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799 results on '"Coombes, R C"'

201. Evaluation of biochemical markers in breast cancer

Author

Coombes, R C, Powles, T J, and Neville, A M

Subjects
C-Reactive Protein, Evaluation Studies as Topic, Ferritins, Humans, Breast Neoplasms, Female, Neoplasm Metastasis, Research Article, Carcinoembryonic Antigen
Published
1977

203. A preliminary clinical study of gossypol in advanced human cancer.

Author

Stein, Robert, Joseph, A., Matlin, Stephen, Cunningham, David, Ford, Hubert, Coombes, R., Stein, R C, Joseph, A E, Matlin, S A, Cunningham, D C, Ford, H T, and Coombes, R C

Subjects
ANTINEOPLASTIC agents, CLINICAL trials, COMPARATIVE studies, HYDROCARBONS, RESEARCH methodology, MEDICAL cooperation, RESEARCH, TUMORS, EVALUATION research, THERAPEUTICS
Abstract

A total of 34 patients with advanced cancer were given weekly or daily escalating doses of oral gossypol, a cottonseed-oil constituent showing evidence of antineoplastic activity in pre-clinical studies. No major adverse events occurred and there was no evidence of haematological or biochemical disturbance. As determined by dose escalation in 17 patients, the dose-limiting toxicity was emesis in 16 patients. There was no evidence of tumour regression in any of the 20 patients assessed for response. We conclude that gossypol is safe but unlikely to be clinically useful in patients with advanced cancer. [ABSTRACT FROM AUTHOR]

Published
1992
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204. A clinical study of nafazatrom in advanced human breast cancer.

Author

Jones, Alison, Powles, Trevor, Forgeson, Gary, Coombes, R., Jones, A L, Powles, T J, Forgeson, G V, and Coombes, R C

Subjects
ANTINEOPLASTIC agents, BREAST tumors, CLINICAL trials, COMPARATIVE studies, CLINICAL drug trials, HETEROCYCLIC compounds, RESEARCH methodology, MEDICAL cooperation, PROSTAGLANDINS, RESEARCH, EVALUATION research, PHARMACODYNAMICS
Abstract

Prostaglandins (PGs) have been shown to inhibit tumour metastases in experimental animal systems. Nafazatrom is a pyrazolinone derivative that increases endogenous prostacyclin (PGI2) and has experimental anti-cancer activity. In the present study, nafazatrom was given to 47 women with advanced breast cancer; objective remission of metastases was seen in 2 patients and stabilisation of disease in 1 case. Nafazatrom was safe and well tolerated. [ABSTRACT FROM AUTHOR]

Published
1991
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205. Oral 4-hydroxyandrostenedione, a new endocrine treatment for disseminated breast cancer.

Author

Cunningham, David, Powles, Trevor, Dowsett, Mitchell, Hutchison, Gillian, Brodie, Angela, Ford, Hubert, Gazet, Jean-Claude, Coombes, R., Cunningham, D, Powles, T J, Dowsett, M, Hutchison, G, Brodie, A M, Ford, H T, Gazet, J C, and Coombes, R C

Abstract

Thirty-one post-menopausal female patients, with locally advanced or disseminated breast cancer were treated with the aromatase inhibitor 4-hydroxyandrostenedione given orally at a dose of 500 mg daily. Twenty-nine patients had assessable disease. Eight patients (28%) had objective evidence of partial response and six remain in remission 7-10 months later. A further four patients (14%) had stabilisation of disease and 11 patients (37%) had progressive disease in spite of treatment. Plasma oestradiol levels were measured throughout therapy in 16 patients and were lowered to 53% +/- 8% of baseline levels within 7 days of commencing 4-hydroxyandrostenedione. With regard to toxicity, one patient developed a transient skin rash and another patient some facial swelling. A further patient developed a transient leucopaenia and treatment was therefore discontinued. Twenty-seven of the 30 evaluable patients (90%) experienced no side effects. These results indicate that oral administration of 4-hydroxyandrostenedione is an acceptable new treatment for post-menopausal women with disseminated breast cancer. [ABSTRACT FROM AUTHOR]

