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198 results on '"Gore, M.E."'

15. Pathogenesis, clinical evolution and outcomes of patients with immune checkpoint inhibitor induced acute liver injury: A multicentre study

Author

Au, L., primary, Nathwani, R., additional, Possamai, L., additional, Barlow, C., additional, Tillett, T., additional, Bowen, R., additional, Spain, L., additional, Thomas, J., additional, Backhouse, M., additional, Gurung, A., additional, Morrison, R., additional, Cross, T., additional, Herbert, C., additional, Goldin, R., additional, Gore, M.E., additional, Larkin, J., additional, Antoniades, C., additional, and Turajlic, S., additional

Published
2018
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16. MEDIOLA: A phase I/II trial of olaparib (PARP inhibitor) in combination with durvalumab (anti-PD-L1 antibody) in pts with advanced solid tumours – new ovarian cancer cohorts

Author

Penson, R.T., primary, Drew, Y., additional, de Jonge, M.J.A., additional, Hong, S.-H., additional, Park, Y.H., additional, Wolfer, A., additional, Brown, J., additional, Ferguson, M., additional, Gore, M.E., additional, Alvarez, R.H., additional, Kaufman, B., additional, Gresty, C., additional, Angell, H.K., additional, Meyer, K., additional, Lanasa, M., additional, Herbolsheimer, P., additional, and Domchek, S., additional

Published
2018
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17. An open-label, phase II basket study of olaparib and durvalumab (MEDIOLA): Results in germline BRCA -mutated ( gBRCA m) platinum-sensitive relapsed (PSR) ovarian cancer (OC)

Author

Drew, Y., primary, de Jonge, M., additional, Hong, S.H., additional, Park, Y.H., additional, Wolfer, A., additional, Brown, J., additional, Ferguson, M., additional, Gore, M.E., additional, Alvarez, R.H., additional, Gresty, C., additional, Angell, H., additional, Meyer, K., additional, Learoyd, M., additional, Tang, M., additional, Lanasa, M., additional, Herbolsheimer, P., additional, and Domchek, S.M., additional

Published
2018
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22. Assessing the impact of evolving evidence in renal cell carcinoma treatment: An update of the Renal Cell Carcinoma Appropriateness-based Treatment Toolkit (ReCATT)

Author

Gore, M.E., primary, Bellmunt, J., additional, Eisen, T., additional, Escudier, B., additional, Mickisch, G., additional, Patard, J., additional, Porta, C., additional, Ravaud, A., additional, Schmidinger, M., additional, Schöffski, P., additional, Sternberg, C.N., additional, Szczylik, C., additional, Lewis, S., additional, and Kirpekar, S., additional

Published
2014
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27. Intensive treatment of multiple myeloma and criteria for complete remission

Author

Gore, M.E., Viner, C., Meldrum, M., Bell, J., Milan, S., Zuiable, A., Slevin, M., Selby, P.J., Clark, P.I., Millar, B., Maitland, J.A., Judson, I.R., Tillyer, C., Malpas, J.S., and McElwain, T.J.

Subjects
Multiple myeloma -- Care and treatment, Methylprednisolone -- Evaluation, Vincristine -- Evaluation, Melphalan -- Evaluation, Doxorubicin -- Evaluation
Published
1989

28. Cediranib monotherapy in patients with advanced renal cell carcinoma: results of a randomised phase II study.

Author

Mulders, P.F.A., Hawkins, R., Nathan, P., Jong, I. de, Osanto, S., Porfiri, E., Protheroe, A., Herpen, C.M.L. van, Mookerjee, B., Pike, L., Jurgensmeier, J.M., Gore, M.E., Mulders, P.F.A., Hawkins, R., Nathan, P., Jong, I. de, Osanto, S., Porfiri, E., Protheroe, A., Herpen, C.M.L. van, Mookerjee, B., Pike, L., Jurgensmeier, J.M., and Gore, M.E.

