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1. Tumor evolution metrics predict recurrence beyond 10 years in locally advanced prostate cancer

Author

Fernandez-Mateos, J, Cresswell, G, Trahearn, N, Webb, K, Sakr, C, Lampis, A, Stuttle, C, Corbishley, C, Stavrinides, V, Zapata, L, Spiteri, I, Heide, T, Gallagher, L, James, C, Ramazzotti, D, Gao, A, Kote-Jarai, Z, Acar, A, Truelove, L, Proszek, P, Murray, J, Reid, A, Wilkins, A, Hubank, M, Eeles, R, Dearnaley, D, Sottoriva, A, Fernandez-Mateos, Javier, Cresswell, George D., Trahearn, Nicholas, Webb, Katharine, Sakr, Chirine, Lampis, Andrea, Stuttle, Christine, Corbishley, Catherine M., Stavrinides, Vasilis, Zapata, Luis, Spiteri, Inmaculada, Heide, Timon, Gallagher, Lewis, James, Chela, Ramazzotti, Daniele, Gao, Annie, Kote-Jarai, Zsofia, Acar, Ahmet, Truelove, Lesley, Proszek, Paula, Murray, Julia, Reid, Alison, Wilkins, Anna, Hubank, Michael, Eeles, Ros, Dearnaley, David, Sottoriva, Andrea, Fernandez-Mateos, J, Cresswell, G, Trahearn, N, Webb, K, Sakr, C, Lampis, A, Stuttle, C, Corbishley, C, Stavrinides, V, Zapata, L, Spiteri, I, Heide, T, Gallagher, L, James, C, Ramazzotti, D, Gao, A, Kote-Jarai, Z, Acar, A, Truelove, L, Proszek, P, Murray, J, Reid, A, Wilkins, A, Hubank, M, Eeles, R, Dearnaley, D, Sottoriva, A, Fernandez-Mateos, Javier, Cresswell, George D., Trahearn, Nicholas, Webb, Katharine, Sakr, Chirine, Lampis, Andrea, Stuttle, Christine, Corbishley, Catherine M., Stavrinides, Vasilis, Zapata, Luis, Spiteri, Inmaculada, Heide, Timon, Gallagher, Lewis, James, Chela, Ramazzotti, Daniele, Gao, Annie, Kote-Jarai, Zsofia, Acar, Ahmet, Truelove, Lesley, Proszek, Paula, Murray, Julia, Reid, Alison, Wilkins, Anna, Hubank, Michael, Eeles, Ros, Dearnaley, David, and Sottoriva, Andrea

Abstract

Cancer evolution lays the groundwork for predictive oncology. Testing evolutionary metrics requires quantitative measurements in controlled clinical trials. We mapped genomic intratumor heterogeneity in locally advanced prostate cancer using 642 samples from 114 individuals enrolled in clinical trials with a 12-year median follow-up. We concomitantly assessed morphological heterogeneity using deep learning in 1,923 histological sections from 250 individuals. Genetic and morphological (Gleason) diversity were independent predictors of recurrence (hazard ratio (HR) = 3.12 and 95% confidence interval (95% CI) = 1.34-7.3; HR = 2.24 and 95% CI = 1.28-3.92). Combined, they identified a group with half the median time to recurrence. Spatial segregation of clones was also an independent marker of recurrence (HR = 2.3 and 95% CI = 1.11-4.8). We identified copy number changes associated with Gleason grade and found that chromosome 6p loss correlated with reduced immune infiltration. Matched profiling of relapse, decades after diagnosis, confirmed that genomic instability is a driving force in prostate cancer progression. This study shows that combining genomics with artificial intelligence-aided histopathology leads to the identification of clinical biomarkers of evolution.

