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16. Basic Science * 208. Stem Cell Factor Expression is Increased in the Skin of Patients with Systemic Sclerosis and Promotes Proliferation and Migration of Fibroblasts in vitro

Author

Karrar, S., primary, Shiwen, X., additional, Nikotorowicz-Buniak, J., additional, Abraham, D. J., additional, Denton, C., additional, Stratton, R., additional, Bayley, R., additional, Kite, K. A., additional, Clay, E., additional, Smith, J. P., additional, Kitas, G. D., additional, Buckley, C., additional, Young, S. P., additional, Ye, L., additional, Zhang, L., additional, Goodall, J., additional, Gaston, H., additional, Xu, H., additional, Lutalo, P. M., additional, Zhao, Y., additional, Meng Choong, L., additional, Sangle, S., additional, Spencer, J., additional, D'Cruz, D., additional, Rysnik, O. J., additional, McHugh, K., additional, Bowness, P., additional, Rump-Goodrich, L., additional, Mattey, D., additional, Kehoe, O., additional, Middleton, J., additional, Cartwright, A., additional, Schmutz, C., additional, Askari, A., additional, Gardner, D. H., additional, Jeffery, L. E., additional, Raza, K., additional, Sansom, D. M., additional, Fitzpatrick, M., additional, Wallace, G., additional, Young, S., additional, Shaw, J., additional, Hatano, H., additional, Cauli, A., additional, Giles, J. L., additional, Mathieu, A., additional, Kollnberger, S., additional, Webster, S., additional, Ellis, L., additional, O'Brien, L. M., additional, Fitzmaurice, T. J., additional, Nazeer Moideen, A., additional, Evans, L., additional, Osgood, L., additional, Williams, A., additional, Jones, S., additional, Thomas, C., additional, O'Donnell, V., additional, Nowell, M., additional, Ouboussad, L., additional, Savic, S., additional, Dickie, L. J., additional, Hintze, J., additional, Wong, C. H., additional, Cook, G. P., additional, Buch, M., additional, Emery, P., additional, McDermott, M. F., additional, Hardcastle, S. A., additional, Gregson, C. L., additional, Deere, K., additional, Davey Smith, G., additional, Dieppe, P., additional, Tobias, J. H., additional, Dennison, E., additional, Edwards, M., additional, Bennett, J., additional, Coggon, D., additional, Palmer, K., additional, Cooper, C., additional, McWilliams, D., additional, Young, A., additional, Kiely, P. D., additional, Walsh, D., additional, Taylor, H. J., additional, Harding, I., additional, Hutchinson, J., additional, Nelson, I., additional, Blom, A., additional, Tobias, J., additional, Clark, E., additional, Parker, J., additional, Bukhari, M., additional, Jayakumar, K., additional, Kiely, P., additional, Diffin, J., additional, Lunt, M., additional, Marshall, T., additional, Chipping, J., additional, Symmons, D., additional, Verstappen, S., additional, Bluett, J., additional, Bowes, J., additional, Ho, P., additional, McHugh, N., additional, Buden, D., additional, Fitzgerald, O., additional, Barton, A., additional, Glossop, J. R., additional, Nixon, N. B., additional, Emes, R. D., additional, Dawes, P. T., additional, Farrell, W. E., additional, Mattey, D. L., additional, Scott, I. C., additional, Steer, S., additional, Seegobin, S., additional, Hinks, A. M., additional, Eyre, S., additional, Morgan, A., additional, Wilson, A. G., additional, Hocking, L., additional, Wordsworth, P., additional, Worthington, J., additional, Cope, A., additional, Lewis, C. M., additional, Guerra, S., additional, Ahmed, B. A., additional, Abraham, D., additional, Fonseca, C., additional, Robinson, J., additional, Taylor, J., additional, Haroon Rashid, L., additional, Flynn, E., additional, Isaacs, J., additional, Barrett, J. H., additional, Kingston, B., additional, Ahmed, M., additional, Kirwan, J. R., additional, Marshall, R., additional, Chapman, K., additional, Pearson, R., additional, Heycock, C., additional, Kelly, C., additional, Rynne, M., additional, Saravanan, V., additional, Hamilton, J., additional, Saeed, A., additional, Coughlan, R., additional, Carey, J. J., additional, Farah, Z., additional, Matthews, W., additional, Bell, C., additional, Petford, S., additional, Tibbetts, L.