Publications
331 results found
Sousa C, Maginn E, Gabra H, et al., 2014, DNA-PKcs inhibition enhances response to DNA damaging agents and is associated with Rad51 downregulation, EUROPEAN JOURNAL OF CANCER, Vol: 50, Pages: S175-S175, ISSN: 0959-8049
Eltom S, Dale N, Raemdonck KRG, et al., 2014, Respiratory Infections Cause the Release of Extracellular Vesicles: Implications in Exacerbation of Asthma/COPD, PLOS One, Vol: 9, ISSN: 1932-6203
BackgroundInfection-related exacerbations of respiratory diseases are a major health concern; thus understanding the mechanisms driving them is of paramount importance. Despite distinct inflammatory profiles and pathological differences, asthma and COPD share a common clinical facet: raised airway ATP levels. Furthermore, evidence is growing to suggest that infective agents can cause the release of extracellular vesicle (EVs) in vitro and in bodily fluids. ATP can evoke the P2X7/caspase 1 dependent release of IL-1β/IL-18 from EVs; these cytokines are associated with neutrophilia and are increased during exacerbations. Thus we hypothesized that respiratory infections causes the release of EVs in the airway and that the raised ATP levels, present in respiratory disease, triggers the release of IL-1β/IL-18, neutrophilia and subsequent disease exacerbations.MethodsTo begin to test this hypothesis we utilised human cell-based assays, ex vivo murine BALF, in vivo pre-clinical models and human samples to test this hypothesis.ResultsData showed that in a murine model of COPD, known to have increased airway ATP levels, infective challenge causes exacerbated inflammation. Using cell-based systems, murine models and samples collected from challenged healthy subjects, we showed that infection can trigger the release of EVs. When exposed to ATP the EVs release IL-1β/IL-18 via a P2X7/caspase-dependent mechanism. Furthermore ATP challenge can cause a P2X7 dependent increase in LPS-driven neutrophilia.ConclusionsThis preliminary data suggests a possible mechanism for how infections could exacerbate respiratory diseases and may highlight a possible signalling pathway for drug discovery efforts in this area.
Fotopoulou C, Gorgy T, Paterson A, et al., 2014, Molecular physiology monitoring of ovarian cancer ex vivo., Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO) / Clinical Science Symposium on Predicting and Improving Adverse Outcomes in Older Adults with Cancer, Publisher: LIPPINCOTT WILLIAMS & WILKINS, 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA, ISSN: 1048-891X
Ghazaly EA, Rizzuto I, Gabra H, et al., 2014, ProGem1: A phase I/II study of a first-in-class nucleotide, Acelarin, in patients with advanced solid tumors, 50th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0732-183X
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- Citations: 1
Al Bakir M, Wang L, Russell K, et al., 2014, Molecular analysis of non-epithelial ovarian cancer by histologic subtype., 50th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0732-183X
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- Citations: 1
Miller DS, Gabra H, Emons G, et al., 2014, ZuptEC: Phase III study or zuptarelin doxorubicin (AEZS-108) te platinum-taxane pretreated endontetrial cancer (Study AEZS-108-050), 50th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0732-183X
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- Citations: 1
Glasspool RM, Brown R, Gore ME, et al., 2014, A randomised, phase II trial of the DNA-hypomethylating agent 5-aza-2 '-deoxycytidine (decitabine) in combination with carboplatin vs carboplatin alone in patients with recurrent, partially platinum-sensitive ovarian cancer, British Journal of Cancer, Vol: 110, Pages: 1923-1929, ISSN: 1532-1827
Background: Our previous laboratory and clinical data suggested that one mechanism underlying the development of platinum resistance inovarian cancer is the acquisition of DNA methylation. We therefore tested the hypothesis that the DNA hypomethylating agent 5-aza-20-deoxycytodine (decitabine) can reverse resistance to carboplatin in women with relapsed ovarian cancer.Methods: Patients progressing 6–12 months after previous platinum therapy were randomised to decitabine on day 1 and carboplatin (AUC 6) onday 8, every 28 days or carboplatin alone. The primary objective was response rate in patients with methylated hMLH1 tumour DNA in plasma.Results: After a pre-defined interim analysis, the study closed due to lack of efficacy and poor treatment deliverability in 15 patients treated withthe combination. Responses by GCIG criteria were 9 out of 14 vs 3 out of 15 and by RECIST were 6 out of 13 vs 1 out of 12 for carboplatin andcarboplatin/decitabine, respectively. Grade 3/4 neutropenia was more common with the combination (60% vs 15.4%) as was G2/3 carboplatinhypersensitivity (47% vs 21%).Conclusions: With this schedule, the addition of decitabine appears to reduce rather than increase the efficacy of carboplatin in partiallyplatinum-sensitive ovarian cancer and is difficult to deliver. Patient-selection strategies, different schedules and other demethylating agents shouldbe considered in future combination studies.