Published
2024

7. Challenges and Solutions during the COVID Pandemic for Patient Retention and Physician Engagement in the Phase 3 ATLAS Study of Apalutamide Added to Androgen Deprivation Therapy (ADT) in High-Risk Localized or Locally Advanced Prostate Cancer (HRLPC)

Author

Sandler, H.M., primary, Shore, N., additional, Dearnaley, D., additional, Freedland, S.J., additional, Smith, M.R., additional, Rosales, R., additional, Brookman-May, S.D., additional, Dicker, A.P., additional, McKenzie, M.R., additional, Bossi, A., additional, Widmark, A., additional, Wiegel, T., additional, Martin, J., additional, Miladinovic, B., additional, Lefresne, F., additional, Ciprotti, M., additional, McCarthy, S.A., additional, Mundle, S.D., additional, Tombal, B.F., additional, and Feng, F.Y., additional

Published
2022
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8. Sequencing of Androgen Deprivation Therapy of Short Duration with Radiotherapy for Non-Metastatic Prostate Cancer (SANDSTORM): A Pooled Analysis of 12 Randomized Trials

Author

Ma, T.M., primary, Sun, Y., additional, Romero, T., additional, Dearnaley, D., additional, Tree, A., additional, Bolla, M., additional, de Reijke, T.M., additional, Maingon, P., additional, Neven, A., additional, Zapatero, A., additional, Malone, S., additional, Roy, S., additional, Sydes, M., additional, Nabid, A., additional, Sandler, H.M., additional, Roach, M., additional, Pisansky, T.M., additional, Spratt, D.E., additional, and Kishan, A.U., additional

Published
2022
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9. 1375P Intermediate clinical endpoints (ICE) as potential surrogates for overall survival (OS) in men with metastatic hormone-sensitive prostate cancer (mHSPC)

Author

Halabi, S., primary, Roy, A., additional, Rydzewska, L., additional, Godolphin, P., additional, Parmar, M.K., additional, Hussain, M., additional, Tangen, C., additional, Thompson, I.M., additional, Xie, W., additional, Carducci, M.A., additional, Smith, M., additional, Morris, M.J., additional, Gravis Mescam, G., additional, Dearnaley, D., additional, Verhagen, P., additional, Goto, T., additional, James, N.D., additional, Buyse, M.E., additional, Tierney, J., additional, and Sweeney, C.J., additional

Published
2022
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11. Natural History after Likely Cure vs. Recurrence vs. after ProsTate RadiOtheRapy (RAPTOR): A Pooled Analysis of More than 13000 Patients from 21 Randomized Controlled Trials

Author

Roy, S., Romero, T., Roach, M., III, Michalski, J.M., Joseph, D.J., Dearnaley, D., Tree, A., Incrocci, L., Heemsbergen, W., Bolla, M., Nabid, A., Armstrong, J.G., Malone, S., Horwitz, E.M., Wong, J.K., Arcangeli, S., Sanguineti, G., Zapatero, A., Spratt, D.E., and Kishan, A.U.

Published
2024
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16. Observation versus screening spinal MRI and pre-emptive treatment for spinal cord compression in patients with castration-resistant prostate cancer and spinal metastases in the UK (PROMPTS): an open-label, randomised, controlled, phase 3 trial

Author

Dearnaley, D, Hinder, V, Hijab, A, Horan, G, Srihari, N, Rich, P, Houston, JG, Henry, AM, Gibbs, S, Venkitaraman, R, Cruickshank, C, Hassan, S, Miners, A, Mason, M, Pedley, I, Payne, H, Brock, S, Wade, R, Robinson, A, Din, O, Lees, K, Graham, J, Worlding, J, Murray, J, Parker, C, Griffin, C, Sohaib, A, Hall, E, and PROMPTS investigators

