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20. Irish Association for Cancer Research: Proceedings of annual scientific meeting held at Kinsale on April 15–16th, 1994

Author

Lawler, M., Locasciulli, A., Bacigalupo, A., Humphries, P., Ljungman, P., McCann, S. R., Nolan, N., McDermott, E. W., Reynolds, J. R., McCann, A., Rafferty, R., Sweeney, P., Carney, D., O’Higgins, N. J., Duffy, M. J., Gardiner, C., Reen, D. J., O’Connell, M. A., Kelleher, D., Hall, N., O’Neill, L. A. J., Long, A., McCarthy, J. V., Fernandes, R. S., Cotter, T. G., Ryan, E., Kitching, A., MacMathuna, P., Mulligan, E., Merriman, R., Dervan, P., Kelly, P., Gorey, T. F., Lennon, J. R., Crowe, J., Bennett, M. A., Kay, E. W., Curran, B., O’Donoghue, D. P., Leader, M., Croke, D. T., O’Connor, J. M., McKelvey-Martin, V. J., McKenna, P. G., O’Riordan, J. M., Tobin, A., O’Mahoney, M., Keogh, F. M., O’Riordan, J., McNamara, C., McEneaney, P., Daly, P. A., Farrell, M., Young, S., Gibbons, D., McCarthy, P., Mulcahy, H., Parfrey, N. A., Sheahan, K., Lambkin, H., Mothersill, C., Chin, D., Sheehan, K., Kelehan, P., Parfrey, N., Morrin, M., Khan, F., Delaney, P., Rowan, D. M., Orminston, W. J., Donnellan, P. P., Khalid, A., Kerin, M., O’Hanlon, D. M., Kent, P., Given, H. F., Kennedy, S. M., McGeoch, G., Spurr, N. K., Barrett, J., O’Sullivan, G., Collins, J. K., Willcocks, T., Kennedy, S., Dolan, J., Gallagher, W., McDermott, E., O’Higgins, N., Hagan, R., McManus, R., Ormiston, W., Daly, P., Sheils, O., McDermott, M., O’Briain, D. S., Maher, D., Costello, P., Flanagan, F., Stack, J., Ennis, J., Grimes, H., Yanni, A., Harrison, M., Lowry, W. S., Russell, S. E. H., Atkinson, R. J., White, P., Hickey, I., Bell, D. W., Biggart, D., Doyle, J., Staunton, M. J., Gaffney, E. F., Dervan, P. A., McCabe, M. M., Fennelly, J. J., Carney, D. N., O’Reilly, M., McMahon, J. N., Moriarty, M., Hurson, B., O’Neill, A. J., Magee, H., O’Loughlin, J., Dervan, P. A., Cremin, P., Orminston, W., McCarthy, J., Redmond, P., Duggan, S., Rea, S., Bouchier-Hayes, D., O’Donnell, J., Duggan, C., Crown, J., Bermingham, D., Nugent, A., Fleming, C., Crosby, P., Wolff, S., McCarthy, D., Walsh, C. Barry, Cassidy, M., Husain, S., Kay, E., Thornhilll, M., Whelan, D., Barry, D., Turner, M., Prenderville, W., Murphy, F., Prendiville, W., Gibson, G., O’Grady, T., Carmody, M., Donohoe, J., Walshe, J., Murphy, G. M., O’Donoghue, J., Kerin, K., Ahern, S., Molloy, K., Goulden, N., Pamphilon, D. H., O’Connell, M., Power, C., Leroux, A., Perricaudet, M., Walls, D., Britton, F., Brennan, L., Barnett, Y. A., Madden, B., Wakelin, L. P. G., Loughrey, H. C., Corley, P., Redmond, H. P., Watson, R. W. G., Keogh, I., O’Hanlon, D., Walsh, S., Callaghan, J., McNamara, M., Benedict-Smith, A., Barnes, C., Neylon, D., Fenton, M., Searcey, M., Topham, C. M., Wakelin, L. G., Howarth, N. M., Purohit, A., Reed, M. J., Potter, B. V. L., Hatton, W. J., McKerr, G., Harvey, D., Carson, J., Hannigan, B. M., McCarthy, P. J., McClean, S., Hill, B. T., Costelloe, C., Denny, W. A., Fingleton, B., McDonnell, S., Butler, M., Corbally, N., Dervan, P. A., Stephens, J. F., Martin, G., McGirl, A., Lawlor, E., Gardiner, N., Lynch, S., Arce, M. de, O’Brien, F., Duggan, A., O’Herlihy, S., Shanahan, F., O’Keeffe, G., McCann, S., Sweeney, K., Neill, A. O., Pamphilon, D., Sheridan, M., Reid, I., Seymour, C. B., Walshe, T., Hennessy, T. P., O’Mahony, A., O’Connell’, J., Lawlor, C., Nolan, S., Morrisey, D., Pedlow, P. J., Walsh, M., Lowry, S. W., McAleer, J. J. A., McKeown, S. R., Afrasiabi, M., Lappin, T. R. J., Joiner, B., Hirst, K. V., Hirst, D. G., Sweeney, E., VanderSpek, J., Murphy, J., and Foss, F.

