FAS system deregulation in T-cell lymphoblastic lymphoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-03

AUTHORS

M Villa-Morales, M A Cobos, E González-Gugel, V Álvarez-Iglesias, B Martínez, M A Piris, A Carracedo, J Benítez, J Fernández-Piqueras

ABSTRACT

The acquisition of resistance towards FAS-mediated apoptosis may be required for tumor formation. Tumors from various histological origins exhibit FAS mutations, the most frequent being hematological malignancies. However, data regarding FAS mutations or FAS signaling alterations are still lacking in precursor T-cell lymphoblastic lymphomas (T-LBLs). The available data on acute lymphoblastic leukemia, of precursor origin as well, indicate a low frequency of FAS mutations but often report a serious reduction in FAS-mediated apoptosis as well as chemoresistance, thus suggesting the occurrence of mechanisms able to deregulate the FAS signaling pathway, different from FAS mutation. Our aim at this study was to determine whether FAS-mediated apoptotic signaling is compromised in human T-LBL samples and the mechanisms involved. This study on 26 T-LBL samples confirms that the FAS system is impaired to a wide extent in these tumors, with 57.7% of the cases presenting any alteration of the pathway. A variety of mechanisms seems to be involved in such alteration, in order of frequency the downregulation of FAS, the deregulation of other members of the pathway and the occurrence of mutations at FAS. Considering these results together, it seems plausible to think of a cumulative effect of several alterations in each T-LBL, which in turn may result in FAS/FASLG system deregulation. Since defective FAS signaling may render the T-LBL tumor cells resistant to apoptotic cell death, the correct prognosis, diagnosis and thus the success of anticancer therapy may require such an in-depth knowledge of the complete scenario of FAS-signaling alterations. More... »

PAGES

e1110

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cddis.2014.83

DOI

http://dx.doi.org/10.1038/cddis.2014.83

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005566918

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24603338


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Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1038/cddis.2014.83'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1038/cddis.2014.83'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1038/cddis.2014.83'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1038/cddis.2014.83'


 

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293 https://www.grid.ac/institutes/grid.412125.1 schema:alternateName King Abdulaziz University
294 schema:name Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, KSA
295 Grupo de Medicina Xenómica, CIBERER, Universidade de Santiago de Compostela, Santiago de Compostela, Spain
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297 https://www.grid.ac/institutes/grid.413448.e schema:alternateName Instituto de Salud Carlos III
298 schema:name Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Madrid, Spain
299 Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain
300 Instituto de Investigación Sanitario Fundación Jiménez Díaz, ISCIII, Madrid, Spain
301 Instituto de Investigación de Enfermedades Raras, ISCIII, Madrid, Spain
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303 https://www.grid.ac/institutes/grid.7719.8 schema:alternateName Spanish National Cancer Research Centre
304 schema:name Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain
305 Human Genetics Group, CNIO, Madrid, Spain
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