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302. Chapter 2.06: Noble Gases as Mantle Tracers.

Author

Hilton, D. R. and Porceli, D.

Abstract

Chapter 6 of the book "Treatise on Geochemistry: The Mantle and the Core," Volume 2, is presented. The chapter focuses on the use of noble gases as geochemical and mantle tracers. It also offers information about the characteristics of mantle noble gases, the core and the chemistry of the lithosphere.

Published
2005

306. The scaffold protein KSR1, a novel therapeutic target for the treatment of Merlin-deficient tumors

Author

Zhou, L, Lyons-Rimmer, J, Ammoun, S, Müller, J, Lasonder, E, Sharma, V, Ercolano, E, Hilton, D, Taiwo, I, Barczyk, M, and Hanemann, C O

Abstract

Merlin has broad tumor-suppressor functions as its mutations have been identified in multiple benign tumors and malignant cancers. In all schwannomas, the majority of meningiomas and 1/3 of ependymomas Merlin loss is causative. In neurofibromatosis type 2, a dominantly inherited tumor disease because of the loss of Merlin, patients suffer from multiple nervous system tumors and die on average around age 40. Chemotherapy is not effective and tumor localization and multiplicity make surgery and radiosurgery challenging and morbidity is often considerable. Thus, a new therapeutic approach is needed for these tumors. Using a primary human in vitromodel for Merlin-deficient tumors, we report that the Ras/Raf/mitogen-activated protein, extracellular signal-regulated kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) scaffold, kinase suppressor of Ras 1 (KSR1), has a vital role in promoting schwannomas development. We show that KSR1 overexpression is involved in many pathological phenotypes caused by Merlin loss, namely multipolar morphology, enhanced cell–matrix adhesion, focal adhesion and, most importantly, increased proliferation and survival. Our data demonstrate that KSR1 has a wider role than MEK1/2 in the development of schwannomas because adhesion is more dependent on KSR1 than MEK1/2. Immunoprecipitation analysis reveals that KSR1 is a novel binding partner of Merlin, which suppresses KSR1’s function by inhibiting the binding between KSR1 and c-Raf. Our proteomic analysis also demonstrates that KSR1 interacts with several Merlin downstream effectors, including E3 ubiquitin ligase CRL4DCAF1. Further functional studies suggests that KSR1 and DCAF1 may co-operate to regulate schwannomas formation. Taken together, these findings suggest that KSR1 serves as a potential therapeutic target for Merlin-deficient tumors.

Published
2016
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318. DAN is a secreted glycoprotein related to Xenopus cerberus

Author

Stanley, E., primary, Biben, C., additional, Kotecha, S., additional, Fabri, L., additional, Tajbakhsh, S., additional, Wang, C-C., additional, Hatzistavrou, T., additional, Roberts, B., additional, Drinkwater, C., additional, Lah, M., additional, Buckingham, M., additional, Hilton, D., additional, Nash, A., additional, Mohun, T., additional, and Harvey, R.P., additional

Published
1998
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319. Irish gerontological society