Abstract

Background Early diagnosis of malignant spinal cord compression (SCC) is crucial because pretreatment neurological status is the major determinant of outcome. In metastatic castration-resistant prostate cancer, SCC is a clinically significant cause of disease-related morbidity and mortality. We investigated whether screening for SCC with spinal MRI, and pre-emptive treatment if radiological SCC (rSCC) was detected, reduced the incidence of clinical SCC (cSCC) in asymptomatic patients with metastatic castration-resistant prostate cancer and spinal metastasis. Methods We did a parallel-group, open-label, randomised, controlled, phase 3, superiority trial. Patients with metastatic castration-resistant prostate cancer were recruited from 45 National Health Service hospitals in the UK. Eligible patients were aged at least 18 years, with an Eastern Co-operative Oncology Group performance status of 0–2, asymptomatic spinal metastasis, no previous SCC, and no spinal MRI in the past 12 months. Participants were randomly assigned (1:1), using a minimisation algorithm with a random element (balancing factors were treatment centre, alkaline phosphatase [normal vs raised, with the upper limit of normal being defined at each participating laboratory], number of previous systemic treatments [first-line vs second-line or later], previous spinal treatment, and imaging of thorax and abdomen), to no MRI (control group) or screening spinal MRI (intervention group). Serious adverse events were monitored in the 24 h after screening MRI in the intervention group. Participants with screen-detected rSCC were offered pre-emptive treatment (radiotherapy or surgical decompression was recommended per treating physician's recommendation) and 6-monthly spinal MRI. All patients were followed up every 3 months, and then at month 30 and 36. The primary endpoint was time to and incidence of confirmed cSCC in the intention-to-treat population (defined as all patients randomly assigned), with the primary timepoint of interest being 1 year after randomisation. The study is registered with ISRCTN, ISRCTN74112318, and is now complete. Findings Between Feb 26, 2013, and April 25, 2017, 420 patients were randomly assigned to the control (n=210) or screening MRI (n=210) groups. Median age was 74 years (IQR 68 to 79), 222 (53%) of 420 patients had normal alkaline phosphatase, and median prostate-specific antigen concentration was 48 ng/mL (IQR 17 to 162). Screening MRI detected rSCC in 61 (31%) of 200 patients with assessable scans in the intervention group. As of data cutoff (April 23, 2020), at a median follow-up of 22 months (IQR 13 to 31), time to cSCC was not significantly improved with screening (hazard ratio 0·64 [95% CI 0·37 to 1·11]; Gray's test p=0·12). 1-year cSCC rates were 6·7% (95% CI 3·8–10·6; 14 of 210 patients) for the control group and 4·3% (2·1–7·7; nine of 210 patients) for the intervention group (difference −2·4% [95% CI −4·2 to 0·1]). Median time to cSCC was not reached in either group. No serious adverse events were reported within 24 h of screening. Interpretation Despite the substantial incidence of rSCC detected in the intervention group, the rate of cSCC in both groups was low at a median of 22 months of follow-up. Routine use of screening MRI and pre-emptive treatment to prevent cSCC is not warranted in patients with asymptomatic castration-resistant prostate cancer with spinal metastasis. Funding Cancer Research UK.

Published
2022

17. A prospective prostate cancer screening programme for men with pathogenic variants in mismatch repair genes (IMPACT): initial results from an international prospective study.

Author

Bancroft E.K., Page E.C., Brook M.N., Thomas S., Taylor N., Pope J., McHugh J., Jones A.-B., Karlsson Q., Merson S., Ong K.R., Hoffman J., Huber C., Maehle L., Grindedal E.M., Stormorken A., Evans D.G., Rothwell J., Lalloo F., Brady A.F., Bartlett M., Snape K., Hanson H., James P., McKinley J., Mascarenhas L., Syngal S., Ukaegbu C., Side L., Thomas T., Barwell J., Teixeira M.R., Izatt L., Suri M., Macrae F.A., Poplawski N., Chen-Shtoyerman R., Ahmed M., Musgrave H., Nicolai N., Greenhalgh L., Brewer C., Pachter N., Spigelman A.D., Azzabi A., Helfand B.T., Halliday D., Buys S., Ramon Y Cajal T., Donaldson A., Cooney K.A., Harris M., McGrath J., Davidson R., Taylor A., Cooke P., Myhill K., Hogben M., Aaronson N.K., Ardern-Jones A., Bangma C.H., Castro E., Dearnaley D., Dias A., Dudderidge T., Eccles D.M., Green K., Eyfjord J., Falconer A., Foster C.S., Gronberg H., Hamdy F.C., Johannsson O., Khoo V., Lilja H., Lindeman G.J., Lubinski J., Axcrona K., Mikropoulos C., Mitra A.V., Moynihan C., Ni Raghallaigh H., Rennert G., Collier R., Offman J., Kote-Jarai Z., Eeles R.A., Bancroft E.K., Page E.C., Brook M.N., Thomas S., Taylor N., Pope J., McHugh J., Jones A.-B., Karlsson Q., Merson S., Ong K.R., Hoffman J., Huber C., Maehle L., Grindedal E.M., Stormorken A., Evans D.G., Rothwell J., Lalloo F., Brady A.F., Bartlett M., Snape K., Hanson H., James P., McKinley J., Mascarenhas L., Syngal S., Ukaegbu C., Side L., Thomas T., Barwell J., Teixeira M.R., Izatt L., Suri M., Macrae F.A., Poplawski N., Chen-Shtoyerman R., Ahmed M., Musgrave H., Nicolai N., Greenhalgh L., Brewer C., Pachter N., Spigelman A.D., Azzabi A., Helfand B.T., Halliday D., Buys S., Ramon Y Cajal T., Donaldson A., Cooney K.A., Harris M., McGrath J., Davidson R., Taylor A., Cooke P., Myhill K., Hogben M., Aaronson N.K., Ardern-Jones A., Bangma C.H., Castro E., Dearnaley D., Dias A., Dudderidge T., Eccles D.M., Green K., Eyfjord J., Falconer A., Foster C.S., Gronberg H., Hamdy F.C., Johannsson O., Khoo V., Lilja H., Lindeman G.J., Lubinski J., Axcrona K., Mikropoulos C., Mitra A.V., Moynihan C., Ni Raghallaigh H., Rennert G., Collier R., Offman J., Kote-Jarai Z., and Eeles R.A.

