133 research outputs found
Unilateral facial pain associated with recurrence of malignant thymoma: a case report
- Publication venue
- 'S. Karger AG'
- Publication date
- 01/01/2003
- Field of study
The Akt inhibitor KP372-1 suppresses Akt activity and cell proliferation and induces apoptosis in thyroid cancer cells
- Author
- Publication venue
- Nature Publishing Group
- Publication date
- 23/05/2005
- Field of study
The phosphatidylinositol 3′ kinase (PI3K)/phosphatase and tensin homologue deleted on chromosome ten/Akt pathway, which is a critical regulator of cell proliferation and survival, is mutated or activated in a wide variety of cancers. Akt appears to be a key central node in this pathway and thus is an attractive target for targeted molecular therapy. We demonstrated that Akt is highly phosphorylated in thyroid cancer cell lines and human thyroid cancer specimens, and hypothesised that KP372-1, an Akt inhibitor, would block signalling through the PI3K pathway and inhibit cell proliferation while inducing apoptosis of thyroid cancer cells. KP372-1 blocked signalling downstream of Akt in thyroid tumour cells, leading to inhibition of cell proliferation and increased apoptosis. As thyroid cancer consistently expresses phosphorylated Akt and KP372-1 effectively blocks Akt signalling, further preclinical evaluation of this compound for treatment of thyroid cancer is warranted
Performance of the CMS Cathode Strip Chambers with Cosmic Rays
- Author
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- Xella S.
- Xie S
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- Zachariadou A
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- Zeidler C
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- Publication venue
- 'IOP Publishing'
- Publication date
- 01/01/2009
- Field of study
The Cathode Strip Chambers (CSCs) constitute the primary muon tracking device
in the CMS endcaps. Their performance has been evaluated using data taken
during a cosmic ray run in fall 2008. Measured noise levels are low, with the
number of noisy channels well below 1%. Coordinate resolution was measured for
all types of chambers, and fall in the range 47 microns to 243 microns. The
efficiencies for local charged track triggers, for hit and for segments
reconstruction were measured, and are above 99%. The timing resolution per
layer is approximately 5 ns
Activated Leukocyte Cell Adhesion Molecule Expression and Shedding in Thyroid Tumors
- Author
- A Jezierska
- A Savina
- A Verma
- AW Zimmerman
- B Jarzab
- C Kahlert
- C Rodriguez-Antona
- CL Fenton
- D Caccia
- D Mezzanzanica
- DD El
- EY Kim
- Francesca Miccichè
- G Garcia-Rostan
- G Riesco-Eizaguirre
- Gordon Langsley
- GW Hart
- GW Swart
- H Peinado
- Italia Bongarzone
- JA King
- KJ Garton
- L Delys
- L Gorla
- LC van Kempen
- Luca Da Riva
- M Landriscina
- M Ryder
- Marco A. Pierotti
- Marina Fabbi
- MG Borrello
- MP Sanderson
- MV Corrias
- NK Haass
- O Rosso
- P Savagner
- Piera Mondellini
- RA Delellis
- S Jain
- S Scarpino
- SA Wells Jr
- Silvana Canevari
- Silvana Pilotti
- Silvano Ferrini
- SR Davies
- T Piazza
- TG Levin
- V Bassi
- V Kulasingam
- VM Faca
- W Weichert
- Z Jin
- Publication venue
- Public Library of Science
- Publication date
- 01/02/2011
- Field of study
Activated leukocyte cell adhesion molecule (ALCAM, CD166) is expressed in various tissues, cancers, and cancer-initiating cells. Alterations in expression of ALCAM have been reported in several human tumors, and cell adhesion functions have been proposed to explain its association with cancer. Here we documented high levels of ALCAM expression in human thyroid tumors and cell lines. Through proteomic characterization of ALCAM expression in the human papillary thyroid carcinoma cell line TPC-1, we identified the presence of a full-length membrane-associated isoform in cell lysate and of soluble ALCAM isoforms in conditioned medium. This finding is consistent with proteolytically shed ALCAM ectodomains. Nonspecific agents, such as phorbol myristate acetate (PMA) or ionomycin, provoked increased ectodomain shedding. Epidermal growth