Published
1995
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21. Irish association for cancer research: Proceedings of the 1993 IACR Annual Scientific Meeting held April 2-3, 1993 in Kilkenny

Author

Gannon, F., Forde, R. C., Nester, P. V., Webb, P., McCaffrey, J., Fennelly, J. J., McCarthy, D., Halligan, J., Crosby, P., Long, A., Kelleher, D., Keane, J., O’Riordan, T., O’Briain, D. S., Daly, P. A., Sheahan, R., Jawas, A. M., O’Reane, J. C., Murnane, M. J., Corbally, N., Devaney, D., Grogan, L., Dervan, P. A., Carney, D. N., Duggan, A., O’Brien, F., O’Sullivan, G., Collins, J. K., Long, H. A., Conway, D. J., Mercer, P. M., Murphy, D., Stokes, M., Sheahan, K., O’Higgins, N. J., Smyth, P. P. A., O’Connell, M. A., Long, A., O’Neill, L., Kelleher, D., Nugent, A., Gallagher, J., Dolan, J., Bermingham, D., McDermott, E., Fennelly, J. J., Higgins, N. O., Duffy, M. J., Mercer, P. M., McDermott, E. W., Stokes, M., Murphy, D. S., Sharp, M., Duffy, M. J., Murphy, J. J., O’Higgins, N., Daly, P. A., Ormiston, W., Donnellan, P., McManus, R., Ashraf, M. S., Brady, J., Breatnach, F., Deasy, P. F., O’Meara., A., Mercer, P. M., Doran, M., McDermott, E. W. M., Smyth, P. P. A., Cassidy, M., Cross, K. S., O’Higgins., N. J., Devaney, D., Corbally, N., Carney, D. N., Dervan., P. A., Gardiner, N., Lawler, M., Humphries, P., McCann., S. R., Mahon, T., O’Neill., L. A. J., Lawler, M., Humphries, P., McCann., S. R., McManus, R., Shiels, O., Gaffney, E., Daly., P. A., Hollywood, D. P., Hurst., W. C., Donnellan, P., Daly., P. A., Lyng, F. M., Mothersill, C., Cottell, D. C., Trosko, J. E., O’Keefe, G., McCann, S., Sweeney., K., Sheridan, M., Mothersill, C., Seymour, C. B., Harney., J., Grehan, D., O’Briain, D. S., Walshe, T., Hickey, K., Hennessy, T., Mercer, P., Reynolds, J., McDermott, E. W., Stokes, M., Murphy, D., Cross, S., O’Higgins., N., Bermingham, D., Fennelly, J. J., O’Higgins, N., Duffy, M. J., Morrissey, D., Lynch, D., Collins, J. K., O’Sullivan., G., Verhaegen, S., Cotter., T., McGahon, A., Cotter, K., Green, D., Cotter., T., McCarthy, D., Samson, D., Evans, M., Treleaven, J., Barrett, J., McMahon, J., Gaffney, E. F., Grehan, D., Sheils, O., McCabe, M., Dervan, P. A., Lambkin, H., Mothersill, C., Kelehane, P., Corbally, N., Devaney, D., Grogan, L., Dervan, P. A., Carney, D. N., Glynn, J. M., Green, D. R., Cotter, T. G., O’Mahony, A. M., Collins, J. K., O’Sullivan, G. C., Molloy, K. M., Lawler, M., Humphries, P., McCann, S. R., O’Riordan, J., Molloy, K., Corbally, N., Devaney, D., McShane, I., McCann, S. R., Kelleher, L., Magee, H., Carney, D. N., Dervan, P. A., O’Byrne, K., Lyons, D., O’Toole, E., O’Donnell, C., O’Hare, N., Freyne, P., Clancy, L., Ennis, J., Prichard, J., McGovern, E., Luke, D., Carney, D., Kenealy, M. R., Keaveney, M., Nestor, P., Gannon, F., Duggan, S., Redmond, H. P., McCarthy, J., Watson, R. G. W., Croke, D. T., Burke, P., Bouchier-Hayes, D., McCarthy, J., Redmond, H. P., Duggan, S., Watson, R. W. G., Bouchier-Hayes, D., O’Donnell, R., McCarthy, M., O’Donovan, N., O’Sullivan, G., Collins., J. K., O’Connell, J., Phelan, D., Hanvajanawong, C., O’Sullivan, G., Collins, J. K., Morrin, M., Kelly, M., Khan, F., Barrett, N., Delaney, P., O’Mahony, A. M., Collins, J. K., and O’Sullivan, G. C.