Published
1987
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211. Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival: an overview of the randomised trials

Author

Abe, O., Abe, R., Enomoto, K., Kikuchi, K., Koyama, H., Masuda, H., Nomura, Y., Sakai, K., Sugimachi, K., Tominaga, T., Uchino, J., Yoshida, M., Haybittle, J. L., Davies, C., Harvey, V. J., Holdaway, T. M., Kay, R. G., Mason, B. H., Forbes, J. F., Wilcken, N., Gnant, M., Jakesz, R., Ploner, M., Yosef, H. M. A., Focan, C., Lobelle, J. P., Peek, U., Oates, G. D., Powell, J., Durand, M., Mauriac, L., Di Leo, A., Dolci, S., Piccart, M. J., Masood, M. B., Parker, D., Price, J. J., Hupperets, P. S. G. J., Jackson, S., Ragaz, J., Berry, D., Broadwater, G., Cirrincione, C., Muss, H., Norton, L., Weiss, R. B., Abu-Zahra, H. T., Portnoj, S. M., Baum, M., Cuzick, J., Houghton, J., Riley, D., Mansel, R. E., Gordon, N. H., Davis, H. L., Beatrice, A., Mihura, J., Naja, A., Lehingue, Y., Romestaing, P., Dubois, J. B., Delozier, T., Mace Lesec'h, J., Rambert, P., Petruzelka, L., Pribylova, O., Owen, J. R., Harbeck, N., Jänicke, F., Meisner, C., Meier, P., Howell, A., Ribeiro, G. C., Swindell, R., Burrett, J., Clarke, M., Collins, R., Darby, S., Elphinstone, P., Evans, V., Godwin, J., Gray, R., Harwood, C., Hicks, C., Jackson, D., James, S., Mackinnon, E., Mcgale, P., Mchugh, T., Mead, G., Morris, P., Oulds, J., Peto, R., Taylor, C., Wang, Y., Albano, J., De Oliveira, C. F., Gervásio, H., Gordilho, J., Johansen, H., Mouridsen, H. T., Gelman, R. S., Harris, J. R., Henderson, I. C., Shapiro, C. L., Christiansen, P., Ejlertsen, B., Møller, S., Overgaard, M., Carstensen, B., Palshof, T., Trampisch, H. J., Dalesio, O., De Vries, E. G. E., Rodenhuis, S., Van Tinteren, H., Comis, R. L., Davidson, N. E., Robert, N., Sledge, G., Tormey, D. C., Wood, W., Cameron, D., Chetty, U., Forrest, P., Jack, W., Rossbach, J., Klijn, J. G. M., Treurniet-Donker, A. D., Van Putten, W. L. J., Costa, A., Veronesi, U., Bartelink, H., Duchateau, L., Legrand, C., Sylvester, R., Van Der Hage, J. A., Van De Velde, C. J. H., Cunningham, M. P., Catalano, R., Creech, R. H., Bonneterre, J., Fargeot, P., Fumoleau, P., Kerbrat, P., Namer, M., Jonat, W., Kaufmann, M., Schumacher, M., Von Minckwitz, G., Bastert, G., Rauschecker, H., Sauer, R., Sauerbrei, W., Schauer, A., De Schryver, A., Vakaet, L., Belfiglio, M., Nicolucci, A., Pellegrini, F., Sacco, M., Valentini, M., Mcardle, C. S., Smith, D. C., Galligioni, E., Boccardo, F., Rubagotti, A., Dent, D. M., Gudgeon, C. A., Hacking, A., Erazo, A., Medina, J. Y., Izuo, M., Morishita, Y., Takei, H., Fentiman, I. S., Hayward, J. L., Rubens, R. D., Skilton, D., Scheurlen, H., Von Fournier, D., Dafni, U., Fountzilas, G., Klefstrom, P., Blomqvist, C., Saarto, T., Margreiter, R., Asselain, B., Salmon, R. J., Vilcoq, J. R., Arriagada, R., Hill, C., Laplanche, A., M. G., Lê, Spielmann, M., Bruzzi, P., Montanaro, E., Rosso, R., Sertoli, M. R., Venturini, M., Amadori, D., Benraadt, J., Kooi, M., Van De Velde, A. O., Van