Abstract

01 maart 2012, Item does not contain fulltext, BACKGROUND: Cediranib is a highly potent vascular endothelial growth factor (VEGF) signalling inhibitor with activity against VEGF receptors 1, 2 and 3. This Phase II, randomised, double-blind, parallel-group study compared the efficacy of cediranib with placebo in patients with metastatic or recurrent clear cell renal cell carcinoma who had not previously received a VEGF signalling inhibitor. METHODS: Patients were randomised (3:1) to cediranib 45 mg/day or placebo. The primary objective was comparison of change from baseline in tumour size after 12 weeks of therapy. Secondary objectives included response rate and duration, progression-free survival (PFS) and safety and tolerability. Patients in the placebo group could cross over to open-label cediranib at 12 weeks or earlier if their disease had progressed. This study has been completed and is registered with ClinicalTrials.gov, number NCT00423332. FINDINGS: Patients (n=71) were randomised to receive cediranib (n=53) or placebo (n=18). The primary study outcome revealed that, after 12weeks of therapy, there was a significant difference in mean percentage change from baseline in tumour size between the cediranib (-20%) and placebo (+20%) arms (p<0.0001). Eighteen patients (34%) on cediranib achieved a partial response and 25 (47%) experienced stable disease. Cediranib treatment prolonged PFS significantly compared with placebo (hazard ratio (HR)=0.45, 90%confidence interval: 0.26-0.76, p=0.017; median PFS 12.1 versus 2.8 months). The most common adverse events in patients receiving cediranib were diarrhoea (74%), hypertension (64%), fatigue (58%) and dysphonia (58%). INTERPRETATION: Cediranib monotherapy demonstrated significant evidence of antitumour activity in patients with advanced renal cell carcinoma. The adverse event profile was consistent with previous studies of cediranib 45 mg.

Published
2012

29. Common variants at 19p13 are associated with susceptibility to ovarian cancer.

Author

Bolton, K.L., Tyrer, J.P., Song, H., Ramus, S.J., Notaridou, M., Jones, C., Sher, T., Gentry-Maharaj, A., Wozniak, E., Tsai, Y.Y., Weidhaas, J., Paik, D., Berg, D.P.G. van den, Stram, D.O., Pearce, C.L., Wu, A.H., Brewster, W., Anton-Culver, H., Ziogas, A., Narod, S., Levine, D.A., Kaye, S.B., Brown, R., Paul, J., Flanagan, J., Sieh, W., McGuire, V., Whittemore, A.S., Campbell, I., Gore, M.E., Lissowska, J., Yang, H.P., Medrek, K., Gronwald, J., Lubinski, J., Jakubowska, A., Le, N.D., Cook, L.S., Keleman, L.E., Brook-Wilson, A., Massuger, L.F.A.G., Kiemeney, L.A.L.M., Aben, K.K.H., Altena, A.M. van, Houlston, R.S., Tomlinson, I., Palmieri, R.T., Moorman, P.G., Schildkraut, J., Iversen, E.S., Phelan, C.M., Vierkant, R.A., Cunningham, J.M., Goode, E.L., Fridley, B.L., Kruger-Kjaer, S., Blaeker, J., Hogdall, E., Hogdall, C., Gross, J., Karlan, B.Y., Ness, R.B., Edwards, R.P., Odunsi, K., Moyisch, K.B., Baker, J.A., Modugno, F., Heikkinenen, T., Butzow, R., Nevanlinna, H., Leminen, A., Bogdanova, N., Antonenkova, N., Doerk, T., Hillemanns, P., Durst, M., Runnebaum, I., Thompson, P.J., Carney, M.E., Goodman, M.T., Lurie, G., Wang-Gohrke, S., Hein, R., Chang-Claude, J., Rossing, M.A., Cushing-Haugen, K.L., Doherty, J., Chen, C., Rafnar, T., Besenbacher, S., Sulem, P., Stefansson, K., Birrer, M.J., Bolton, K.L., Tyrer, J.P., Song, H., Ramus, S.J., Notaridou, M., Jones, C., Sher, T., Gentry-Maharaj, A., Wozniak, E., Tsai, Y.Y., Weidhaas, J., Paik, D., Berg, D.P.G. van den, Stram, D.O., Pearce, C.L., Wu, A.H., Brewster, W., Anton-Culver, H., Ziogas, A., Narod, S., Levine, D.A., Kaye, S.B., Brown, R., Paul, J., Flanagan, J., Sieh, W., McGuire, V., Whittemore, A.S., Campbell, I., Gore, M.E., Lissowska, J., Yang, H.P., Medrek, K., Gronwald, J., Lubinski, J., Jakubowska, A., Le, N.D., Cook, L.S., Keleman, L.E., Brook-Wilson, A., Massuger, L.F.A.G., Kiemeney, L.A.L.M., Aben, K.K.H., Altena, A.M. van, Houlston, R.S., Tomlinson, I., Palmieri, R.T., Moorman, P.G., Schildkraut, J., Iversen, E.S., Phelan, C.M., Vierkant, R.A., Cunningham, J.M., Goode, E.L., Fridley, B.L., Kruger-Kjaer, S., Blaeker, J., Hogdall, E., Hogdall, C., Gross, J., Karlan, B.Y., Ness, R.B., Edwards, R.P., Odunsi, K., Moyisch, K.B., Baker, J.A., Modugno, F., Heikkinenen, T., Butzow, R., Nevanlinna, H., Leminen, A., Bogdanova, N., Antonenkova, N., Doerk, T., Hillemanns, P., Durst, M., Runnebaum, I., Thompson, P.J., Carney, M.E., Goodman, M.T., Lurie, G., Wang-Gohrke, S., Hein, R., Chang-Claude, J., Rossing, M.A., Cushing-Haugen, K.L., Doherty, J., Chen, C., Rafnar, T., Besenbacher, S., Sulem, P., Stefansson, K., and Birrer, M.J.