Published
1994
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25. Proceedings of meeting of Irish Association for Cancer Research May 16/17, 1985

Author

Doyle, C. T., McCann, J. P., Ardill, J. E. S., Johnston, C. F., McKee, C. M., Stevenson, H. M., Gibbons, J. R., Buchanan, K. D., Collins, P. B., Johnson, A. H., Duignan, J. P., Brady, K., Bouchier-Hayes, D., Reynolds, Maura, McCann, S. R., Mulgrew, S., Mothersill, C., Moriarity, M., Shine, Helen, Collins, J. K., Thornes, R. D., Clarke, R., Moorwood, Janet, van den Berg, H. W., Nelson, J., Murphy, R. F., Hickey, Dorinda, McCann, Shaun R., Melinn, M., Kennedy, D. G., Dickson, G. R., McCann, A., Seymour, C. B., Afdhal, N., O’Donoghue, D. P., Malone, J. F., Moriarty, M., Ardill, Joy, Shaw, C., Casey, M., Conroy, R., Daly, L., Fennelly, J., Herity, P., Hilliard, N., McCambridge, M., Walsh, Ena, Smyth, Honor, Conere, T. J., Church, S., Lowry, W. S., Dooley, Margaret, and Clynes, Martin

Published
1986
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26. Irish association for cancer research Proceedings of 23rd Annual Meeting held in Cork, May, 1966

Author

McCann, S. R., Farrell, D., McDonnell, S., Neenan, S., Moriarty, M., Lynch, V., Kelehan, P., Clynes, M., O’Boyle, C., Herity, B., Hilliard, N., Houston, R. F., Cremin, M., Clarke, R., Nelson, J., Murphy, R. F., Mothersill, Carmel, Seymour, C. B., Hennessy, T. P., McCann, A., Afdhal, N., O’Donoghue, D., O’Byrne, P., Johnson, A. H., Collins, P. B., Duignan, J. B., Bouchier-Hayes, D., Atkinson, R. J., Carney, D. N., Teeling, Mary T., Coughlan, M. B., O’Neill, H., Ennis, J. T., Duffy, M. J., O’Grady, P., Devaney, D., O’Siorain, L., Lijnen, H. R., Daly, M., O’Meara, A., Hallinan, F. M., O’Sullivan, G., Kiely, D., Lee, G., Clifford, Concepta A., Headon, D. R., Casey, B., Pratt, I., Ryan, M. P., and Carney, D.

