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7 results on '"E. W. McDermott"'

1. Incidental Phaeochromocytoma on Staging PET-CT in a Patient with a Sigmoid Tumour and Situs Inversalis Totalis

Author

M. R. Boland, A. J. Lowery, S. Walsh, D. Beddy, R. S. Prichard, D. O’Shea, S. J. Skehan, and E. W. McDermott

Subjects
Surgery, RD1-811
Abstract

An adrenal “incidentaloma” is defined as an unexpected finding on radiological imaging performed for unrelated indications. Improvements in radiological technology have seen a dramatic increase in this phenomenon. We report the unique case of a 60-year-old female presenting with a 6-month history of abdominal pain, altered bowel habit, and rectal bleeding. Her past medical history included situs inversus totalis and a patent ductus arteriosus. Colonoscopy revealed an ulcerated tumour in her sigmoid colon. Staging PET-CT confirmed a sigmoid tumour and also identified a large heterogenous enhancing FDG-avid right adrenal mass. Biochemical testing/MIBG imaging confirmed a right adrenal phaeochromocytoma. Hypertension was controlled and excision was performed via a transperitoneal laparoscopic adrenalectomy, in the left lateral decubitus position. Uniquely, liver retraction was not required due to its position in the left hypochondrium. Histology confirmed a benign 46 mm phaeochromocytoma. Subsequent uncomplicated sigmoid colectomy/right salpingo-oophorectomy for a locally advanced colonic tumour was performed with adjuvant chemotherapy. This case highlights the importance of accurately identifying functioning adrenal tumours before elective surgery as undiagnosed phaeochromocytomas carry significant intraoperative morbidity/mortality. Right adrenalectomy was made easier in this patient by the liver’s unique position. Uncomplicated colorectal resection was made possible by combined preoperative functional/anatomical imaging.

Published
2014
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2. Protein kinase Cdelta expression in breast cancer as measured by real-time PCR, western blotting and ELISA

Author

K. O’Brien, E. W. McDermott, Michael J. Duffy, Viktor Magdolen, Anneke Geurts-Moespot, D Evoy, Eadaoin McKiernan, John W.M. Martens, Fred C.G.J. Sweep, Anieta M. Sieuwerts, Nicolai Grebenchtchikov, J.P. Crown, and Medical Oncology

Subjects
Gene isoform, Cancer Research, Blotting, Western, Breast Neoplasms, Enzyme-Linked Immunosorbent Assay, Aetiology, screening and detection [ONCOL 5], Biology, Polymerase Chain Reaction, breast cancer, SDG 3 - Good Health and Well-being, Translational research [ONCOL 3], Humans, RNA, Messenger, Protein kinase A, Molecular Diagnostics, Protein kinase C, Molecular diagnosis, prognosis and monitoring [UMCN 1.2], Messenger RNA, Endocrinology and reproduction [UMCN 5.2], Reverse Transcriptase Polymerase Chain Reaction, Kinase, Hormonal regulation [IGMD 6], Middle Aged, Survival Analysis, protein kinase Cδ, Molecular biology, Blot, Protein Kinase C-delta, Real-time polymerase chain reaction, Oncology, Apoptosis, Disease Progression, Female
Abstract

Contains fulltext : 71340.pdf (Publisher’s version ) (Closed access) The protein kinase C (PKC) family of genes encode serine/threonine kinases that regulate proliferation, apoptosis, cell survival and migration. Multiple isoforms of PKC have been described, one of which is PKCdelta. Currently, it is unclear whether PKCdelta is involved in promoting or inhibiting cancer formation/progression. The aim of this study was therefore to investigate the expression of PKCdelta in human breast cancer and relate its levels to multiple parameters of tumour progression. Protein kinase Cdelta expression at the mRNA level was measured using real-time PCR (n=208) and at protein level by both immunoblotting (n=94) and ELISA (n=98). Following immunoblotting, two proteins were identified, migrating with molecular masses of 78 and 160 kDa. The 78 kDa protein is likely to be the mature form of PKCdelta but the identity of the 160 kDa form is unknown. Levels of both these proteins correlated weakly but significantly with PKCdelta concentrations determined by ELISA (for the 78 kDa form, r=0.444, P

Published
2008

3. Expression of survivin and its splice variants survivin-2B and survivin-ΔEx3 in breast cancer

Author

Arnold D.K. Hill, Michael J. Duffy, E. W. McDermott, Brigid C. Browne, Bríd M. Ryan, John Crown, Niall O'Higgins, Caroline O'Shea, and Norma O'Donovan

Subjects
Cancer Research, Programmed cell death, Survivin, Breast Neoplasms, Biology, Inhibitor of apoptosis, Inhibitor of Apoptosis Proteins, Breast cancer, medicine, Humans, Breast, breast carcinoma, skin and connective tissue diseases, Molecular Diagnostics, programmed cell death, neoplasms, Messenger RNA, apoptosis, medicine.disease, Fibroadenoma, Neoplasm Proteins, Alternative Splicing, Oncology, Apoptosis, inhibitor of apoptosis, Cancer research, Female, Breast carcinoma, Microtubule-Associated Proteins
Abstract