Dongen, J. A., Vermorken, J. B., Castiglione, M., Cavalli, F., Coates, A., Collins, J., Forbes, J., Gelber, R. D., Goldhirsch, A., Lindtner, J., Price, K. N., Rudenstam, C. M., Senn, H. J., Bliss, J. M., Chilvers, C. E. D., Coombes, R. C., Hall, E., Marty, M., Borovik, R., Brufman, G., Hayat, H., Robinson, E., Wigler, N., Bonadonna, G., Camerini, T., De Palo, G., Del Vecchio, M., Formelli, F., Valagussa, P., Martoni, A., Pannuti, F., Cocconi, G., Colozza, A., Camisa, R., Aogi, K., Takashima, S., Ikeda, T., Inokuchi, K., Sawa, K., Sonoo, H., Korzeniowski, S., Skolyszewski, J., Ogawa, M., Yamashita, J., Bonte, J., Christiaens, R., Paridaens, R., Van Den Bogaert, W., Martin, P., Geniez, ROMAIN SYLVAIN JEAN, Hakes, T., Hudis, C. A., Wittes, R., Giokas, G., Kondylis, D., Lissaios, B., De La Huerta, R., Sainz, M. G., Altemus, R., Cowan, K., Danforth, D., Lichter, A., Lippman, M., O'Shaughnessy, J., Pierce, L. J., Steinberg, S., Venzon, D., Zujewski, J. A., Paradiso, A., De Lena, M., Schittulli, F., Myles, J. D., Pater, J. L., Pritchard, K. I., Whelan, T., Anderson, S., Bass, G., Brown, A., Bryant, J., Costantino, J., Dignam, J., Fisher, B., Redmond, C., Wieand, S., Wolmark, N., Jackson, I. M., Palmer, M. K., Ingle, J. N., Suman, V. J., Bengtsson, N. O., Jonsson, H., Larsson, L. G., Lythgoe, J. P., Kissin, M., Erikstein, B., Hannisdal, E., Jacobsen, A. B., Varhaug, J. E., Gundersen, S., Hauer-Jensen, M., Høst, H., Nissen-Meyer, R., Blamey, R. W., Mitchell, A. K., Morgan, D. A. L., Robertson, J. F. R., Di Palma, M., Mathé, G., Misset, J. L., Clark, R. M., Levine, M., Morimoto, K., Takatsuka, Y., Crossley, E., Harris, A., Talbot, D., Taylor, M., Di Blasio, B., Ivanov, V., Semiglazov, V., Brockschmidt, J., Cooper, M. R., Ueo, H., Falkson, C. I., A'Hern, R., Ashley, S., Powles, T. J., Smith, I. E., Yarnold, J. R., Gazet, J. C., Corcoran, N., Deshpande, N., Di Martino, L., Douglas, P., Lindtner, A., Notter, G., Bryant, A. J. S., Ewing, G. H., Firth, L. A., Krushen-Kosloski, J. L., Foster, L., George, W. D., Stewart, H. J., Stroner, P., Malmström, P., Möller, T. R., Rydén, S., Tengrup, I., Tennvall-Nittby, L., Carstenssen, J., Dufmats, M., Hatschek, T., Nordenskjöld, B., Söderberg, M., Carpenter, J. T., Albain, K., Crowley, J., Green, S., Martino, S., Osborne, C. K., Ravdin, P. M., Glas, U., Johansson, U., Rutqvist, L. E., Singnomklao, T., Wallgren, A., Maibach, R., Thürlimann, B., Brenner, H., Hercbergs, A., Yoshimoto, M., Deboer, G., Paterson, A. H. G., Meakin, J. W., Panzarella, T., Shan, Y., Shao, Y. F., Wang, X., Zhao, D. B., Chen, Z. M., Pan, H. C., Bahi, J., Reid, M., Spittle, M., Deutsch, G. P., Senanayake, F., Kwong, D. L. W., Bianco, A. R., Carlomagno, C., De Laurentiis, M., De Placido, S., Buzdar, A. U., Smith, T., Bergh, J., Holmberg, L., Liljegren, G., Nilsson, J., Seifert, M., Sevelda, P., Zielinsky, C. C., Buchanan, R. B., Cross, M., Royle, G. T., Dunn, J. A., Hills, R. K., Lee, M., Morrison, J. M., Spooner, D., Litton, A., Chlebowski, R. T., Caffier, H., Clarke, M, Collins, R, Darby, S, Davies, C, Elphinstone, P, Evans, E, Godwin, J, Gray, R, Hicks, C, James, S, MacKinnon, E, McGale, P, McHugh, T, Peto, R, Taylor, C, and Wang, Y