-M., additional, Douglas, K. M. J., additional, Holden, W., additional, Ledingham, J., additional, Fletcher, M., additional, Winfield, R., additional, Price, Z., additional, Mackay, K., additional, Dixon, C., additional, Oppong, R., additional, Jowett, S., additional, Nicholls, E., additional, Whitehurst, D., additional, Hill, S., additional, Hammond, A., additional, Hay, E., additional, Dziedzic, K., additional, Righetti, C., additional, Lebmeier, M., additional, Manning, V. L., additional, Hurley, M., additional, Scott, D. L., additional, Choy, E., additional, Bearne, L., additional, Nikiphorou, E., additional, Morris, S., additional, James, D., additional, Wong, E. C., additional, Long, J., additional, Fletcher, A., additional, Holmes, S., additional, Hockey, P., additional, Abbas, M., additional, Chattopadhyay, C., additional, Flint, J., additional, Gayed, M., additional, Schreiber, K., additional, Arthanari, S., additional, Nisar, M., additional, Khamashta, M., additional, Gordon, C., additional, Giles, I., additional, Robson, J., additional, Kiran, A., additional, Maskell, J., additional, Arden, N., additional, Hutchings, A., additional, Emin, A., additional, Culliford, D., additional, Dasgupta, B., additional, Hamilton, W., additional, Luqmani, R., additional, Jethwa, H., additional, Rowczenio, D., additional, Trojer, H., additional, Russell, T., additional, Loeffler, J., additional, Hawkins, P., additional, Lachmann, H., additional, Verma, I., additional, Syngle, A., additional, Krishan, P., additional, Garg, N., additional, McGowan, S. P., additional, Gerrard, D. T., additional, Chinoy, H., additional, Ollier, W. E., additional, Cooper, R. G., additional, Lamb, J. A., additional, Taborda, L., additional, Correia Azevedo, P., additional, Isenberg, D., additional, Leyland, K. M., additional, Judge, A., additional, Hunter, D., additional, Hart, D., additional, Javaid, M. K., additional, Edwards, M. H., additional, Litwic, A. E., additional, Jameson, K. A., additional, Deeg, D., additional, Cushnaghan, J., additional, Aihie Sayer, A., additional, Jagannath, D., additional, Parsons, C., additional, Stoppiello, L., additional, Mapp, P., additional, Ashraf, S., additional, Wilson, D., additional, Hill, R., additional, Scammell, B., additional, Wenham, C., additional, Shore, P., additional, Hodgson, R., additional, Grainger, A., additional, Aaron, J., additional, Hordon, L., additional, Conaghan, P., additional, Bar-Ziv, Y., additional, Beer, Y., additional, Ran, Y., additional, Benedict, S., additional, Halperin, N., additional, Drexler, M., additional, Mor, A., additional, Segal, G., additional, Lahad, A., additional, Haim, A., additional, Rath, U., additional, Morgensteren, D. M., additional, Salai, M., additional, Elbaz, A., additional, Vasishta, V. G., additional, Derrett-Smith, E., additional, Hoyles, R., additional, Khan, K., additional, Ezeonyeji, A., additional, Takhar, G., additional, Ong, V., additional, Loughrey, L., additional, Bissell, L.-A., additional, Hensor, E., additional, Abignano, G., additional, Redmond, A., additional, Del Galdo, F., additional, Hall, F. C., additional, Malaviya, A., additional, Baker, S., additional, Furlong, A., additional, Mitchell, A., additional, Godfrey, A. L., additional, Ruddlesden, M., additional, Hadjinicolaou, A., additional, Hughes, M., additional, Moore, T., additional, O'Leary, N., additional, Tracey, A., additional, Ennis, H., additional, Dinsdale, G., additional, Roberts, C., additional, Herrick, A., additional, Denton, C. P., additional, Guillevin, L., additional, Hunsche, E., additional, Rosenberg, D., additional, Schwierin, B., additional, Scott, M., additional, Krieg, T., additional, Anderson, M., additional, Matucci-Cerinic, M., additional, Alade, R., additional, Xu, S., additional, Nihtyanova, S., additional, Clark, K. E., additional, Tam, F. W. K., additional, Unwin, R., additional, Stratton, R. J., additional, Schreiber, B., additional, Seng