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862 results on '"Lunec, J."'

10. Histological profile of tumours from MYCN transgenic mice

Author

Moore, H.C., Wood, K.M., Jackson, M.S., Lastowska, M.A., Hall, D., Imrie, H., Redfern, C.P.F., Lovat, P.E., Ponthan, F., O'Toole, K., Lunec, J., and Tweddle, D.A.

Subjects
Animal models in research -- Usage, Animal models in research -- Genetic aspects, Neuroblastoma -- Research, Neuroblastoma -- Genetic aspects, Proto-oncogenes -- Research, Proto-oncogenes -- Physiological aspects, Health
Published
2008

11. Age Dependency of the Prognostic Impact of Tumor Genomics in Localized Resectable MYCN -Nonamplified Neuroblastomas. Report From the SIOPEN Biology Group on the LNESG Trials and a COG Validation Group

Author

Ambros IM, Tonini GP, Pötschger U, Gross N, Mosseri V, Beiske K, Berbegall AP, Bénard J, Bown N, Caron H, Combaret V, Couturier J, Defferrari R, Delattre O, Jeison M, Kogner P, Lunec J, Marques B, Martinsson T, Mazzocco K, Noguera R, Schleiermacher G, Valent A, Van Roy N, Villamon E, Janousek D, Pribill I, Glogova E, Attiyeh EF, Hogarty MD, Monclair TF, Holmes K, Valteau-Couanet D, Castel V, Tweddle DA, Park JR, Cohn S, Ladenstein R, Beck-Popovic M, De Bernardi B, Michon J, Pearson ADJ, and Ambros PF

Subjects
neoplasms
Abstract

For localized, resectable neuroblastoma without MYCN amplification, surgery only is recommended even if incomplete. However, it is not known whether the genomic background of these tumors may influence outcome.

Published
2020

12. The role of the tumour suppressor [p33.sup.ING1b] in human neoplasia. (Review)

Author

Nouman, G.S., Anderson, J.J., Lunec, J., and Angus, B.

Subjects
Genetic research -- Genetic aspects, Tumor suppressor genes -- Research -- Genetic aspects, Cancer -- Genetic aspects, Health, Genetic aspects, Research
Abstract

The inhibitor of growth (ING) genes (ING1-4) probably descend from tumour suppressor genes. ING] was the first to be identified and later isolated using an approach to detect genes whose [...]

Published
2003

13. Downregulation of nuclear expression of the [p33.sup.INGlb] inhibitor of growth protein in invasive carcinoma of the breast. (Original Article)

Author

Nouman, G.S., Anderson, J.J., Crosier, S., Shrimankar, J., Lunec, J., and Angus, B.

Subjects
Oncology, Experimental -- Genetic aspects -- Physiological aspects, Genetic research -- Physiological aspects -- Genetic aspects, Breast cancer -- Genetic aspects -- Physiological aspects, Cancer -- Research, Health, Physiological aspects, Genetic aspects
Abstract

Background/Aims: The inhibitor of growth gene 1 (INGl) is a modulator of cell cycle checkpoints, apoptosis, and cellular senescence. The most widely expressed INGl isoform is [p33.sup.INGlb], which can modulate [...]

Published
2003

14. Loss of nuclear expression of the [p33.sup.ING1b] inhibitor of growth protein in childhood acute lymphoblastic leukaemia. (Original Article)

Author

Nouman, G.S., Anderson, J.J., Wood, K.M., Lunec, J., Hall, A.G., Reid, M.M., and Angus, B.

Subjects
Tumor suppressor genes -- Research -- Physiological aspects, Acute lymphocytic leukemia -- Physiological aspects -- Research, Health, Physiological aspects, Research
Abstract

Background/Aims: [p33.sup.ING1b] is a tumour suppressor protein involved in growth control and apoptosis. Suppression of [p33.sup.ING1b] expression is associated with the loss of cellular growth control and immortalisation, whereas its [...]