Subjects
medicine.medical_specialty, Time Factors, medicine.medical_treatment, Breast Neoplasms, Rate ratio, Breast Conservation Treatment, Disease-Free Survival, Breast cancer, Cause of Death, Breast-conserving surgery, Medicine, Humans, Lung cancer, Aged, Probability, Randomized Controlled Trials as Topic, business.industry, Female, Middle Aged, Neoplasm Recurrence, Local, Medicine (all), General Medicine, medicine.disease, Surgery, Radiation therapy, Unilateral Breast Neoplasms, Neoplasm Recurrence, Local, business, Mastectomy
Abstract

Background In early breast cancer, variations in local treatment that substantially affect the risk of locoregional recurrence could also affect long-term breast cancer mortality. To examine this relationship, collaborative meta-analyses were undertaken, based on individual patient data, of the relevant randomised trials that began by 1995. Methods Information was available on 42 000 women in 78 randomised treatment comparisons (radiotherapy vs no radiotherapy, 23 500; more vs less surgery, 9300; more surgery vs radiotherapy, 9300). 24 types of local treatment comparison were identified. To help relate the effect on local (ie, locoregional) recurrence to that on breast cancer mortality, these were grouped according to whether or not the 5-year local recurrence risk exceeded 10% (10%, 25 000 women). Findings About three-quarters of the eventual local recurrence risk occurred during the first 5 years. In the comparisons that involved little (10%) differences, however, 5-year local recurrence risks were 7% active versus 26% control (absolute reduction 19%), and 15-year breast cancer mortality risks were 44·6% versus 49·5% (absolute reduction 5·0%, SE 0·8, 2p These 25 000 women included 7300 with breast-conserving surgery (BCS) in trials of radiotherapy (generally just to the conserved breast), with 5-year local recurrence risks (mainly in the conserved breast, as most had axillary clearance and node-negative disease) 7% versus 26% (reduction 19%), and 15-year breast cancer mortality risks 30·5% versus 35·9% (reduction 5·4%, SE 1·7, 2p=0·0002; overall mortality reduction 5·3%, SE 1·8, 2p=0·005). They also included 8500 with mastectomy, axillary clearance, and node-positive disease in trials of radiotherapy (generally to the chest wall and regional lymph nodes), with similar absolute gains from radiotherapy; 5-year local recurrence risks (mainly at these sites) 6% versus 23% (reduction 17%), and 15-year breast cancer mortality risks 54·7% versus 60·1% (reduction 5·4%, SE 1·3, 2p=0·0002; overall mortality reduction 4·4%, SE 1·2, 2p=0·0009). Radiotherapy produced similar proportional reductions in local recurrence in all women (irrespective of age or tumour characteristics) and in all major trials of radiotherapy versus not (recent or older; with or without systemic therapy), so large absolute reductions in local recurrence were seen only if the control risk was large. To help assess the life-threatening side-effects of radiotherapy, the trials of radiotherapy versus not were combined with those of radiotherapy versus more surgery. There was, at least with some of the older radiotherapy regimens, a significant excess incidence of contralateral breast cancer (rate ratio 1·18, SE 0·06, 2p=0·002) and a significant excess of non-breast-cancer mortality in irradiated women (rate ratio 1·12, SE 0·04, 2p=0·001). Both were slight during the first 5 years, but continued after year 15. The excess mortality was mainly from heart disease (rate ratio 1·27, SE 0·07, 2p=0·0001) and lung cancer (rate ratio 1·78, SE 0·22, 2p=0·0004). Interpretation In these trials, avoidance of a local recurrence in the conserved breast after BCS and avoidance of a local recurrence elsewhere (eg, the chest wall or regional nodes) after mastectomy were of comparable relevance to 15-year breast cancer mortality. Differences in local treatment that substantially affect local recurrence rates would, in the hypothetical absence of any other causes of death, avoid about one breast cancer death over the next 15 years for every four local recurrences avoided, and should reduce 15-year overall mortality.