Edwin Lim, C., additional, Corsiero, E., additional, Sutcliffe, N., additional, Wardemann, H., additional, Pitzalis, C., additional, Bombardieri, M., additional, Tahir, H., additional, Donnelly, S., additional, Greenwood, M., additional, Smith, T. O., additional, Easton, V., additional, Bacon, H., additional, Jerman, E., additional, Armon, K., additional, Poland, F., additional, Macgregor, A., additional, van der Heijde, D., additional, Sieper, J., additional, Elewaut, D., additional, Pangan, A. L., additional, Nguyen, D., additional, Badenhorst, C., additional, Kirby, S., additional, White, D., additional, Harrison, A., additional, Garcia, J. A., additional, Stebbings, S., additional, MacKay, J. W., additional, Aboelmagd, S., additional, Gaffney, K., additional, Deodhar, A., additional, Braun, J., additional, Mack, M., additional, Hsu, B., additional, Gathany, T., additional, Han, C., additional, Inman, R. D., additional, Cooper-Moss, N., additional, Packham, J., additional, Strauss, V., additional, Freeston, J. E., additional, Coates, L., additional, Nam, J., additional, Moverley, A. R., additional, Helliwell, P., additional, Wakefield, R., additional, Mease, P., additional, Fleischmann, R., additional, Wollenhaupt, J., additional, Kielar, D., additional, Woltering, F., additional, Stach, C., additional, Hoepken, B., additional, Arledge, T., additional, Gladman, D., additional, Coteur, G., additional, Kavanaugh, A., additional, Purcaru, O., additional, McInnes, I., additional, Gottlieb, A. B., additional, Puig, L., additional, Rahman, P., additional, Ritchlin, C., additional, Li, S., additional, Wang, Y., additional, Mendelsohn, A., additional, Doyle, M., additional, Tillett, W., additional, Jadon, D., additional, Shaddick, G., additional, Cavill, C., additional, Robinson, G., additional, Sengupta, R., additional, Korendowych, E., additional, de Vries, C., additional, Thomas, R. C., additional, Shuto, T., additional, Busquets-Perez, N., additional, Marzo-Ortega, H., additional, McGonagle, D., additional, Richards, G., additional, Bingham, S., additional, John Hamlin, P., additional, Adshead, R., additional, Cambridge, S., additional, Suppiah, P., additional, Cullinan, M., additional, Nolan, A., additional, Thompson, W. M., additional, Mathieson, H. R., additional, Mackie, S. L., additional, Bryer, D., additional, Krutikov, M., additional, Gray, L., additional, Bruce, E., additional, Keat, A., additional, Innes, W., additional, Pandit, R., additional, Kay, L., additional, Lapshina, S., additional, Myasoutova, L., additional, Erdes, S., additional, Wallis, D., additional, Waldron, N., additional, Thorne, I., additional, Harris, C., additional, Vohra, K., additional, Khinchi, D., additional, Kaur, L., additional, Jones, A., additional, Harrison, N., additional, Harris, D., additional, Jones, T., additional, Rees, J., additional, Bennett, A., additional, Fazal, S., additional, Tugnet, N., additional, Barkham, N., additional, Basu, N., additional, McClean, A., additional, Harper, L., additional, Amft, E. N., additional, Dhaun, N., additional, Luqmani, R. A., additional, Little, M. A., additional, Jayne, D. R., additional, Flossmann, O., additional, McLaren, J., additional, Kumar, V., additional, Reid, D. M., additional, Macfarlane, G. J., additional, Jones, G., additional, Yates, M., additional, Watts, R. A., additional, Igali, L., additional, Mukhtyar, C., additional, Doll, H., additional, Yew, S., additional, Suppiah, R., additional, Hoglund, P., additional, Jayne, D., additional, Westman, K., additional, Win Maw, W., additional, Patil, P., additional, Williams, M., additional, Adizie, T., additional, Christidis, D., additional, Borg, F., additional, Robertson, A., additional, Croft, A. P., additional, Smith, S., additional, Carr, S., additional, Youssouf, S., additional, Salama, A., additional, Pusey, C., additional, and Morgan, M., additional