Abstract

BACKGROUND: Lynch syndrome is a rare familial cancer syndrome caused by pathogenic variants in the mismatch repair genes MLH1, MSH2, MSH6, or PMS2, that cause predisposition to various cancers, predominantly colorectal and endometrial cancer. Data are emerging that pathogenic variants in mismatch repair genes increase the risk of early-onset aggressive prostate cancer. The IMPACT study is prospectively assessing prostate-specific antigen (PSA) screening in men with germline mismatch repair pathogenic variants. Here, we report the usefulness of PSA screening, prostate cancer incidence, and tumour characteristics after the first screening round in men with and without these germline pathogenic variants. METHOD(S): The IMPACT study is an international, prospective study. Men aged 40-69 years without a previous prostate cancer diagnosis and with a known germline pathogenic variant in the MLH1, MSH2, or MSH6 gene, and age-matched male controls who tested negative for a familial pathogenic variant in these genes were recruited from 34 genetic and urology clinics in eight countries, and underwent a baseline PSA screening. Men who had a PSA level higher than 3.0 ng/mL were offered a transrectal, ultrasound-guided, prostate biopsy and a histopathological analysis was done. All participants are undergoing a minimum of 5 years' annual screening. The primary endpoint was to determine the incidence, stage, and pathology of screening-detected prostate cancer in carriers of pathogenic variants compared with non-carrier controls. We used Fisher's exact test to compare the number of cases, cancer incidence, and positive predictive values of the PSA cutoff and biopsy between carriers and non-carriers and the differences between disease types (ie, cancer vs no cancer, clinically significant cancer vs no cancer). We assessed screening outcomes and tumour characteristics by pathogenic variant status. Here we present results from the first round of PSA screening in the IMPACT study. This

Published
2022

19. OC-0105 PROMPTS RCT of screening MRI for spinal cord compression in prostate cancer (ISRCTN74112318)

Author

Dearnaley, D., primary, Hinder, V., additional, Hijab, A., additional, Horan, G., additional, Srihari, N., additional, Rich, P., additional, Houston, G., additional, Henry, A., additional, Gibbs, S., additional, Venkitaraman, R., additional, Cruickshank, C., additional, Hassan, S., additional, Mason, M., additional, Pedley, I., additional, Payne, H., additional, Brock, S., additional, Wade, R., additional, Robinson, A., additional, Din, O., additional, Lees, K., additional, Murray, J., additional, Parker, C., additional, Griffin, C., additional, Sohaib, A., additional, and Hall, E., additional

Published
2022
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23. Prevalence of the HOXB13 G84E germline mutation in British men and correlation with prostate cancer risk, tumour characteristics and clinical outcomes

