Sunitinib-induced asthenia: from molecular basis to clinical relief
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Sunitinib-induced asthenia: from molecular basis to clinical reliefData
2011-11-01Cita bibliográfica
Antón Aparicio LM, Grande Pulido E, Aparicio Gallego G. Sunitinib-induced asthenia: from molecular basis to clinical relief. Cancer Biol Therap. 2011;12(9):765-771
Resumo
[Abstract] Asthenia-fatigue syndrome (AFS) is defined as a persistent, subjective sense of tiredness related to cancer or its treatment and greatly impacts quality of life among cancer patients. All tyrosine kinase inhibitors, but especially sunitinib, may induce AFS. The reason for sunitinib-induced AFS is not yet well understood. Adverse events caused by sunitinib associated with AFS may include anemia, hypothyroidism, nausea and vomiting. However, AFS is also reported when active treatment with sunitinib is ongoing, and no other relevant adverse event can justify it. The molecular mechanisms by which sunitinib triggers AFS remain elusive. Sunitinib displays multiple off-target tyrosine-kinase interactions and competitively inhibits multiple proteins through the blockade of their ATP-binding sites. The broad spectrum of kinases inhibited may play a key role not only in terms of activity but also in terms of toxicity induced by sunitinib. This study considered different clinical observations and current metabolic and pharmacological knowledge, leading to hypotheses regarding which molecular mechanisms may be involved in sunitinib-induced AFS in cancer patients. Deeper knowledge of the molecular mode of action of sunitinib may lead to improved optimization of its clinical use.
Palabras chave
Asthenia
Cancer
Energy
Sunitinib
Tyrosine kinase inhibitors
Cancer
Energy
Sunitinib
Tyrosine kinase inhibitors
Versión do editor
Dereitos
This is an accepted manuscript of an article published by Taylor & Francis in "Cancer Biology & Therapy" on 2011, avaliable online at Taylor & Francis Online
ISSN
1538-4047
1555-8576
1555-8576