Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Retinoic acid and interferon signaling cross talk in normal and RA-resistant APL cells
Autore:
Chelbi-Alix, MK; Pelicano, L;
Indirizzi:
Hop St Louis, CNRS, UPR 9051, F-75475 Paris 10, France Hop St Louis Paris France 10 s, CNRS, UPR 9051, F-75475 Paris 10, France
Titolo Testata:
LEUKEMIA
fascicolo: 8, volume: 13, anno: 1999,
pagine: 1167 - 1174
SICI:
0887-6924(199908)13:8<1167:RAAISC>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE PROMYELOCYTIC LEUKEMIA; INDUCIBLE GENE-EXPRESSION; PML GROWTH-SUPPRESSOR; TRANSCRIPTION FACTOR; NB4 CELLS; IFN-ALPHA; GENOMIC STRUCTURE; PROTEIN-KINASE; HUMAN CANCER; INDUCTION;
Keywords:
Stat1; IRF-1; IRF-3; p21(WAF/CIP1); interferon; retinoic acid; differentiation;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
107
Recensione:
Indirizzi per estratti:
Indirizzo: Chelbi-Alix, MK Hop St Louis, CNRS, UPR 9051, 1 Ave Vellefaux, F-75475 Paris 10, France Hop St Louis 1 Ave Vellefaux Paris France 10 s 10, France
Citazione:
M.K. Chelbi-Alix e L. Pelicano, "Retinoic acid and interferon signaling cross talk in normal and RA-resistant APL cells", LEUKEMIA, 13(8), 1999, pp. 1167-1174

Abstract

Retinoic acid (RA) and interferon (IFN) potentiate each other to induce biological responses. Their combination has shown synergistic differentiating, antiproliferative and antiviral activities in various cell lines including those derived from the acute promyelocytic leukemia (APL). IFNs have demonstrated broad applications in cancer, as well as in virologic diseases. RAhas variable effectiveness in therapy. Its real success is in APL where itprovides the first example of a differentiation therapy. However, completeclinical remission with RA alone is always transient as RA resistance develops in the treated patients as well as in vitro. In various cell lines, including those derived from APL, RA induces directly the expression of two transcription factors, Stat1 and IRF-1 which play central roles in the IFN signal transduction. In addition, RA induces IFN-alpha synthesis and enhances the IFN-induced Stat activation. Here, we review the molecular mechanismsby which RA and IFNs can cooperate in inducing differentiation, inhibitionof cell growth or viral replication focusing on recent results derived from normal and RA-resistant APL cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 00:55:12