Author

Kote-Jarai, Z., Mikropoulos, C., Leongamornlert, D. A., Dadaev, T., Tymrakiewicz, M., Saunders, E. J., Jones, M., Jugurnauth-Little, S., Govindasami, K., Guy, M., Hamdy, F. C., Donovan, J. L., Neal, D. E., Lane, J. A., Dearnaley, D., Wilkinson, R. A., Sawyer, E. J., Morgan, A., Antoniou, A. C., Eeles, R. A., Hall, Per, Berchuck, Andrew, Dennis, Joe, Dunning, Alison M., Lee, Andrew, Dicks, Ed, Simard, Jacques, Tessier, Daniel C., Bacot, Francois, Vincent, Daniel, LaBoissière, Sylvie, Robidoux, Frederic, Bojesen, Stig E., Nielsen, Sune F., and Nordestgaard, Borge G.

Published
2015
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32. A prospective prostate cancer screening programme for men with pathogenic variants in mismatch repair genes (IMPACT): initial results from an international prospective study

Author

Bancroft, EK, Page, EC, Brook, MN, Thomas, S, Taylor, N, Pope, J, McHugh, J, Jones, A-B, Karlsson, Q, Merson, S, Ong, KR, Hoffman, J, Huber, C, Maehle, L, Grindedal, EM, Stormorken, A, Evans, DG, Rothwell, J, Lalloo, F, Brady, AF, Bartlett, M, Snape, K, Hanson, H, James, P, McKinley, J, Mascarenhas, L, Syngal, S, Ukaegbu, C, Side, L, Thomas, T, Barwell, J, Teixeira, MR, Izatt, L, Suri, M, Macrae, FA, Poplawski, N, Chen-Shtoyerman, R, Ahmed, M, Musgrave, H, Nicolai, N, Greenhalgh, L, Brewer, C, Pachter, N, Spigelman, AD, Azzabi, A, Helfand, BT, Halliday, D, Buys, S, Cajal, TRY, Donaldson, A, Cooney, KA, Harris, M, McGrath, J, Davidson, R, Taylor, A, Cooke, P, Myhill, K, Hogben, M, Aaronson, NK, Ardern-Jones, A, Bangma, CH, Castro, E, Dearnaley, D, Dias, A, Dudderidge, T, Eccles, DM, Green, K, Eyfjord, J, Falconer, A, Foster, CS, Gronberg, H, Hamdy, FC, Johannsson, O, Khoo, V, Lilja, H, Lindeman, GJ, Lubinski, J, Axcrona, K, Mikropoulos, C, Mitra, A, Moynihan, C, Raghallaigh, HN, Rennert, G, Collier, R, Offman, J, Kote-Jarai, Z, Eeles, RA, Bancroft, EK, Page, EC, Brook, MN, Thomas, S, Taylor, N, Pope, J, McHugh, J, Jones, A-B, Karlsson, Q, Merson, S, Ong, KR, Hoffman, J, Huber, C, Maehle, L, Grindedal, EM, Stormorken, A, Evans, DG, Rothwell, J, Lalloo, F, Brady, AF, Bartlett, M, Snape, K, Hanson, H, James, P, McKinley, J, Mascarenhas, L, Syngal, S, Ukaegbu, C, Side, L, Thomas, T, Barwell, J, Teixeira, MR, Izatt, L, Suri, M, Macrae, FA, Poplawski, N, Chen-Shtoyerman, R, Ahmed, M, Musgrave, H, Nicolai, N, Greenhalgh, L, Brewer, C, Pachter, N, Spigelman, AD, Azzabi, A, Helfand, BT, Halliday, D, Buys, S, Cajal, TRY, Donaldson, A, Cooney, KA, Harris, M, McGrath, J, Davidson, R, Taylor, A, Cooke, P, Myhill, K, Hogben, M, Aaronson, NK, Ardern-Jones, A, Bangma, CH, Castro, E, Dearnaley, D, Dias, A, Dudderidge, T, Eccles, DM, Green, K, Eyfjord, J, Falconer, A, Foster, CS, Gronberg, H, Hamdy, FC, Johannsson, O, Khoo, V, Lilja, H, Lindeman, GJ, Lubinski, J, Axcrona, K, Mikropoulos, C, Mitra, A, Moynihan, C, Raghallaigh, HN, Rennert, G, Collier, R, Offman, J, Kote-Jarai, Z, and Eeles, RA