Published
2002

26. Quality Assessment of Genetic Markers Used for Therapy Stratification

Author

Ambros, I.M., Benard, J., Boavida, M., Bown, N., Caron, H., Combaret, V., Couturier, J., Darnfors, C., Delattre, O., Freeman-Edward, J., Gambini, C., Gross, N., Hattinger, C.M., Luegmayr, A., Lunec, J., Martinsson, T., Mazzocco, K., Navarro, S., Noguera, R., O’Neill, S., Pötschger, U., Rumpler, S., Speleman, F., Tonini, G.P., Valent, A., Van Roy, N., Amann, G., De Bernardi, B., Kogner, P., Ladenstein, R., Michon, J., Pearson, A.D.J., and Ambros, P.F.

Published
2003

35. Age-dependency of the prognostic impact of tumor genomics in localized resectable MYCN non-amplified neuroblastomas Report from the SIOPEN Biology Group on the LNESG Trials

Author

Ambros, I.M., Tonini, G.P., Gross, N., Mosseri, V., Pötschger, U., Beiske, K., Berbegall, A.P., Bénard, J., Bown, N., Caron, H., Combaret, V., Couturier, J., Defferrari, R., Delattre, O., Jeison, M., Kogner, P., Lunec, J., Marques, B., Martinsson, T., Mazzocco, K., Noguera, R., Schleiermacher, G., Valent, A., Van Roy, N., Villamon, E., Janousek, D., Pribill, I., Glogova, E., Attiyeh, E.F., Hogarty, M.D., Monclair, T., Holmes, K., Valteau-Couanet, D., Pearson ADJ, A.D.J., Castel, V., Tweddle, D.A., Park, J.R., Cohn, S., Ladenstein, R., Beck-Popovic, M., De Bernardi, B., Michon, J., and Ambros, P.F.

Subjects
Neuroblastoma, Tumor Genomics, MYCN, Doenças Genéticas
Abstract

BACKGROUND: Biology based treatment reduction, i.e. surgery alone also in case of not totally resected tumors, was advised in neuroblastoma patients with localized resectable disease without MYCN amplification. However, whether the genomic background of these tumors may influence outcome was unknown and therefore scrutinized in a meta-analysis comprising two prospective therapy studies and a ‘validation’ cohort. PATIENTS AND METHODS: Diagnostic samples were derived from 406 INSS stages 1/2A/2B tumors from three cohorts: LNESGI/II and COG. Genomic data were analyzed in two age groups (cut-off: 18 months) and quality controlled by the SIOPEN Biology Group. RESULTS: In both patient age groups stage 2 tumors led to similarly reduced event-free survival (5y-EFS: 83+3% versus 80+4%), but overall survival was only decreased in patients >18m (5y-OS: 97+1% versus 87+4%; p=0.001). In the latter age subgroup, only tumors with SCA led to relapses, with 11q loss as the strongest marker (5y-EFS: 40+15% versus 89+5%; p18m but not

Published
2018

44. Chain breaking antioxidant status in rheumatoid arthritis: clinical and laboratory correlates

Author

Situnayake, R.D., Thurnham, D.I., Kootathep, S., Chirico, S., Lunec, J., Davis, M., and McConkey, B.

Subjects
Rheumatoid arthritis -- Physiological aspects, Antioxidants -- Measurement, Active oxygen in the body -- Physiological aspects, Health
Abstract

Rheumatoid arthritis (RA) is a disease that causes inflammation of the joints. During the process of inflammation, oxygen radicals (highly reactive atoms with unpaired electrons) are generated within the joint tissue. When samples of joint tissue are grown in culture and oxygen radicals are added, the radicals damage (oxidize) and destroy the joint tissue. In this way, oxygen radicals are thought to be involved in RA. Under normal circumstances, the body makes its own proteins, called antioxidants, that inactivate oxygen radicals and prevent them from causing tissue damage. These antioxidants include specific enzymes and vitamins E and C (ascorbic acid). In order to investigate the relationship between oxygen radicals and RA, blood samples from 20 patients with RA and 20 healthy volunteers were tested for the presence of antioxidants. The levels of antioxidants (vitamin E, ascorbic acid and urate) present in the blood samples were determined by measuring the amount of protein damage that occurred following the addition of oxygen radicals to the blood. The patients with RA had lower blood levels of antioxidants than those without RA. Lower blood levels of antioxidants appeared to be related to morning joint stiffness, pain and grip strength. Also, the blood samples that contained high levels of urate were less susceptible to damage by oxygen radicals. These findings indicate that patients with RA are more susceptible to tissue damage caused by oxygen radicals than people who do not have RA. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

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