Published
1987
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28. Irish association for cancer research: Scientific meeting held in Queen’s University, Belfast, on September 23rd, 1983. The Sixth Irish Cancer Society Lecture was delivered by Professor D. G. Harnden, Director of the Paterson Labboratories, Christie Hospital and Holt Radium Institute, Manchester on “Cancer genes, chromosomes and cancer”

Author

Abram, W. P., Jones, F., McGuigan, M., Corbally, N., Malone, J. F., Mothersill, C., Seymour, C., Martin, W. M. C., Mulgrew, S., Moriarty, M., Bailey, D., Duignan, J. P., Morrissey, B., Crowe, J., Lennon, J., O’Malley, E., Atkinson, R. J., Lowry, W. S., O’Loughlin, G., Herity, N., Blake, P., Conroy, R., Buchanan, K. D., O’Hare, M. M. T., Kennedy, T. L., Hadden, D. R., Thornes, R. D., Reynolds, Maura, McCann, S. R., McCormick, Derek, Clarke, R., VandenBerg, H. W., Murphy, R. F., McCluskey, D. R., Russell, R. J., Earls, B. J. P., VandenBerg, H. W., Wilson, R., Kennedy, D. G., O’Hare, M. M. T., Huda, I., Gibbons, J. R. P., Kennedy, T. L., Buchanan, K. D., Johnston, C. F., Shaw, C., Buchanan, K. D., Headon, Bernadette B., Reen, Denis J., Kennedy, D. G., VandenBerg, H. W., Murphy, R. F., Lowry, W. S., Rottger, J., O’Reilly, D., Mullins, L., McCarthy, M., Collins, J. K., Seymour, C. B., Mothersill, Carmel, Moriarty, M., Malone, J. F., Conere, T. J., El-Badawi, M. G., Koriech, O., Horton, P. W., Gordon, L., Lowry, W. S., Wallace, Ian, and Meldrum, R. A.

Published
1984
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29. Proceedings of The Irish Association for Cancer Research Meeting: Universiiy College, Galway, 21St September, 1984

Author

Corridan, J. P., Moran, M. A., Herity, B., Hilliard, N., Moriarty, M., Fennelly, J., McCambridge, M. M., Casey, M., Quigley, M., Moriarty, M., Hunt, S., Gordon, Lynn, Lowry, W. S., Moriarty, M., Prendiville, J., Raftery, H., Blake, P., Herity, B., Robinson, A., Conroy, R., Pomeroy, M., Herity, Bernadette, Murphy, J. F., Daly, Leslie, Atkinson, R. J., Pomeroy, M., Kelly, D., McCabe, M., Fennelly, J. J., Moriarty, M., Duffy, G., Duff, F., Robinson, A., Duffy, J., Reynolds, Maura, McCann, S. R., Keeling, P., Byrne, P. J., Mealy, K., Whelan, A., Feighery, C., Hennessy, T. P. J., Mealy, K., Keeling, P., Byrne, P. J., Whelan, A., Feighery, C., Hennessy, T. P. J., Duffy, M. J., O’Connell, M., Cantwell, B., Fennelly, J., O’Siorain, L., Conroy, R., Duffy, M. J., O’Ccnnel, M., Fennelly, J., O’Siorain, L., Conroy, R., Simon, J., Harrington, M. G., O’Siorain, Li, O’Briain, S., McDonnell, S., Moriarty, M., Clynes, M., Seymour, C. B., Mothersill, C., Byrne, P., Hennessy, T. P. J., Moriarty, M., Lavelle, S. M., Lomhair, M. Mac, O’Reilly, D., Mullins, E., Canty, S., Collins, J. K., Davis, J., Conroy, J., Collins, J. K., Keatinge, M. B., Collins, P. B., Duignan, J. P., Dickson, B., Johnson, A. H., McCann, A., Seymour, C., Mothersill, C., Long, A., Moriarty, M., O’Donoghue, D., Mulgrew, S., Seymour, C., Mothersill, C., Moriarty, M., Conere, T. J., Church, S. W., Lowry, Sidney, Earls, B., and Russell, R. J.

Published
1985
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43. DOSE CALCULATIONS FOR [131I] META-IODOBENZYLGUANIDINEINDUCED BYSTANDER EFFECTS.

Author

Gow, M. D., Seymour, C. B., Boyd, M., Mairs, R. J., Prestiwch, W. V., and Mothersill, C. E.