Curry EWJ, Stronach EA, Rama NR, et al., 2014, Molecular subtypes of serous borderline ovarian tumor show distinct expression patterns of benign tumor and malignant tumor-associated signatures, MODERN PATHOLOGY, Vol: 27, Pages: 433-442, ISSN: 0893-3952
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- Citations: 8
Fotopoulou C, Gabra H, 2014, Endometrial cancer, Treatment of Cancer, Sixth Edition, Pages: 405-416, ISBN: 9781482214949
Cancer of the endometrium or endometrial carcinoma (EC) is the most common gynaecologic malignancy in developed countries and the second-most common in developing countries, where cervical cancer is more common. EC is a hormonally driven cancer for the majority of cases, with 80% of endometrial cancers being due to either an excess of oestrogen or lack of progestin. There are two main types of EC: Type-I, estrogen-related, which usually presents histologically as a low-grade endometrioid tumour and is associated with atypical endometrial hyperplasia. Type-II tumours account for 10% 20% of EC. In the very small subgroup of patients with serous EC confined only to the endometrium risk of recurrence is only very small compared to those with myometrial invasion. In women with well or moderately differentiated EC and minimal invasion, progestins may be used to induce regression if fertility is to be preserved.
Fotopoulou C, Vergote I, Mainwaring P, et al., 2014, Weekly AUC2 carboplatin in acquired platinum resistant ovarian cancer with or without oral phenoxodiol, a sensitizer of platinum cytotoxicity: the phase Ill OVATURE multicenter randomized study, ANNALS OF ONCOLOGY, Vol: 25, Pages: 160-165, ISSN: 0923-7534
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- Citations: 24
Cheraghchi-Bashi-Astaneh A, De Sousa CH, Maginn E, et al., 2013, DNA-PK inhibition resensitizes ovarian cancer cells to cisplatin in vivo and is associated with modulation of AKT pathway signaling, CLINICAL CANCER RESEARCH, Vol: 19, ISSN: 1078-0432
Fotopoulou C, Spiers L, Adjogatse D, et al., 2013, Management of ascites via the alfa-pump closed system in platinum-resistant-ovarian-cancer (PROC): A model of sequential non-invasive tumor-cell sampling through the urinary bladder, CLINICAL CANCER RESEARCH, Vol: 19, ISSN: 1078-0432
Gabra H, 2013, Targeting acquired platinum resistance in ovarian cancer, CLINICAL CANCER RESEARCH, Vol: 19, ISSN: 1078-0432
Hopkins TG, Stavraka C, Hood C, et al., 2013, THE IMPACT OF OVARIAN CANCER TREATMENT ON WOMEN'S SEXUAL WELLBEING, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 23, ISSN: 1048-891X
Fotopoulou C, Spiers L, Pickford E, et al., 2013, CONTINUOUS LOW-FLOW ASCITES-DRAINAGE AND SEQUENTIAL NON-INVASIVE TUMOR-CELL SAMPLING THROUGH THE URINARY BLADDER VIA THE ALFA-PUMP CLOSED SYSTEM IN PLATINUM-RESISTANT-OVARIAN-CANCER (PROC), INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 23, ISSN: 1048-891X
Hopkins TG, Jayantha C, Gabra H, et al., 2013, OUTCOMES IN MUCINOUS OVARIAN CARCINOMAS: 10 YEARS OF EXPERIENCE IN A TERTIARY CENTRE, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 23, ISSN: 1048-891X
Browne A, Sriraksa R, Guney T, et al., 2013, Differential expression of IL-8 and IL-8 receptors in benign, borderline and malignant ovarian epithelial tumours, CYTOKINE, Vol: 64, Pages: 413-421, ISSN: 1043-4666
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- Citations: 24
O'Cathail SM, Shaboodien R, Mahmoud S, et al., 2013, Intravenous Versus Oral Dexamethasone Premedication in Preventing Paclitaxel Infusion Hypersensitivity Reactions in Gynecological Malignancies, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 23, Pages: 1318-1325, ISSN: 1048-891X
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- Citations: 8
Frede J, Fraser SP, Oskay-Oezcelik G, et al., 2013, Ovarian cancer: Ion channel and aquaporin expression as novel targets of clinical potential, EUROPEAN JOURNAL OF CANCER, Vol: 49, Pages: 2331-2344, ISSN: 0959-8049