Alternative splicing of survivin mRNA gives rise to multiple isoforms, that is, survivin and 3 splice variants, survivin-2B, survivin-3B and survivin-DeltaEx3. The aim of this study was to compare the expression of survivin, survivin-2B and survivin-DeltaEx3 in normal breast tissue, fibroadenomas, primary breast cancer and axillary nodal metastases. Survivin, survivin-2B and survivin-DeltaEx3 mRNA were measured using semiquantitative RT-PCR. In the primary carcinomas, we related mRNA for each form of survivin to both survivin protein and apoptosis. For each type of breast tissue, survivin was the predominant form detected, being present in 146 out of 156 (93.6%) primary breast carcinomas, 11 out of 11 (100%) axillary nodal metastases, 21 out of 31 (67.7%) fibroadenomas and five out of 22 (22.7%) specimens of normal breast tissue. Levels of the three forms of survivin were significantly higher in the carcinomas compared to normal breast tissue (P0.0001). Levels of both survivin-2B and survivin-DeltaEx3 but not survivin were significantly higher in nodal metastases than primary carcinomas. Survivin mRNA levels correlated significantly with survivin protein. Finally, both survivin and survivin-DeltaEx3 but not survivin-2B correlated positively with apoptosis. Although survivin, survivin-2B and survivin-DeltaEx3 were all detected in both malignant and nonmalignant breast tissue, the predominant form was survivin. Our results suggest that the different forms of survivin may have different roles in apoptosis in breast cancer.

Published
2004
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5. Sylvester o’halloran surgical scientific meeting

Author

N. Relihan, G. McGreal, M. Murray, E. W. McDermott, N. J. O’Higgins, M. J. Duffy, D. A. McNamara, J. Harmey, J. H. Wang, D. Donovan, T. N. Walsh, D. J. Bouchier-Hayes, E. Kay, J. D. Kelly, H. P. Weir, P. F. Keane, S. R. Johnston, K. E. Williamson, P. W. Hamilton, D. McManus, M. Morrin, P. V. Delaney, D. C. Winter, B. J. Harvey, J. P. Geibel, G. C. O’Sullivan, C. P. Delaney, R. Coffey, T. F. Gorey, J. M. Fitzpatrick, N. F. Fanning, W. Kirwan, T. Cotter, D. Bouchier-Hayes, H. P. Redmond, G. Pidgeon, F. Fennessy, C. Kelly, R. Flavin, A. M. Rasheed, A. Leahy, E. E. Lang, M. T. P. Caldwell, W. A. Tanner, P. D. Kiely, M. O’Reilly, S. Tierney, M. Barry, J. Drumm, P. A. Grace, C. M. Gallagher, D. C. Grant, P. Connell, M. K. Barry, O. Traynor, J. M. P. Hyland, M. J. O’Sullivan, D. Evoy, W. O. Kirwan, B. Cannon, L. Kenny-Walshe, M. J. Whelton, H. O’Grady, S. O’Neill, J. M. Hyland, S. H. Teh, S. O’Ceallaigh, M. K. O’Donohoe, F. B. Keane, G. C. O’Toole, J. Calleary, L. Basso, S. B. Amjad, Z. Khan, L. McMullin, W. P. Joyce, P. J. Balfe, M. T. Caldwell, S. Teahan, K. Al-Brekeit, A. Rasheed, A. Cullen, C. O’Keane, J. MacFarlane, M. Walsh, T. McGloughlin, P. Grace, D. Colgan, P. Madhavan, S. Sultan, M. P. Colgan, D. Moore, G. Shanik, N. McEniff, M. Molloy, E. Eguare, C. Fiuza, P. Burke, R. Maher, M. Creamer, C. J. Cronin, H. H. Sigurdsso, W. Kim, G. Linklater, K. S. Cross, W. G. Simpson, J. A. M. Shaw, D. W. M. Pearson, P. Fitzgerald, P. Quinn, C. M. Brady, S. M. A. Shah, M. Ehtisham, M. S. Khan, H. D. Flood, M. Loubani, K. Sweeney, B. Lenehan, V. Lynch, A. Joy, D. Reidy, K. Mahalingam, W. Cashman, E. D. Mulligan, T. Purcell, B. Dunne, M. Griffin, N. Noonan, D. Hollywood, N. Keeling, J. V. Reynolds, T. P. J. Hennessy, D. O’Halloran, P. Neary, D. Hamilton, N. Haider, N. Aherne, R. G. K. Watson, D. Walsh, M. Murphy, M. Joyce, S. Johnston, O. Clinton, H. F. Given, A. Brannigan, M. O’Donohoe, J. Donohoe, T. Corrigan, M. Bresnihan, T. M. Feeley, M. P. McMonagle, D. Quinlan, D. Kelly, P. K. Hegarty, B. Tan, C. Cronin, M. P. Brady, M. Zeeshan, D. J. McAvinchey, C. Mooney, D. Coyle, G. Khayyat, E. Masterson, T. Thambi-Pillai, K. Farah, M. B. Codd, G. G. Tsiotos, C. D. Johnson, M. G. Sarr, M. R. Kell, M. Lynch, D. Ryan, A. O’Donovan, M. Cassidy, M. Doyle, G. Fulton, P. R. O’Connell, R. Kingston, M. Dillon, E. McDermott, N. O’Higgins, R. G. O’Sullivan, and J. A. O’Donnell