Author

Finucane, P., primary, Giles, L., additional, O’Sullivan, C., additional, Duggan, J., additional, Sexton, A., additional, Atkins, N., additional, O’Brien, E., additional, Freyne, A., additional, Wrigley, M., additional, Maguire, C. P., additional, Rowan, M., additional, O’Neill, D., additional, Lawlor, B. A., additional, Walsh, J. B., additional, Coakley, D., additional, Cagney, M., additional, Harbison, J., additional, Crowe, M., additional, Keating, D., additional, Coen, R. F., additional, O’Boyle, C. A., additional, Doyle, R. M., additional, Kennedy, N. P., additional, Doyle, S., additional, Gerrard-Dunne, P., additional, Weir, D. G., additional, Coen, R., additional, Mulpeter, K., additional, McNally, B., additional, Daly, E., additional, Harmon, D., additional, Stokes, E., additional, Kennedy, N., additional, Gilchriest, D., additional, Heaney, A. E., additional, Young, I. S., additional, Beringer, T. R. O., additional, Kirby, M., additional, Swanwick, G. R. J., additional, Bruce, I., additional, Buggy, F., additional, Beausang, P., additional, O’Connor, M., additional, Hyland, M., additional, Twomey, C., additional, MacMahon, M., additional, Smith, T., additional, Love, Wm. C., additional, Foy, C. J., additional, Passmore, A. P., additional, Vahidassr, M. D., additional, Smye, M., additional, Young, I., additional, Cunningham, C., additional, Horgan, N. F., additional, Keane, N., additional, Connolly, P., additional, Mannion, A., additional, Kelly, A., additional, Power, M., additional, Greene, J., additional, Fan, C. W., additional, McDonnell, B., additional, Johnson, Z., additional, Doona, M., additional, Lawlor, R., additional, Magee, C., additional, McCormack, P., additional, Nolan, D., additional, Ó Mathúna, P., additional, Lyons, D., additional, Allain, T. J., additional, Roy, S., additional, Polkey, M., additional, Swift, C. G., additional, Heraty, M., additional, Keane, E. M., additional, O’Broin, S., additional, Kelleher, B., additional, O’Connor, M. P., additional, Gaynor, C., additional, Lynch, D., additional, Hyland, C. M., additional, Hanlon, D., additional, Harrington, P., additional, Ryan, M., additional, Doyle, R., additional, St. John Coss, D., additional, Junejo, S., additional, Donnellan, C. A., additional, Gosney, M. A., additional, Clinch, D., additional, Hilton, D., additional, O’Malley, B., additional, Albloushi, S., additional, Lavan, J. N., additional, Courtney, M. G., additional, Hardiman, E., additional, Bolger, M., additional, Pooransingh, S., additional, Flannery, W., additional, O’Malley, C., additional, Horkan, E. M., additional, Lundstrom, F., additional, Webster, R., additional, Threadgold, M., additional, Hamill, R., additional, Tracey, F., additional, McConnell, J. G., additional, Taylor, I. C., additional, Duggan, E., additional, Murphy, A., additional, Nelson, S. J., additional, Rea, I. M., additional, Ward, M., additional, McNulty, H., additional, O’Loughlin, A., additional, Collas, D. M., additional, Tannock, C., additional, Walker, Z., additional, and Katona, C., additional

Published
1998
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328. Preface

Author

Staudigel, H., primary, Albarède, F., additional, Hilton, D., additional, and Elliott, T., additional

Published
1995
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337. Axl/Gas6/NFκB signalling in schwannoma pathological proliferation, adhesion and survival.

Author

Ammoun, S, Provenzano, L, Zhou, L, Barczyk, M, Evans, K, Hilton, D A, Hafizi, S, and Hanemann, C O

Subjects
NF-kappa B, NEUROMAS, CANCER cell proliferation, CELL adhesion, PROTEIN-tyrosine kinases, MULTIDRUG resistance, NEOPLASTIC cell transformation, NEOVASCULARIZATION
Abstract

TAM family receptor tyrosine kinases comprising Tyro3 (Sky), Axl, and Mer are overexpressed in some cancers, correlate with multidrug resistance and contribute to tumourigenesis by regulating invasion, angiogenesis, cell survival and tumour growth. Mutations in the gene coding for a tumour suppressor merlin cause development of multiple tumours of the nervous system such as schwannomas, meningiomas and ependymomas occurring spontaneously or as part of a hereditary disease neurofibromatosis type 2. The benign character of merlin-deficient tumours makes them less responsive to chemotherapy. We previously showed that, amongst other growth factor receptors, TAM family receptors (Tyro3, Axl and Mer) are significantly overexpressed in schwannoma tissues. As Axl is negatively regulated by merlin and positively regulated by E3 ubiquitin ligase CRL4DCAF1, previously shown to be a key regulator in schwannoma growth we hypothesized that Axl is a good target to study in merlin-deficient tumours. Moreover, Axl positively regulates the oncogene Yes-associated protein, which is known to be under merlin regulation in schwannoma and is involved in increased proliferation of merlin-deficient meningioma and mesothelioma. Here, we demonstrated strong overexpression and activation of Axl receptor as well as its ligand Gas6 in human schwannoma primary cells compared to normal Schwann cells. We show that Gas6 is mitogenic and increases schwannoma cell-matrix adhesion and survival acting via Axl in schwannoma cells. Stimulation of the Gas6/Axl signalling pathway recruits Src, focal adhesion kinase (FAK) and NFκB. We showed that NFκB mediates Gas6/Axl-mediated overexpression of survivin, cyclin D1 and FAK, leading to enhanced survival, cell-matrix adhesion and proliferation of schwannoma. We conclude that Axl/FAK/Src/NFκB pathway is relevant in merlin-deficient tumours and is a potential therapeutic target for schwannoma and other merlin-deficient tumours. [ABSTRACT FROM AUTHOR]

Published
2014
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