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dc.contributor.authorGhidini, M
dc.contributor.authorHahne, J
dc.contributor.authorFrizziero, Melissa
dc.contributor.authorTomasello, G
dc.contributor.authorTrevisani, F
dc.contributor.authorLampis, A
dc.contributor.authorPassalacqua, R
dc.contributor.authorValeri, N
dc.date.accessioned2018-09-15T19:26:25Z
dc.date.available2018-09-15T19:26:25Z
dc.date.issued2018-08
dc.identifier.citationMicroRNAs as mediators of resistance mechanisms to small-molecule tyrosine kinase inhibitors in solid tumours. 2018, 13(4): 423-436 Target Oncolen
dc.identifier.issn1776-260X
dc.identifier.pmid30006826
dc.identifier.doi10.1007/s11523-018-0580-3
dc.identifier.urihttp://hdl.handle.net/10541/621241
dc.description.abstractReceptor tyrosine kinases (RTKs) are widely expressed transmembrane proteins that act as receptors for growth factors and other extracellular signalling molecules. Upon ligand binding, RTKs activate intracellular signalling cascades, and as such are involved in a broad variety of cellular functions including differentiation, proliferation, migration, invasion, angiogenesis, and survival under physiological as well as pathological conditions. Aberrant RTK activation can lead to benign proliferative conditions as well as to various forms of cancer. Indeed, more than 70% of the known oncogene and proto-oncogene transcripts involved in cancer code for RTKs. Consequently, these receptors are broadly studied as targets in the treatment of different tumours, and a large variety of small-molecule tyrosine kinase inhibitors (TKIs) are approved for therapy. In most cases, patients develop resistance to the TKIs within a short time. MicroRNAs are short (18-22 nucleotides) non-protein-coding RNAs that fine-tune cell homeostasis by controlling gene expression at the post-transcriptional level. Deregulation of microRNAs is common in many cancers, and increasing evidence exists for an important role of microRNAs in the development of resistance to therapies, including TKIs. In this review we focus on the role of microRNAs in mediating resistance to small-molecule TKIs in solid tumours.
dc.language.isoenen
dc.rightsArchived with thanks to Targeted oncologyen
dc.titleMicroRNAs as mediators of resistance mechanisms to small-molecule tyrosine kinase inhibitors in solid tumours.en
dc.typeArticleen
dc.contributor.departmentMedical Department, Division of Oncology, ASST di Cremona, Ospedale di Cremona, Cremona, Italyen
dc.identifier.journalTargeted Oncologyen
html.description.abstractReceptor tyrosine kinases (RTKs) are widely expressed transmembrane proteins that act as receptors for growth factors and other extracellular signalling molecules. Upon ligand binding, RTKs activate intracellular signalling cascades, and as such are involved in a broad variety of cellular functions including differentiation, proliferation, migration, invasion, angiogenesis, and survival under physiological as well as pathological conditions. Aberrant RTK activation can lead to benign proliferative conditions as well as to various forms of cancer. Indeed, more than 70% of the known oncogene and proto-oncogene transcripts involved in cancer code for RTKs. Consequently, these receptors are broadly studied as targets in the treatment of different tumours, and a large variety of small-molecule tyrosine kinase inhibitors (TKIs) are approved for therapy. In most cases, patients develop resistance to the TKIs within a short time. MicroRNAs are short (18-22 nucleotides) non-protein-coding RNAs that fine-tune cell homeostasis by controlling gene expression at the post-transcriptional level. Deregulation of microRNAs is common in many cancers, and increasing evidence exists for an important role of microRNAs in the development of resistance to therapies, including TKIs. In this review we focus on the role of microRNAs in mediating resistance to small-molecule TKIs in solid tumours.


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