factor receptor stimulation also enhanced ALCAM secretion through an ADAM17/TACE-dependent pathway. ADAM17/TACE was expressed in the TPC-1 cell line, and ADAM17/TACE silencing by specific small interfering RNAs reduced ALCAM shedding. In addition, the CGS27023A inhibitor of ADAM17/TACE function reduced ALCAM release in a dose-dependent manner and inhibited cell migration in a wound-healing assay. We also provide evidence for the existence of novel O-glycosylated forms and of a novel 60-kDa soluble form of ALCAM, which is particularly abundant following cell stimulation by PMA. ALCAM expression in papillary and medullary thyroid cancer specimens and in the surrounding non-tumoral component was studied by western blot and immunohistochemistry, with results demonstrating that tumor cells overexpress ALCAM. These findings strongly suggest the possibility that ALCAM may have an important role in thyroid tumor biology
Biological activity of the thyroid TRK-T3 oncogene requires signalling through Shc
- Author
- A Greco
- A Greco
- A Greco
- A Obermeier
- C Miranda
- C Miranda
- CM Boney
- D Thomas
- DR Kaplan
- E Fournier
- E Mercalli
- E Migliaccio
- E Migliaccio
- E Roccato
- E Ulrich
- G Pelicci
- H Gu
- H Kouhara
- I Bongarzone
- I Dikic
- JIS MacDonald
- K Li
- LE Stevenson
- M A Pierotti
- M Ashcroft
- M Gishizki
- M Mencinger
- M Mencinger
- MA Pierotti
- MG Borrello
- N Canu
- N Gotoh
- N Gotoh
- P Van der Geer
- R Possenti
- RM Stephens
- SH Ong
- SJ Rabin
- SO Meakin
- V Ranzi
- X Qian
- Y Muragaki
- Publication venue
- Nature Publishing Group
- Publication date
- Field of study
The thyroid TRK-T3 oncogene, produced by a chromosomal translocation, is a chimeric, constitutively activated version of the NTRK1/NGF receptor and it is able to transform NIH3T3 cells and differentiate PC12 cells. TRK-T3 oncoprotein triggers multiple signal transduction pathways. Among others, TRK-T3 binds and phosphorylates the Shc and SNT1/FRS2 adaptor proteins both involved in coupling the receptor tyrosine kinase to the mitogen-activated protein kinase pathway by recruiting Grb2/SOS. We were interested in defining the role of Shc in the oncogenesis by TRK-T3. The mutation of TRK-T3 tyrosine 291, docking site for both Shc and FRS2, abrogates the oncogene biological activity. To directly explore the role of Shc we used the ShcY317F mutant, which carries the mutation of a tyrosine residue involved in Grb2 recruitment. We demonstrated that the ShcY317F mutant exerts an inhibitory effect on TRK-T3 transforming activity. Such effect can be modulated by the amount of ShcY317F protein and affects the viability of cells expressing TRK-T3 by means of a mechanism involving apoptosis. Our results indicate a definitive role of the adaptor protein Shc in TRK-T3 transforming activity
RET PLCγ Phosphotyrosine Binding Domain Regulates Ca2+ Signaling and Neocortical Neuronal Migration
- Author
- Branden Nelson
- BS Schmutzler
- C Canibano
- CB Guan
- D Natarajan
- DE Clapham
- DS Richardson
- E Arighi
- E Pozas
- G Paratcha
- GR Dressler
- GR Monteith
- HL Roderick
- I Plaza-Menacho
- J Anders
- J Mijatovic
- JP Golden
- JQ Zheng
- Katsutoshi Nakahata
- L Desfrere
- L Jiao
- LN Borodinsky
- M Coulpier
- M Jijiwa
- M Santoro
- M Takahashi
- M Uchida
- MG Borrello
- MJ Berridge
- MJ Berridge
- MJ Berridge
- MR Rusciano
- MS Airaksinen
- N Asai
- N Asai
- Nicolas Fritz
- P Runeberg-Roos
- P Uhlen
- Paola Rebellato
- Per Uhlén
- R Zhou
- RAM Daza
- S Bourane
- S Eketjall
- S Jain
- S Kjaer
- S Malmersjo
- S Manie
- S Seino
- SJ Cook
- Songbai Zhang
- T Fukuda
- T Saito
- T Watanabe
- T Yu
- T. Kalle Lundgren
- TK Lundgren
- VM Leppanen
- Publication venue
- Public Library of Science
- Publication date
- 15/02/2012
- Field of study