243. The treatment of postmenopausal women with advanced breast cancer with buserelin

Author

Waxman, J. H., Harland, S. J., Coombes, R. C., Wrigley, P. F. M., Malpas, J. S., Powles, T., and Lister, T. A.

Abstract

Repeated administration of long-acting analogues of gonadotrophin-releasing hormone down-regulates the pituitary gonadotrophins and gonadal hormones. The activity of these compounds in premenopausal women with breast cancer has been previously noted. In an attempt to cause a highly selective medical hypophysectomy 18 consecutive postmenopausal women with symptomatic advanced breast cancer were treated with intranasal buserelin in divided dosages of either 600 or 1000 µg daily. The pituitary gonadotrophins were suppressed in all patients, without objective evidence of response. This is in contrast with an earlier finding that the long-acting analogues of gonadotrophin-releasing hormone were effective in postmenopausal patients with breast cancer.

Published
1985
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244. Mitomycin C, melphalan and methotrexate combination chemotherapy for palliation of disseminated breast cancer

Author

Perez, D. J., Powles, T. J., Gazet, J. -C., Ford, H. T., and Coombes, R. C.

Abstract

Fifty-seven patients with metastatic breast carcinoma have been treated with mitomycin C (10 mg/m2 IV 6-weekly), melphalan (6 mg/m2 POx3 days, 3-weekly), and methotrexate (35 mg/m2 IV 3-weekly) to assess the efficacy and toxicity of this regimen. Of 48 evaluable patients 19 (40%) responded for a median period of 5 months and 12 (25%) had stabilisation of disease. Of the 12 patients previously treated with adriamycin only one responded, whereas 18 of the 36 patients without previous chemotherapy responded. Although healing of bone metastases was infrequent control of hypercalcaemia was commonly seen. Generally the treatment was well tolerated and treatment was stopped in only five patients because of toxicity. Cummulative marrow toxicity was observed but was not a significant problem in the first 6 months of treatment. Mitomycin C, melphalan, and methotrexate (MMM) appears to provide an effective, well tolerated chemotherapy combination for metastatic breast carcinoma.

Published
1984
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245. The role of RIP140 and FOXA1 in breast cancer endocrine sensitivity and resistance.

Author

Harada.-Shoji, N., Coombes, R. C., and Lam, E. W.-F.

Subjects
*ESTROGEN receptors, *HORMONE therapy, *TAMOXIFEN, *CANCER cell growth, *DRUG resistance
Abstract