Abstract

Contains fulltext : 89441.pdf (publisher's version ) (Closed access)

Published
2010

30. A genome-wide association study identifies susceptibility loci for ovarian cancer at 2q31 and 8q24.

Author

Goode, E.L., Chenevix-Trench, G., Song, H., Ramus, S.J., Notaridou, M., Lawrenson, K., Widschwendter, M., Vierkant, R.A., Larson, M.C., Kjaer, S.K., Birrer, M.J., Berchuck, A., Schildkraut, J., Tomlinson, I.P., Kiemeney, L.A.L.M., Cook, L.S., Gronwald, J., Garcia-Closas, M., Gore, M.E., Campbell, I., Whittemore, A.S., Sutphen, R., Phelan, C.M., Anton-Culver, H., Pearce, C.L., Lambrechts, D., Rossing, M.A., Chang-Claude, J., Moysich, K.B., Goodman, M.T., Dork, T., Nevanlinna, H., Ness, R.B., Rafnar, T., Hogdall, E., Fridley, B.L., Cunningham, J.M., Sieh, W., McGuire, V., Godwin, A.K., Cramer, D.W, Hernandez, D., Levine, D., Lu, K., Iversen, E.S., Palmieri, R.T., Houlston, R.S., Altena, A.M. van, Aben, K.K.H., Massuger, L.F.A.G., Brooks-Wilson, A., Kelemen, L.E., Le, N.D., Jakubowska, A., Lubinski, J., Medrek, K., Stafford, A., Easton, D.F., Tyrer, J.P., Bolton, K.L., Harrington, P., Eccles, D., Chen, A., Molina, A.N., Davila, B.N., Arango, H., Tsai, Y.Y., Chen, Z., Risch, H.A., McLaughlin, J., Narod, S., Ziogas, A., Brewster, W., Gentry-Maharaj, A., Menon, U., Wu, A.H., Stram, D.O., Pike, M.C., Beesley, J., Webb, P.M., Chen, X., Ekici, A.B., Thiel, F.C., Beckmann, M.W., Yang, H., Wentzensen, N., Lissowska, J., Fasching, P.A., Despierre, E., Amant, F., Vergote, I., Doherty, J., Hein, R., Wang-Gohrke, S., Lurie, G., Carney, M.E., Thompson, P., Goode, E.L., Chenevix-Trench, G., Song, H., Ramus, S.J., Notaridou, M., Lawrenson, K., Widschwendter, M., Vierkant, R.A., Larson, M.C., Kjaer, S.K., Birrer, M.J., Berchuck, A., Schildkraut, J., Tomlinson, I.P., Kiemeney, L.A.L.M., Cook, L.S., Gronwald, J., Garcia-Closas, M., Gore, M.E., Campbell, I., Whittemore, A.S., Sutphen, R., Phelan, C.M., Anton-Culver, H., Pearce, C.L., Lambrechts, D., Rossing, M.A., Chang-Claude, J., Moysich, K.B., Goodman, M.T., Dork, T., Nevanlinna, H., Ness, R.B., Rafnar, T., Hogdall, E., Fridley, B.L., Cunningham, J.M., Sieh, W., McGuire, V., Godwin, A.K., Cramer, D.W, Hernandez, D., Levine, D., Lu, K., Iversen, E.S., Palmieri, R.T., Houlston, R.S., Altena, A.M. van, Aben, K.K.H., Massuger, L.F.A.G., Brooks-Wilson, A., Kelemen, L.E., Le, N.D., Jakubowska, A., Lubinski, J., Medrek, K., Stafford, A., Easton, D.F., Tyrer, J.P., Bolton, K.L., Harrington, P., Eccles, D., Chen, A., Molina, A.N., Davila, B.N., Arango, H., Tsai, Y.Y., Chen, Z., Risch, H.A., McLaughlin, J., Narod, S., Ziogas, A., Brewster, W., Gentry-Maharaj, A., Menon, U., Wu, A.H., Stram, D.O., Pike, M.C., Beesley, J., Webb, P.M., Chen, X., Ekici, A.B., Thiel, F.C., Beckmann, M.W., Yang, H., Wentzensen, N., Lissowska, J., Fasching, P.A., Despierre, E., Amant, F., Vergote, I., Doherty, J., Hein, R., Wang-Gohrke, S., Lurie, G., Carney, M.E., and Thompson, P.