The receptor tyrosine kinase RET plays an essential role during embryogenesis in regulating cell proliferation, differentiation, and migration. Upon glial cell line-derived neurotrophic factor (GDNF) stimulation, RET can trigger multiple intracellular signaling pathways that in concert activate various downstream effectors. Here we report that the RET receptor induces calcium (Ca2+) signaling and regulates neocortical neuronal progenitor migration through the Phospholipase-C gamma (PLCγ) binding domain Tyr1015. This signaling cascade releases Ca2+ from the endoplasmic reticulum through the inositol 1,4,5-trisphosphate receptor and stimulates phosphorylation of ERK1/2 and CaMKII. A point mutation at Tyr1015 on RET or small interfering RNA gene silencing of PLCγ block the GDNF-induced signaling cascade. Delivery of the RET mutation to neuronal progenitors in the embryonic ventricular zone using in utero electroporation reveal that Tyr1015 is necessary for GDNF-stimulated migration of neurons to the cortical plate. These findings demonstrate a novel RET mediated signaling pathway that elevates cytosolic Ca2+ and modulates neuronal migration in the developing neocortex through the PLCγ binding domain Tyr1015
Selective inhibition of RET mediated cell proliferation in vitro by the kinase inhibitor SPP86
- Author
- A Arora
- A Boulay
- A Gattelli
- A Kim
- A Morandi
- A Pardanani
- A Preto
- BP Fox
- C Lanzi
- C Lanzi
- C Wang
- D Caccia
- D Lipson
- DB Mendel
- DW Kim
- F Carlomagno
- F Carlomagno
- F Ciardiello
- FM Yakes
- G Cassinelli
- G Cassinelli
- H Murakami
- HJ Meulenbeld
- I Plaza-Menacho
- I Plaza-Menacho
- I Plaza-Menacho
- IS Lucet
- J Bain
- J Bain
- J Jiang
- JA Knauf
- JA McCubrey
- JE Phay
- JH Hanke
- JK Slack-Davis
- John P Alao
- JP Alao
- JP Alao
- K Moelling
- K Takeuchi
- L Gonzalez
- L Mologni
- L Mologni
- LC Murphy
- LM Mulligan
- M Croyle
- M Putyrski
- M Saiselet
- MG Borrello
- Morten Grøtli
- N Akeno-Stuart
- N Simiantonaki
- P Cohen
- P Diner
- Per Sunnerhagen
- Peter Dinér
- PI Poulikakos
- R St Bernard
- R Wimmer
- RL Yamnik
- S Wilhelm
- Sona Michlikova
- T Kohno
- T O'Hare
- T Pilli
- W Brandt
- WH Chappell
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
CMS Data Processing Workflows during an Extended Cosmic Ray Run
- Author
- Abadjiev K
- Abbaneo D
- Abbiendi G
- Abbrescia M
- Abdullin S
- Abelev B
- Acosta D
- Acosta JG
- Acosta MV
- Actis O
- Adam N
- Adam W
- Adams MR
- Adams T
- Adiguzel A
- Adler V
- Adolphi R
- Adzic P
- Afaq MA
- Agostino L
- Agram JL
- Aguilar-Benitez M
- Ahmad M
- Ahmad WH
- Ahmed I
- Ahmed W
- Ahuja S
- Aisa D
- Aisa S
- Akchurin N
- Akgun B
- Akgun U
- Akimenko S
- Akin IV
- Alagoz E
- Alampi G
- Albajar C
- Albayrak EA
- Alberdi J
- Albergo S
- Albert E
- Albrow M
- Alexander J
- Alidra M
- Aliev T
- Allfrey P
- Almeida N
- Altenhofer G
- Altsybeev I
- Alver B
- Alverson G
- Alves GA
- Amaglobeli N
- Amapane N
- Ambroglini F
- Amsler C
- Anagnostou G
- Ananthan B
- Anastassov A
- Andelin D
- Anderson M
- Andrea J
- Andreev V
- Andreev Y
- Anghel IM
- Anguelov T
- Anisimov A
- Antillon E
- Antipov P
- Antonelli L
- Anttila E
- Antunes JR
- Antunovic Z
- Apanasevich L
- Apollinari G
- Apresyan A
- Arce P
- Arcidiacono R
- Arenton MW
- Arfaei H
- Argiro S
- Arisaka K
- Arneodo M
- Arnold B
- Arora S
- Artamonov A
- Asaadi J
- Asghar MI
- Ashby S
- Askew A
- Atac M
- Atramentov O
- Auffray E
- Aurisano A
- Autermann C
- Avery P
- Avetisyan A
- Avila C
- Awan MIM
- Ayan AS
- Ayhan A
- Azhgirey I
- Aziz T
- Azzi P
- Azzurri P
- Baarmand MM
- Babb J
- Babucci E
- Baccaro S
- Bacchetta N
- Bacchi W
- Bachtis M
- Baden D
- Badgett W
- Baechler J
- Baer H
- Baesso P
- Baffioni S
- Bagby L
- Bagliesi G
- Bahk SY
- Bailleux D
- Baillon P
- Bainbridge R
- Bakhshiansohi H
- Bakirci MN
- Bakken JA
- Balazs M
- Baldin B
- Ball AH
- Ball G
- Ballin J
- Bally SL
- Ban Y
- Bandurin D
- Banerjee S
- Banerjee S
- Banicz K
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- Banzuzi K
- Barashko V
- Barbagli G
- Barberis E
- Barbone L
- Barcala JM
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- Bargassa P
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- Barnes VE
- Barnett BA
- Barney D
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- Bartalini P
- Bartoloni A
- Bartz E
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- Battilana C
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- Baud A
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- Beauceron S