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- Citations: 52
Chatterjee J, Hopkins T, Wahba J, et al., 2013, Early stage mucinous ovarian carcinomas: 10 years of experience in a tertiary centre, BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Vol: 120, Pages: 282-283, ISSN: 1470-0328
Fotopoulou C, Spiers L, Pickford E, et al., 2013, Continuous low-flow ascites drainage and sequential non-invasive tumor-cell sampling through the urinary bladder via the alfa-pump closed system in platinum-resistant ovarian cancer (PROC): First clinical experience in a cancer patient., 49th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0732-183X
Pinato DJ, Graham J, Gabra H, et al., 2013, Evolving concepts in the management of drug resistant ovarian cancer: Dose dense chemotherapy and the reversal of clinical platinum resistance, CANCER TREATMENT REVIEWS, Vol: 39, Pages: 153-160, ISSN: 0305-7372
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- Citations: 49
Stemke-Hale K, Shipman K, Kitsou-Mylona I, et al., 2013, Frequency of mutations and polymorphisms in borderline ovarian tumors of known cancer genes, MODERN PATHOLOGY, Vol: 26, Pages: 544-552, ISSN: 0893-3952
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- Citations: 14
Banerjee S, Rustin G, Paul J, et al., 2013, A multicenter, randomized trial of flat dosing versus intrapatient dose escalation of single-agent carboplatin as first-line chemotherapy for advanced ovarian cancer: an SGCTG (SCOTROC 4) and ANZGOG study on behalf of GCIG, ANNALS OF ONCOLOGY, Vol: 24, Pages: 679-687, ISSN: 0923-7534
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- Citations: 35
Shaboodien R, Diamantis N, Blagden S, et al., 2013, Feasibility of Trials in Ovarian Cancer by Line of Therapy and Platinum Sensitivity, INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER, Vol: 23, Pages: 481-487, ISSN: 1048-891X
Singh RK, Mizuno K, Wasmeier C, et al., 2013, Distinct and opposing roles for Rab27a/Mlph/MyoVa and Rab27b/Munc13-4 in mast cell secretion, FEBS JOURNAL, Vol: 280, Pages: 892-903, ISSN: 1742-464X
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- Citations: 60
Chee JLY, Saidin S, Lane DP, et al., 2013, Wild-type and mutant p53 mediate cisplatin resistance through interaction and inhibition of active caspase-9, CELL CYCLE, Vol: 12, Pages: 278-288, ISSN: 1538-4101
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- Citations: 46
Ghazali E, Joel S, Gribben J, et al., 2013, ProGem1: Phase I first-in- human study of the novel nucleotide NUC-1031 in adult patients with advanced solid tumors., 49th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), AMER SOC CLINICAL ONCOLOGY
Recchi C, Seabra MC, 2012, Novel functions for Rab GTPases in multiple aspects of tumour progression, Biochemical Society Transactions, Vol: 40, Pages: 1398-1403, ISSN: 1470-8752
Rab GTPases are master regulators of intracellular trafficking and, in recent years, their role in the control of different aspects of tumour progression has emerged. In the present review, we show that Rab GTPases are disregulated in many cancers and have central roles in tumour cell migration, invasion, proliferation, communication with stromal cells and the development of drug resistance. As a consequence, Rab proteins may be novel potential candidates for the development of anticancer drugs and, in this context, the preliminary results obtained with an inhibitor of Rab function are also discussed.
Perumal M, Stronach EA, Gabra H, et al., 2012, Evaluation of 2-Deoxy-2-[<SUP>18</SUP>F]Fluoro-D-glucose- and 3′-Deoxy-3′-[<SUP>18</SUP>F]Fluorothymidine-Positron Emission Tomography as Biomarkers of Therapy Response in Platinum-Resistant Ovarian Cancer, MOLECULAR IMAGING AND BIOLOGY, Vol: 14, Pages: 753-761, ISSN: 1536-1632
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- Citations: 22
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