Published
2013
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36. Bromocriptine and Dopamine Mediate Independent and Synergistic Apoptotic Pathways in Pituitary Cells.

Author

Rowther, F. B., Richardson, A., Clayton, R. N., and Farrell, W. E.

Subjects
DOPAMINE, PROLACTINOMA, PROLACTIN, PITUITARY tumors, BROMOCRIPTINE, APOPTOSIS
Abstract

Dopamine (DA) agonists are the primary treatment choice for prolactinoma, effectively suppressing prolactin expression and reducing tumour size. However, the intracellular pathway(s) through which either DA or its agonists impact on proliferation or lead to tumour shrinkage are incompletely understood. To identify the mediators in the apoptotic cascades after DA or DA agonist challenges we used a well-characterized model system, the rodent somatolactotroph cell line GH3. In these cells, we show that apoptosis induced by the DA agonist bromocriptine (BC), but not DA, is initiated through activation of the JNK pathway. However, both DA and BC activate the terminal effector caspase, caspase-3. Kinetic studies and chemical inhibitor co-incubation experiments support a role for JNK activation preceding caspase-9 activation in BC challenged cells, however, engagement of these mediators was not apparent in DA challenge cells. These studies suggest that apoptosis induced by BC or DA is mediated through distinct and independent pathways that converge with activation of the terminal caspase, caspase-3. These observations were further reinforced by our findings that DA and BC, in co-incubation experiments, synergistically induce apoptosis. These findings raise the possibility that drugs acting through the same pathway as DA may be clinically beneficial when combined with BC. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2010
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37. A Novel Apoptosis Gene Identified in the Pituitary Gland.

Author

Farrell, W. E.

Subjects
*PITUITARY tumors, *ADENOMA, *PITUITARY gland, *APOPTOSIS, *GENES
Abstract

Although multiple different cancers have been described, it is likely that these tumour types share a small, and common, number of newly acquired functional capabilities. Tumours that arise within the pituitary gland are no exception with respect to these new functional capabilities. Although compelling evidence for self-sufficiency in growth signals is presented, loss of functional tumour suppressor genes by classic mechanisms has not been clearly established. However, and in this context, methylation-mediated or -associated gene silencing, in particular of tumour suppressor genes, has been reported by numerous investigators in this tumour type. More recently, a search for novel genes on the basis of their inappropriate methylation has led to identification of a novel pro-apoptotic gene. Its pituitary tumour derivation and role in drug-induced apoptosis resulted in the acronym PTAG (pituitary tumour apoptosis gene) being assigned to this gene. In a model pituitary tumour cell line, AtT20, expression of PTAG per se had no discernible effects on proliferation, cell cycle profile or viability. However, enforced expression was associated with a significantly increased sensitivity to the apoptotic effects induced by bromocriptine challenge. Apoptosis was mediated through caspase activation and associated with DNA fragmentation as determined by TUNEL labelling. Similar findings are also evident in the rodent pituitary cell line, GH3 and our data shows that drugs other than bromocriptine, and that engage characterized receptors, elicit a PTAG-augmented apoptotic response. The isolation of novel genes, on the basis of their methylation status, offers a significant advantage with respect to our understanding of tumorigenesis in both the pituitary and other tumour types. The reversal of apparent gene silencing may lead to tumour cell ‘sensitisation’ to chemo- and radiotherapeutic treatment strategies. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2006
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40. Sporadic Colorectal Polyps: Management Options and Guidelines.

Author

Anwar, Suhail, White, J., Hall, C., Farrell, W. E., Deakin, M., and Elder, J. B.

Subjects
COLON cancer, RISK management in business
Abstract

Focuses on the management and guidelines of sporadic colorectal polyps. Classification of colorectal polyps; Association of adenomatous polyps and villous adenoma with high-grade dysplasia; Need of postpolypectomy surveillance.

Published
1999
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46. Cyclin D1 (CCND1) genotype is associated with tumour grade in sporadic pituitary adenomas.