Subjects
*CANCER radiotherapy, *RADIOBIOLOGY, *ABSORBED dose, *CELL lines, *CONTROL groups, *RADIOPHARMACEUTICALS, *NORADRENALINE regulation
Abstract

Targeted radiotherapy is a potentially useful treatment for some cancers and may be potentiated by bystander effects. However, without estimation of absorbed dose, it is difficult to compare the effects with conventional external radiation treatment. Methods: Using the Vynckier - Wambersie dose point kernel, a model for dose rate evaluation was created allowing for calculation of absorbed dose values to two cell lines transfected with the noradrenaline transporter (NAT) gene and treated with [131I]MIBG. Results: The mean doses required to decrease surviving fractions of UVW/NAT and EJ138/NAT cells, which received medium from [131I]MIBG-treated cells, to 25 - 30% were 1.6 and 1.7 Gy respectively. The maximum mean dose rates achieved during [131I]MIBG treatment were 0.09 - 0.75 Gy/h for UVW/NAT and 0.07 - 0.78 Gy/h for EJ138/NAT. These were significantly lower than the external beam gamma radiation dose rate of 15 Gy/h. In the case of control lines which were incapable of [131I]MIBG uptake the mean absorbed doses following radiopharmaceutical were 0.03 - 0.23 Gy for UVW and 0.03 - 0.32 Gy for EJ138. Conclusion: [131I]MIBG treatment for ICCM production elicited a bystander doseresponse profile similar to that generated by external beam gamma irradiation but with significantly greater cell death. [ABSTRACT FROM AUTHOR]

Published
2014
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47. Dose– and time–response relationships for lethal mutations and chromosomal instability induced by ionizing radiation in an immortalized human keratinocyte cell line.

Author

Mothersill, C., Kadhim, M. A., O'Reilly, S., Papworth, D., Marsden, S. J., Seymour, C. B., and Wright, E. G.

Subjects
IONIZING radiation, CHROMOSOME abnormalities, IRRADIATION, KERATINOCYTES
Abstract

Purpose: To investigate the relationship between two well-established delayed effects of ionizing radiation, experiments were conducted to determine the induction and expression of lethal mutations (delayed reproductive death) and chromosomal instability with respect to dose and time in a human immortalized keratinocyte cell line. Methods: HPV-G cells were γ- or α-irradiated and maintained in culture for up to 72 population doublings. At intervals, measurements were made of cloning efficiency and the cells examined for apoptosis and cytogenetic aberrations. Results: The descendants of cells surviving 1 or 3 Gy γ-irradiation, but not 0.5 Gy γ-irradiation, exhibited a reduced colony-forming efficiency. The reduction persisted at a constant rate of 15–20% clonogenic cell loss per population doubling for up to 72 population doublings. Apoptosis was demonstrated in all colonies in the 1 and 3 Gy groups at 30 and 72 population doublings post-irradiation but not in the 0.5 Gy group. A significant persistent reduction in colony-forming ability (~80%) was demonstrated in the progeny of cells irradiated with 0.5 Gy α-particles. After 30 population doublings, the proportion of chromosomally aberrant cells was significantly greater than control values for all doses of both high- and low-LET radiations. The major cytogenetic aberrations (chromatid breaks, chromosome fragments and minutes) were consistent with the transmission of chromosomal instability. The expression of instability declined between 30 and 72 population doublings in the 0.5Gy and 3 Gy gamma-irradiation groups, but persisted up to 72 population doublings in the 1 Gy group. The expression of chromosomal instability was greater in the descendants of alpha-irradiated cells and showed little evidence of reduction with time. Conclusions: Unstable aberrations characteristic of radiation-induced chromosomal instability may commonly result in apoptosis and account for a component of the delayed reproductive death/lethal mutation phenotype in HPV-G cells. However, the absence of lethal mutations in the descendants of 0.5 Gy γ-irradiated cells indicates a low-LET threshold effect for this particular endpoint. Overall, and particularly at low doses, there is no direct correlation between the two endpoints, indicating the absence of a simple relationship between these manifestations of radiation-induced genomic instability. [ABSTRACT FROM AUTHOR]

Published
2000
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48. Involvement of energy metabolism in the production of ‘bystander effects’ by radiation.

