Genetic instability, a hallmark of solid tumors including thyroid cancers, is thought to represent the mean by which premalignant cells acquire novel functional capabilities responsible for cancer cell growth and tumour progression. Over the last few years, the knowledge of the molecular processes controlling the mitotic phase of the cell cycle has increased considerably, and different mitotic proteins, whose expression or function has been found altered in human cancer tissues, have been associated to tumour genetic instability and aneuploidy. These include the three members of the Aurora kinase family (Aurora-A, -B and -C), serine/threonine kinases that regulate multiple aspects of chromosome segregation and cytokinesis. The genes encoding the Aurora kinases have been shown to induce cell malignant transformation, and their overexpression has been detected in several tumor derived cell lines and tissues, being often associated with a poor prognosis. Over the last decade, specific inhibitors of Aurora kinases exhibited in preclinical and early phase clinical studies a good therapeutic efficacy against several tumour types, including the highly aggressive anaplastic thyroid cancer and the medullary thyroid cancer. In the present review we'll first focus on the Aurora mitotic functions in normal cells; then we shall describe the main implications of their overexpression in the onset of genetic instability and consequent aneuploidy. We shall finally discuss on the effects of the functional inhibition of Aurora kinases on thyroid cancer cells growth and tumorigenicity. Clin Ter 2012; 163(6):e457-462

Aurora kinases: new molecular targets in thyroid cancer therapy / Baldini, Enke; Sorrenti, Salvatore; E., D'Armiento; N., Prinzi; E., Guaitoli; P., Favoriti; Gnessi, Lucio; C., Moretti; M., Bianchini; S., Alessandrini; Catania, Antonio; DE ANTONI, Enrico; Ulisse, Salvatore. - In: LA CLINICA TERAPEUTICA. - ISSN 0009-9074. - ELETTRONICO. - 163:6(2012), pp. e457-e462.

Aurora kinases: new molecular targets in thyroid cancer therapy

BALDINI, ENKE;SORRENTI, Salvatore;GNESSI, Lucio;CATANIA, Antonio;DE ANTONI, Enrico;ULISSE, SALVATORE
2012

Abstract

Genetic instability, a hallmark of solid tumors including thyroid cancers, is thought to represent the mean by which premalignant cells acquire novel functional capabilities responsible for cancer cell growth and tumour progression. Over the last few years, the knowledge of the molecular processes controlling the mitotic phase of the cell cycle has increased considerably, and different mitotic proteins, whose expression or function has been found altered in human cancer tissues, have been associated to tumour genetic instability and aneuploidy. These include the three members of the Aurora kinase family (Aurora-A, -B and -C), serine/threonine kinases that regulate multiple aspects of chromosome segregation and cytokinesis. The genes encoding the Aurora kinases have been shown to induce cell malignant transformation, and their overexpression has been detected in several tumor derived cell lines and tissues, being often associated with a poor prognosis. Over the last decade, specific inhibitors of Aurora kinases exhibited in preclinical and early phase clinical studies a good therapeutic efficacy against several tumour types, including the highly aggressive anaplastic thyroid cancer and the medullary thyroid cancer. In the present review we'll first focus on the Aurora mitotic functions in normal cells; then we shall describe the main implications of their overexpression in the onset of genetic instability and consequent aneuploidy. We shall finally discuss on the effects of the functional inhibition of Aurora kinases on thyroid cancer cells growth and tumorigenicity. Clin Ter 2012; 163(6):e457-462
2012
mitosis; aurora kinases; thyroid cancer; cell cycle; aneuploidy; thyroid cancers; therapy
01 Pubblicazione su rivista::01a Articolo in rivista
Aurora kinases: new molecular targets in thyroid cancer therapy / Baldini, Enke; Sorrenti, Salvatore; E., D'Armiento; N., Prinzi; E., Guaitoli; P., Favoriti; Gnessi, Lucio; C., Moretti; M., Bianchini; S., Alessandrini; Catania, Antonio; DE ANTONI, Enrico; Ulisse, Salvatore. - In: LA CLINICA TERAPEUTICA. - ISSN 0009-9074. - ELETTRONICO. - 163:6(2012), pp. e457-e462.
File allegati a questo prodotto
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/502984
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? 7
  • Scopus 16
  • ???jsp.display-item.citation.isi??? 15
social impact