Author

Simpson, D J, Fryer, A A, Grossman, A B, Wass, J A, Pfeifer, M, Kros, J M, Clayton, R N, and Farrell, W E

Abstract

The cyclin D1 (CCND1) gene contains a frequent A/G polymorphism within the splice donor region of exon 4/intron 4. CCND1 genotype is associated with clinical outcome in a number of malignancies although prognostic significance varies with tumour type. We examined CCND1 allele frequencies and genotype distribution in 294 patients with sporadic pituitary adenomas of various histologies. CCND1 allele frequencies and distribution of genotypes were similar in the 294 cases compared with previously reported control populations. Analysis according to tumour subtype showed no statistical difference in allele frequencies compared with controls. However, CCND1 genotype distribution in the somatotrophinomas showed a significant difference compared with normal controls (P = 0.008). We next examined CCND1 allele frequencies and genotype distribution across the tumour grades. Within the total tumour cohort the CCND1 allele frequencies showed a significant inverse relationship across the tumour grades (P = 0.005). The CCND1 A allele progressively increased from grade 1 (0.37) through to grade 4 (0.62) tumours, whilst the CCND1 G allele frequency progressively decreased from grade 1 (0.63) through to grade 4 (0.38) tumours. Trend analysis of CCND1 genotypes showed a significant progressive increase in AA frequency from grade 1 (15%) through to grade 4 (46%) tumours (P = 0.005). The CCND1 GG genotype progressively decreased from grade 1 (41%) through to grade 4 (23%) tumours (P = 0.204). No statistical significance was observed between CCND1 AG genotype and tumour grades. While the functional significance of the observed segregation of the CCND1 A/G polymorphism and tumour grade is unclear, our data suggest that CCND1 allele frequencies and genotype distributions show significant differences between tumour grades in sporadic pituitary adenomas. Since CCND1 genotype may be determined by analysis of peripheral blood samples it may provide a useful predictive marker for those tumours likely to show invasive behaviour. This may be clinically useful in indicating which tumours should receive adjunctive treatment (e.g. radiotherapy) immediately after surgical resection.

Published
2001
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47. Aberrant expression of G(1)/S regulators is a frequent event in sporadic pituitary adenomas.

Author

Simpson, D J, Frost, S J, Bicknell, J E, Broome, J C, McNicol, A M, Clayton, R N, and Farrell, W E

Abstract

Components of the pRb/p16/cyclin D1/CDK4 pathway are frequent targets in numerous tumour types, including those of pituitary origin. However, previous studies of pituitary tumours have examined individual components of this pathway. Therefore, to determine their overall contribution we have simultaneously examined the immunohistochemical status of pRb, p16 and cyclin D1 and analysed the CDK4 gene for a characterized activating mutation. Of the total pituitary tumour cohort (29 clinically non-functioning adenomas and 16 somatotrophinomas) abnormal expression of either pRb, p16 or cyclin D1 was observed in 36 of 45 (80%) tumours and was significantly (P = 0.005) associated with non-functioning tumours (27/29; 93%) compared with somatotrophinomas (9/16, 56%). Loss of either pRb or p16 expression was mutually exclusive in 23 of 45 (51%) tumours, whilst concomitant loss of pRb and p16 expression was observed in five tumours. Cyclin D1 overexpression was observed in 22 of 45 (49%) tumours, however, there was no significant association between overexpression of cyclin D1 and the expression status of either pRb or p16. In addition, no activating mutations within codon 24 of the CDK4 gene were detected. This study provides evidence for the first time that components of the pRb/p16/cyclin D1/CDK4 pathway, either alone or in combination, are frequently deregulated in human pituitary tumours, suggesting that this pathway may be a useful target in drug or gene therapeutic approaches.

Published
2001
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50. Pro-opiomelanocortin gene expression and peptide secretion in human small-cell lung cancer cell lines

Author

White, A., Stewart, M. F., Farrell, W. E., Crosby, S. R., Lavender, P. M., Twentyman, P. R., Rees, L. H., and Clark, A. J. L.

Abstract

Expression of the RNA coding for the ACTH—β-lipotrophin precursor, pro-opiomelanocortin (POMC), has been demonstrated in five human small-cell lung cancer (SCLC) cell lines. Using Northern and slot-blot hybridization analysis of RNA and a bovine POMC cDNA as probe, the processed POMC RNA from SCLC cells was found to be approximately 1350 nucleotides in length, which is larger than that found in the normal human pituitary. Expression of the POMC gene was confirmed by measurement of ACTH precursors secreted by the cells, using a novel two-site immunoradiometric assay based on monoclonal antibodies, which directly quantifies both POMC and pro-ACTH but does not recognize ACTH. Levels of POMC in medium accumulated throughout the growth of the cells, in contrast to POMC RNA which showed a relatively constant level of expression. We conclude that human SCLC cell lines are valuable models for studying the aberrant expression and regulation of the human POMC gene.

Published
1989
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