Abstract

BACKGROUND: Lynch syndrome is a rare familial cancer syndrome caused by pathogenic variants in the mismatch repair genes MLH1, MSH2, MSH6, or PMS2, that cause predisposition to various cancers, predominantly colorectal and endometrial cancer. Data are emerging that pathogenic variants in mismatch repair genes increase the risk of early-onset aggressive prostate cancer. The IMPACT study is prospectively assessing prostate-specific antigen (PSA) screening in men with germline mismatch repair pathogenic variants. Here, we report the usefulness of PSA screening, prostate cancer incidence, and tumour characteristics after the first screening round in men with and without these germline pathogenic variants. METHODS: The IMPACT study is an international, prospective study. Men aged 40-69 years without a previous prostate cancer diagnosis and with a known germline pathogenic variant in the MLH1, MSH2, or MSH6 gene, and age-matched male controls who tested negative for a familial pathogenic variant in these genes were recruited from 34 genetic and urology clinics in eight countries, and underwent a baseline PSA screening. Men who had a PSA level higher than 3·0 ng/mL were offered a transrectal, ultrasound-guided, prostate biopsy and a histopathological analysis was done. All participants are undergoing a minimum of 5 years' annual screening. The primary endpoint was to determine the incidence, stage, and pathology of screening-detected prostate cancer in carriers of pathogenic variants compared with non-carrier controls. We used Fisher's exact test to compare the number of cases, cancer incidence, and positive predictive values of the PSA cutoff and biopsy between carriers and non-carriers and the differences between disease types (ie, cancer vs no cancer, clinically significant cancer vs no cancer). We assessed screening outcomes and tumour characteristics by pathogenic variant status. Here we present results from the first round of PSA screening in the IMPACT study. This s

Published
2021

33. 1837P Assessing PSA

Author

Halabi, S., Roy, A., Guo, S., Rydzewska, L., Godolphin, P.J., Parmar, M.K., Hussain, M., Tangen, C., Thompson, I.M., Carducci, M.A., Smith, M.R., Morris, M.J., Gravis, G., Dearnaley, D., Verhagen, P., Goto, T., James, N.D., Buyse, M.E., Tierney, J., and Sweeney, C.

Published
2023
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37. Hormone-sensitive prostate cancer: a case of ETS gene fusion heterogeneity

Author

Attard, G., Jameson, C., Moreira, J., Flohr, P., Parker, C., Dearnaley, D., Cooper, C.S., and de Bono, J.S.

Subjects
Prostate cancer -- Diagnosis, Prostate cancer -- Demographic aspects, Prostate cancer -- Prognosis, Prostate cancer -- Genetic aspects, Hormones -- Research, Gene fusion -- Research, Health
Published
2009

38. The Intensity-Modulated Pelvic Node and Bladder Radiotherapy (IMPART) Trial:A Phase II Single-Centre Prospective Study

Author

Tan, M. P., Harris, V., Warren-Oseni, K., McDonald, F., McNair, H., Taylor, H., Hansen, V., Sharabiani, M., Thomas, K., Jones, K., Dearnaley, D., Hafeez, S., and Huddart, R. A.

