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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Colabufo, N.A. et al.

Nicola A. Colabufo, Marialessandra Contino, Mauro Niso, Francesco Berardi, Marcello Leopoldo, Roberto Perrone,

EGFR tyrosine kinase inhibitors and multidrug resistance: perspectives.

Aim of present review is to provide an evidence-based update of mechanisms responsible for the onset of resistance to drug therapy by EGFR inhibitors, particularly with regards to TKIs. Among ABC transporters involved in MDR, P-glycoprotein and BCRP have been considered the pumps responsible for TKIs treatment failure. Moreover, two subtypes of EGFR mutations have been described: mutations of the exons coding for tyrosine kinase domain (18 to 21) and truncating mutations (exons 2 to 7) that involve downstream effectors such as MAPK, PI3K/Akt, STAT. The first group of mutations can be considered as a hallmark of NSCLC and are responsible for the failure of TKIs while the second group of mutations leads to resistance. The strategies to overcome MDR and to bypass the kinase domain mutations have been addressed. Finally, for some first generation TKIs some perspectives as radiotracers for PET/SPECT diagnosis in tumor displaying P-gp and BCRP overexpression have been suggested.[1]

References

EGFR tyrosine kinase inhibitors and multidrug resistance: perspectives. Colabufo, N.A., Contino, M., Niso, M., Berardi, F., Leopoldo, M., Perrone, R. Front. Biosci. (2011) [Pubmed]

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