Subjects
business.industry, Foundation (engineering), Medicine, Library science, General Medicine, business
Published
1998
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6. The role of oestrogen receptor {alpha} in human thyroid cancer: contributions from coregulatory proteins and the tyrosine kinase receptor HER2

Author

E. Myers, Arnold D.K. Hill, D. Kavanagh, Leonie S. Young, Marie McIlroy, E. W. McDermott, Fiona T Bane, and Thomas Crotty

Subjects
Adult, Male, Cancer Research, medicine.medical_specialty, Adolescent, Receptor, ErbB-2, Endocrinology, Diabetes and Metabolism, Receptor tyrosine kinase, Young Adult, Endocrinology, Cyclin D1, Internal medicine, Coactivator, Adenocarcinoma, Follicular, medicine, Tumor Cells, Cultured, Humans, Thyroid Neoplasms, Receptor, Follicular thyroid cancer, Child, Thyroid cancer, Aged, Aged, 80 and over, biology, Thyroid, Carcinoma, Estrogen Receptor alpha, Receptor Protein-Tyrosine Kinases, Middle Aged, medicine.disease, Survival Analysis, medicine.anatomical_structure, Oncology, Case-Control Studies, Child, Preschool, biology.protein, Trans-Activators, Female, Co-Repressor Proteins, Proto-oncogene tyrosine-protein kinase Src, Transcription Factors
Abstract

Epidemiological, clinical, and molecular studies suggest a role for oestrogen in thyroid cancer. How oestrogen mediates its effects and the consequence of it on clinical outcome has not been fully elucidated. The participation of coregulatory proteins in modulating oestrogen receptor (ER) function and input of crosstalk with the tyrosine kinase receptor HER2 was investigated. Oestrogen induced cell proliferation in the follicular thyroid cancer (FTC)-133 cells, but not in the anaplastic 8305C cell line. Knockdown of the coactivator steroid receptor coactivator (SRC)-1 inhibited FTC-133 basal, but not oestrogen induced, cell proliferation. Oestrogen also increased protein expression of SRC-1 and the ER target gene cyclin D1 in the FTC-133 cell line. ERα, ERβ, the coregulatory proteins SRC-1 and nuclear corepressor (NCoR), and the tyrosine kinase receptor HER2 were localised by immunohistochemistry and immnofluorescence in paraffin-embedded tissue from thyroid tumour patients (n=111). ERα was colocalised with both SRC-1 and NCoR to the nuclei of the tumour epithelial cells. Expression of ERα and NCoR was found predominantly in non-anaplastic tumours and was significantly associated with well-differentiated tumours and reduced incidence of disease recurrence. In non-anaplastic tumours, HER2 was significantly associated with SRC-1, and these proteins were associated with poorly differentiated tumours, capsular invasion and disease recurrence. Totally, 87% of anaplastic tumours were positive for SRC-1. Kaplan–Meier estimates of disease-free survival indicated that in thyroid cancer, SRC-1 strongly correlates with reduced disease-free survival (PP

Published
2009

7. ADAM-17 predicts adverse outcome in patients with breast cancer.

Author

P. M. McGowan, E. McKiernan, F. Bolster, B. M. Ryan, A. D. K. Hill, E. W. McDermott, D. Evoy, N. OHiggins, J. Crown, and M. J. Duffy

Subjects
*METALLOPROTEINASES, *ENZYMES, *LIGANDS (Biochemistry), *CANCER, *HEPARIN
Abstract

ADAM-17 is a matrix metalloproteinase-like enzyme involved in the release of several ligands that have been shown to promote both cancer formation and progression. These ligands include transforming growth factor-a, amphiregulin, heparin-binding epidermal growth factor, epiregulin and tumor necrosis factor-a. In this investigation, we measured the expression of total ADAM-17 by enzyme-linked immunosorbent assay in 153 invasive breast cancers. We also measured the precursor and active forms by western blotting in 140 invasive breast cancers. Expression of ADAM-17 was significantly increased in high-grade compared with low-grade tumors and was independent of tumor size, lymph node metastasis and estrogen receptor status. Patients with high expression of ADAM-17 had a significantly shorter overall survival compared with those with low expression. Significantly, the prognostic impact of ADAM-17 was independent of conventional prognostic factors for breast cancer. Our results are further evidence that ADAM-17 is involved in breast cancer progression and thus provides further impetus for exploiting ADAM-17 as new target for cancer treatment. [ABSTRACT FROM AUTHOR]

Published
2008
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