 2010, Current Academic Clinical Trials in Ovarian Cancer <i>Gynecologic Cancer Intergroup and US National Cancer Institute Clinical Trials Planning Meeting</i>, <i>May 2009</i>, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 20, Pages: 1284-1298, ISSN: 1048-891X
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- Citations: 7
Harrington KJ, Hingorani M, Tanay MA, et al., 2010, Phase I/II Study of Oncolytic HSV<SUP>GM-CSF</SUP> in Combination with Radiotherapy and Cisplatin in Untreated Stage III/IV Squamous Cell Cancer of the Head and Neck, CLINICAL CANCER RESEARCH, Vol: 16, Pages: 4005-4015, ISSN: 1078-0432
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- Citations: 192
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