Author

Mothersill, C, Stamato, T D, Perez, M L, Cummins, R, Mooney, R, and Seymour, C B

Subjects
ENERGY metabolism, RADIATION chemistry, MITOCHONDRIA
Abstract

These experiments were done to determine if interference with energy metabolism and REDOX biochemistry during low LET radiation exposure would alter the ability of medium harvested from the irradiated cells to induce a bystander effect in unirradiated cells. Human keratinocyte cells and CHO-K1 mutant cell lines were irradiated using cobalt 60. Clonogenic assays were used to determine the reproductive death of the cells exposed to direct irradiation or medium from irradiated cells. The persistence in progeny was also examined. Use of apoptosis inhibitors or medium from the LDH or G6PD null cell lines, reduced or prevented the bystander effect. Transfection with G6PD recovered the effect. Treatment with anti-oxidant substances, L-lactate and L-deprenyl prevented bystander factor associated cell kill. The lactate analogue, oxamate, was less effective. Data from experiments where media harvested from the different cell lines was exchanged suggest that signal production and cellular response may involve different mechanisms. The effects on exposed cells were transmitted to progeny which also showed excessive levels of cell death for several generations. The results suggest that energy/REDOX metabolism may be involved in the expression of a radiation induced bystander response. Given the aberrant energy metabolism in tumour cells, this may have implications for dose escalation in radiotherapy. [ABSTRACT FROM AUTHOR]

Published
2000

49. Effect of docetaxel (taxotere) on expression of radiation-induced lethal mutations in human cell lines.

Author

Creane, M., Seymour, C. B., and Mothersill, C.

Subjects
*DOCETAXEL, *LETHAL mutations, *PHYSIOLOGY
Abstract

Purpose: To investigate if docetaxel, ionizing radiation or a combination of both induces delayed cell death in selected human normal or tumour cell lines. Materials and methods: The initial and residual surviving fractions were determined for two malignant human colon cell lines of widely different radiosensitivity (SW 48 and HT29) and for an immortal but non-malignant human keratinocyte line (HaCaT). Results: Lethal mutations were observed only after the treatment of SW48 and HaCaT cells with radiation alone. No lethal mutations were found in the HT29 cell line. No lethal mutations were observed for any cell line treated with Docetaxel and the plating efficiency of progeny was actually increased above the control level. Conclusion: In all cases a combination of radiation and docetaxel prevented induction of lethal mutations despite the fact that radiation alone induced lethal mutations in the SW48 and HaCaT cell lines. This suggests that the effects of pre-treating with Docetaxel are in some way blocking or inhibiting the lethal mutation pathway. There appears to be a link between the tendency of the cell line to undergo apoptosis and lethal mutation expression. [ABSTRACT FROM AUTHOR]

Published
1999
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50. Radiobiological effects of docetaxel (Taxotere): a potential radiation sensitizer.

Author

Creane, M., Seymour, C. B., Colucci, S., and Mothersill, C.

Subjects
*DOCETAXEL, *RADIATION-sensitizing agents
Abstract

Purpose: To investigate the ability of docetaxel (Taxotere) to radiosensitize human cell lines of differing malignant status, intrinsic radiosensitivity and p53 status. Materials and methods: Cell survival following treatment with drug and/or radiation was determined by colony-forming assay on two malignant human colon cell lines of widely different radiosensitivity (HT29 and SW48). An immortal human keratinocyte line (HaCaT), which does not form tumours in nude mice, was used to assess the effect on non-malignant human epithelium. Results: The experiments indicate that docetaxel had the greatest cytotoxic and radiosensitizing effect on the SW48 (p53wt) cell line. The degree of radiosensitization was not improved by increasing the drug concentration, although the overall cytotoxicity was increased with increasing concentrations of the two agents. Both p53m ut lines were less sensitive to the drug, irrespective of their malignant potential. Conclusion: The results support a role for Taxotere as a weak radiosensitizer of the three cell lines tested. The p53 status and intrinsic radiosensitivity may be relevant to the mechanism. [ABSTRACT FROM AUTHOR]

Published
1999
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