13-cis-Retinoic acid represents a well-established clinical strategy for the management of minimal residual disease of high risk neuroblastoma (NB) patients. However, the clinical efficacy on the overall survival of these patients remains limited, addressing the issue of better understanding the molecular mechanisms and intracellular pathways mediating Retinoic Acid (RA) clinical effects.

Di Francesco, A., Cusano, G., Franzese, O., Orienti, I., Falconi, M., Vesci, L., et al. (2015). Resistance to the atypical retinoid ST1926 in SK-N-AS cells selected the subline rAS-ST with enhanced sensitivity to ATRA mediated by not conventional mechanisms: DNA damage, G2 accumulation and late telomerase inhibition. TOXICOLOGY IN VITRO, 29(7), 1628-1638 [10.1016/j.tiv.2015.06.017].

Resistance to the atypical retinoid ST1926 in SK-N-AS cells selected the subline rAS-ST with enhanced sensitivity to ATRA mediated by not conventional mechanisms: DNA damage, G2 accumulation and late telomerase inhibition

FRANZESE, ORNELLA;
2015-01-01

Abstract

13-cis-Retinoic acid represents a well-established clinical strategy for the management of minimal residual disease of high risk neuroblastoma (NB) patients. However, the clinical efficacy on the overall survival of these patients remains limited, addressing the issue of better understanding the molecular mechanisms and intracellular pathways mediating Retinoic Acid (RA) clinical effects.
2015
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/14 - FARMACOLOGIA
English
Con Impact Factor ISI
Differentiation; Neuroblastoma; Retinoic acid; ST1926; Telomerase; Adamantane; Antineoplastic Agents; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Cinnamates; Comet Assay; DNA Damage; Drug Resistance, Neoplasm; Humans; Proto-Oncogene Proteins c-akt; Receptors, Retinoic Acid; Telomerase; Tretinoin
Di Francesco, A., Cusano, G., Franzese, O., Orienti, I., Falconi, M., Vesci, L., et al. (2015). Resistance to the atypical retinoid ST1926 in SK-N-AS cells selected the subline rAS-ST with enhanced sensitivity to ATRA mediated by not conventional mechanisms: DNA damage, G2 accumulation and late telomerase inhibition. TOXICOLOGY IN VITRO, 29(7), 1628-1638 [10.1016/j.tiv.2015.06.017].
Di Francesco, A; Cusano, G; Franzese, O; Orienti, I; Falconi, M; Vesci, L; Riccardi, R
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/167152
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