Subjects
Bladder cancer, IMRT, pelvic nodes, radiotherapy
Abstract

Aims: Node-positive bladder cancer (NPBC) carries a poor prognosis and has traditionally been treated palliatively. However, surgical series suggest that a subset of NPBC patients can achieve long-term control after cystectomy and lymph node dissection. There is little published data regarding the use of radiotherapy to treat NPBC patients. This is in part due to concerns regarding the toxicity of whole-pelvis radiotherapy using conventional techniques. We hypothesised that, using intensity-modulated radiotherapy (IMRT), the pelvic nodes and bladder could be treated within a radical treatment volume with acceptable toxicity profiles. Materials and methods: The Intensity-modulated Pelvic Node and Bladder Radiotherapy (IMPART) trial was a phase II single-centre prospective study designed to assess the feasibility of delivering IMRT to treat the bladder and pelvic nodes in patients with node-positive or high-risk node-negative bladder cancer (NNBC). The primary end point was meeting predetermined dose constraints. Secondary end points included acute and late toxicity, pelvic relapse-free survival and overall survival. Results: In total, 38 patients were recruited and treated between June 2009 and November 2012; 22/38 (58%) had NPBC; 31/38 (81.6%) received neoadjuvant chemotherapy; 18/38 (47%) received concurrent chemotherapy; 37/38 (97%) patients had radiotherapy planned as per protocol. Grade 3 gastrointestinal and genitourinary acute toxicity rates were 5.4 and 20.6%, respectively. At 1 year, the grade 3 late toxicity rate was 5%; 1-, 2- and 5-year pelvic relapse-free survival rates were 55, 37 and 26%, respectively. The median overall survival was 1.9 years (95% confidence interval 1.1–3.8) with 1-, 2- and 5-year overall survival rates of 68, 50 and 34%, respectively. Conclusion: Delivering IMRT to the bladder and pelvic nodes in NPBC and high-risk NNBC is feasible, with low toxicity and low pelvic nodal recurrence rates. Long-term control seems to be achievable in a subset of patients. However, relapse patterns suggest that strategies targeting both local recurrence and the development of distant metastases are required to improve patient outcomes.

Published
2020

40. Processing of radical prostatectomy specimens for correlation of data from histopatological, molecular biological, and radiological studies: a new whole organ technique

Author

JhEeles, R Avar, S G, Fisher, C, Jackson, S A, Reinsberg, S A, Dennis, N, Falconer, A, Dearnaley, D, Edwards, S M, Leach, M O, Edwards, S E, Cummings, C, Christmas,, T, Thompson, A, Woodhouse, C, Sandhu, S, Cooper, C S, and Eeles, R A

Subjects
Tissue microarrays -- Research, Tissue microarrays -- Diagnosis, Prostatectomy -- Methods, Prostatectomy -- Research, Prostate cancer -- Research, Prostate cancer -- Prognosis, Prostate cancer -- Diagnosis, Preoperative care -- Methods, Preoperative care -- Analysis, Pathology, Molecular -- Diagnosis, Pathology, Molecular -- Research, Pathology, Molecular -- Analysis, Health
Published
2005

50. Targeted prostate cancer screening in men with mutations in BRCA1 and BRCA2 detects aggressive prostate cancer: preliminary analysis of the results of the IMPACT study

Author

Mitra, Anita V., Bancroft, Elizabeth K., Barbachano, Yolanda, Page, Elizabeth C., Foster, C. S., Jameson, C., Mitchell, G., Lindeman, G. J., Stapleton, A., Suthers, G., Evans, D. G., Cruger, D., Blanco, I., Mercer, C., Kirk, J., Maehle, L., Hodgson, S., Walker, L., Izatt, L., Douglas, F., Tucker, K., Dorkins, H., Clowes, V., Male, A., Donaldson, A., Brewer, C., Doherty, R., Bulman, B., Osther, P. J., Salinas, M., Eccles, D., Axcrona, K., Jobson, I., Newcombe, B., Cybulski, C., Rubinstein, W. S., Buys, S., Townshend, S., Friedman, E., Domchek, S., Ramon y Cajal, T., Spigelman, A., Teo, S. H., Nicolai, N., Aaronson, N., Ardern-Jones, A., Bangma, C., Dearnaley, D., Eyfjord, J., Falconer, A., Grönberg, H., Hamdy, F., Johannsson, O., Khoo, V., Kote-Jarai, Z., Lilja, H., Lubinski, J., Melia, J., Moynihan, C., Peock, S., Rennert, G., Schröder, F., Sibley, P., Suri, M., Wilson, P., Bignon, Y. J., Strom, S., Tischkowitz, M., Liljegren, A., Ilencikova, D., Abele, A., Kyriacou, K., van Asperen, C., Kiemeney, L., Easton, D. F., and Eeles, Rosalind A.

Published
2011
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