Abstract

Contains fulltext : 89180.pdf (publisher's version ) (Closed access)

Published
2010

31. Interferon alfa-2a versus combination therapy with interferon alfa-2a, interleukin-2, and fluorouracil in patients with untreated metastatic renal cell carcinoma (MRC RE04/EORTC GU 30012): an open-label randomised trial.

Author

Gore, M.E., Griffin, C.L., Hancock, B., Patel, P.M., Pyle, L., Aitchison, M., James, N., Oliver, R.T.D., Mardiak, J., Hussain, T., Sylvester, R., Parmar, M.K., Royston, P., Mulders, P.F.A., Gore, M.E., Griffin, C.L., Hancock, B., Patel, P.M., Pyle, L., Aitchison, M., James, N., Oliver, R.T.D., Mardiak, J., Hussain, T., Sylvester, R., Parmar, M.K., Royston, P., and Mulders, P.F.A.

Abstract

Item does not contain fulltext, BACKGROUND: In metastatic renal cell carcinoma combinations of interferon alfa-2a, interleukin-2, and fluorouracil produce higher response rates and longer progression-free survival than do single agents. We aimed to compare overall survival in patients receiving combination treatment or interferon alfa-2a. METHODS: RE04/30012 was an open-label randomised trial undertaken in 50 centres across eight countries. 1006 treatment-naive patients diagnosed with advanced metastatic renal cell carcinoma were randomly allocated (1 to 1) by minimisation to receive interferon alfa-2a alone or combination therapy with interferon alfa-2a, interleukin-2, and fluorouracil. Treatment was not masked. The primary endpoint was overall survival. Treatment groups were compared with a non-stratified log-rank test. Analysis was by intention to treat. This study is registered, number ISRCTN 46518965. FINDINGS: 502 patients were randomly assigned to receive interferon alfa-2a and 504 to receive combined treatment. Median follow-up was 37.2 months (24.8-52.3). Median overall survival was 18.8 months (17.0-23.2) for patients receiving interferon alfa-2a versus 18.6 months (16.5-20.6) for those receiving combination therapy. Overall survival did not differ between the two groups (hazard ratio 1.05 [95% CI 0.90-1.21], p=0.55; absolute difference 0.3% (-5.1 to 5.6) at 1 year and 2.7% (-8.2 to 2.9) at 3 years). Serious adverse events were reported in 113 (23%) patients receiving interferon alfa-2a and 131 (26%) of those receiving combined treatment. INTERPRETATION: Although combination therapy does not improve overall or progression-free survival compared with interferon alfa-2a alone, immunotherapy might still have a role because it can produce remissions that are of clinically relevant length in some patients. Identification of patients who will benefit from immunotherapy is crucial. FUNDING: UK Medical Research Council.