Background: The estrogen receptor-a (ERa) is implicated in the initiation and progression of breast cancer. Endocrine therapeutics, including tamoxifen (OHT) and fulvestrant (ICI182780; ICI) improve disease-free survival. Despite positive effects, de novo or acquired resistance to endocrine therapies frequently occurs. It has recently been published that nuclear receptor-interacting protein 1, NRIP1, also called RIP140, encodes an ER corepressor RIP140 and has a role in the regulation of breast cancer cell growth in response to anti-estrogens. FOXA1 has previously been shown to function as a 'pioneer factor' and dictate ER dependent gene expression in both normal and malignant breast epithelial cells. In this study we investigated the expression of ERa cofactors RIP140 and FOXA1 and their roles in hormonal therapy and endocrine resistance. Methods: Tamoxifen sensitive or resistant breast cancer cell lines were analysed for protein and mRNA expression by western blotting and quantitative real-time PCR with or without the inhibition of ERa with tamoxifen or ICI. To determine the functional role of RIP140 and FOXA1 as well as their interaction in breast cancer, tamoxifen sensitive breast cancer cells (eg. MCF-7 and ZR-75-1) were transfected with either RIP140 or FOXA1 expression vector and examined for the expression of ER-target genes by Western blot and RT-qPCR analysis. The consequence of depletion of RIP140 and FOXA1 by RNA interference (RNAi) was also studied in these breast cancer cells. The expression of RIP140 and FOXA1 and potential target genes were also validated in breast cancer patient samples by Immunohistochemistry. Results: We first examined the basal expression levels of RIP140 and FOXA1 in tamoxifen sensitive as well as resistant breast cancer cell lines. The expression levels of RIP140 were low in the resistance cells compared with their parental sensitive counterparts, while that of FOXA1 had no significant difference between the cell lines. The degradation of ERa by ICI treatment resulted in the down-regulation of RIP140 and FOXA1 expression in the endocrine sensitive. Our experiments also demonstrated the functional interaction between RIP140 and FOXA1 and showed that depletion of RIP140 by RNA interference (RNAi) in sensitive cells resulted in reduction of FOXA1 expression. We also indentified from this work, a number of ER-regulated genes which are activated by FOXA1 and repressed by RIP140 expression. The regulation of these target genes by ERa, FOXA1 and RIP140 were also confirmed in the breast cancer patient samples. Conclusion: The results from this study demonstrated that RIP140 and FOXA1 play a pivotal role in dictating hormonal sensitivity and resistance in breast cancer. Moreover, this work also identified a number of ERa-regulated genes which are downstream targets of FOXA1 and RIP140, and as such, they may be reliable prognostic markers for endocrine sensitivity in breast cancer. [ABSTRACT FROM AUTHOR]

Published
2012
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246. A randomized trial of exemestane after two to three years of tamoxifen therapy in postmenopausal women with primary breast cancer.

Author

Coombes, R. C., Hall, E., Gibson, L. J., Paridaens, R., Jassem, J., Delozier, T., Jones, S. E., Alvarez, I., Bertelli, G., Ortmann, O., Coates, A. S., Bajetta, E., Dodwell, D., Coleman, R. E., Fallowfield, L. J., Mickiewicz, E., Andersen, J., Lonning, P. E., Cocconi, G., and Stewart, A.

Subjects
*BREAST cancer, *CANCER treatment, *AROMATASE, *TAMOXIFEN, *CYTOCHROME P-450
Abstract

Presents the results of a study on the disease-free survival of postmenopausal women with primary breast cancer who switched to the aromatase inhibitor exemestane after tamoxifen therapy. Characteristics of the aromatase inhibitor; Number of first events that occurred in the study, including metastatic recurrence; Hazard ratio of reduced incidence of contralateral breast cancer in the exemestane group.

Published
2004
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247. Resolution of late-onset asthma following high-dose chemotherapy.

Author

Palmieri, C, Gillmore, R, Menzies-Gow, A, Fishpool, S, Robinson, D, Shaw, R, and Coombes, R C

Subjects
ASTHMA, DRUG therapy, STEM cells, CELL transplantation, TRANSPLANTATION of organs, tissues, etc.
Abstract

Summary:We describe a patient with moderately severe (British Thorax Society Step IV/V) asthma requiring regular inhaled and oral corticosteroids to control symptoms who experienced resolution of her asthma following high-dose chemotherapy and autologous stem cell transplantation for breast cancer. As far as the authors are aware this is the first reported case.Bone Marrow Transplantation (2003) 32, 847-848. doi:10.1038/sj.bmt.1704268 [ABSTRACT FROM AUTHOR]

Published
2003
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