- Beaudette F
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- Beliy N
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- Bellato M
- Bellinger JN
- Belotelov I
- Benaglia A
- Bencze G
- Bendavid J
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- Benedetti D
- Benelli G
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- Benvenuti AC
- Berengueres JOL
- Beretvas A
- Bergauer H
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- Berry D
- Berry E
- Berryhill J
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- Bertl W
- Bertoldi M
- Berzano U
- Besancon M
- Besson A
- Betchart B
- Betev B
- Betts RR
- Beuselinck R
- Bhat PC
- Bhatnagar V
- Bhattacharya S
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- Bhatti A
- Biallass P
- Bianchini L
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- Biery K
- Biino C
- Bilei GM
- Bilki B
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- Bisello D
- Bitioukov S
- Blaha J
- Blekman F
- Bloch D
- Bloch I
- Bloch P
- Bloom K
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- Blum P
- Blumenfeld B
- Blyweert S
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- Bodek A
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- Borgia MA
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- Borras K
- Borrello L
- Borsato E
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- Chetluru V
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- Chien CY
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- Publication venue
- INSTITUTE OF PHYSICS PUBLISHING
- Publication date
- 01/01/2009
- Field of study
Peer reviewe
Aligning the CMS Muon Chambers with the Muon Alignment System during an Extended Cosmic Ray Run
- Author
- Abadjiev K
- Abbaneo D
- Abbiendi G
- Abbrescia M
- Abdullin S
- Abelev B
- Acosta D
- Acosta JG
- Acosta MV
- Actis O
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- Adam W
- Adams MR
- Adams T
- Adiguzel A
- Adler V
- Adolphi R
- Adzic P
- Afaq MA
- Agostino L
- Agram JL
- Aguilar Benitez M
- Ahmad M
- Ahmad WH
- Ahmed I
- Ahmed W
- Ahuja S
- Aisa D
- Aisa S
- Akchurin N
- Akgun B
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- Akimenko S
- Akin IV
- Alagoz E
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- Albayrak EA
- Alberdi J
- Albergo S
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- Alexander J
- Alidra M
- Aliev T
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- Almeida N
- Altenhofer G
- Altsybeev I
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- Alverson G
- Alves GA
- Amaglobeli N
- Amapane N
- Ambroglini F
- Amsler C
- Anagnostou G
- Ananthan B
- Anastassov A
- Andelin D
- Anderson M
- Andrea J
- Andreev V
- Andreev Y
- Anghel IM
- Anguelov T
- Anh T. Vu
- Anisimov A
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- Asghar MI
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- Publication venue
- Publication date
- 01/01/2009
- Field of study
Peer reviewe
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
- Author
- A Abbott
- A Abou-Raya
- A Aljandali
- A Ambesi-Impiombato
- A Aydin
- A Balcerczyk
- A Besarab
- A Brzezinski
- A Campbell
- A Carrillo-Vico
- A Cavalli
- A Chattopadhyay
- A Chattopadhyay
- A Cherubini
- A Dey
- A Doms
- A Donovan
- A Donovan
- A Dávalos
- A Gaeta
- A Garny
- A Gnjec
- A Gomes
- A Gopalakrishnan
- A Hald
- A Henney
- A Hirayama
- A Hoffmann
- A Huber
- A Hugman
- A Iannetti
- A Ide-Ektessabi
- A Jacobs
- A Jeyabalan
- A Kahvejian
- A Karrar
- A Kasztler
- A Kibel
- A Kocyigit
- A Kotha
- A Kumral
- A Lass
- A Lecube
- A Lewén
- A Lotery
- A Maggio
- A Malek
- A Malik
- A Mantovani
- A Matsuzawa
- A Mitra
- A Monge
- A Murakami
- A Murakami
- A Murakami
- A Murakami
- A Mutti
- A Nijnik
- A Nunomura
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- The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group
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- Publication venue
- Publication date
- 09/08/2008
- Field of study
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
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