Published
2010

32. Establishing the role of cytokine therapy in advanced renal cell carcinoma.

Author

Gore, M.E., Mulder, P.H.M. de, Gore, M.E., and Mulder, P.H.M. de

Abstract

Item does not contain fulltext, Tribute to Professor Pieter De Mulder, from Martin Gore. Pieter and I were often pitted against each other in debates at international meetings on the role of cytokine therapy. The truth is that there was little disagreement between us, but we both thought such set pieces were a good way to highlight the issues surrounding the use of cytokines. He wanted our true joint view to be put on record, and the result is this article. Pieter himself suffered from kidney cancer for many years and he died in April as we were putting the finishing touches to this manuscript. Pieter was a remarkable man in so many ways. He was a physician of great compassion, immense intellect, utter integrity and unshakeable scientific rigor. These qualities meant that his perspective on many clinical controversies was in great demand internationally. The European oncology community has lost one of its giants and I, a dear friend. This manuscript is dedicated to the memory of Professor Pieter de Mulder.

Published
2008

34. Docetaxel in platiunim-pretreated patients

Author

Piccart, M.J., Rustin, G.J.S., Gore, M.E., ten Bokkel Huinink, W., van Oosterom, Allan T., van der Burg, M.E.L., Nelstrop, A., Selleslags, J., te Velde, A., Wanders, J., and Kaye, S.B.

Published
1996

44. 1006 ORAL Prognostic Factors for Progression-free Survival (PFS), Overall Survival (OS), and Long-term OS (LT-OS) With Sunitinib in 1,059 Patients, Treated on Clinical Trials, With Metastatic Renal Cell Carcinoma (mRCC)

Author

Motzer, R.J., primary, Escudier, B., additional, Bukowski, R., additional, Rini, B.I., additional, Hutson, T.E., additional, Barrios, C.H., additional, Lin, X., additional, Fly, K., additional, Matczak, E., additional, and Gore, M.E., additional

Published
2011
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45. Revised U.K. guidelines for the management of cutaneous melanoma 2010

Author

Marsden, J.R., primary, Newton-Bishop, J.A., additional, Burrows, L., additional, Cook, M., additional, Corrie, P.G., additional, Cox, N.H., additional, Gore, M.E., additional, Lorigan, P., additional, MacKie, R., additional, Nathan, P., additional, Peach, H., additional, Powell, B., additional, and Walker, C., additional

Published
2010
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48. Tumour necrosis factor, cholestatic jaundice, and chronic liver disease

Author

Jones, A., Selby, P.J., Viner, C., Hobbs, S., Gore, M.E., and McElwain, T.J.

Subjects
Liver function tests -- Abnormalities, Tumor necrosis factor -- Adverse and side effects, Mutation breeding -- Usage, Jaundice -- Causes of, Health
Abstract

Tumor necrosis factor (TNF) is a protein produced by activated macrophages (immune system cells) in response to circulating toxins. One important physiological effect of TNF is to produce necrosis (tissue death) of experimentally induced tumors. With the cloning of the gene for human TNF, large quantities of the substance have become available, and experiments have been carried out investigating its possible use as an anti-cancer agent. The authors discuss previous studies of TNF performed by themselves and others. Complications of this treatment regimen, especially alterations in the levels of liver enzymes, were reported. Patients developed hyperbilirubinemia (high blood levels of bilirubin, a liver bile constituent), as well as jaundice induced by inhibition of bile flow (cholestatic jaundice). The possibility that these effects were caused by spread of the cancer to the liver was ruled out by noting the abatement of liver symptoms with cessation of TNF treatment. Liver biopsies were not performed, so no biochemical or microscopic analysis of liver tissue was possible in these cases. The observations suggest that TNF has direct pathogenic effects on the liver, and the hypothesis is put forward that disruptions in liver function seen in conditions where TNF levels would be increased (following viral infections, in liver failure, and in chronic liver disease) may be directly attributable to TNF. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

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