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dc.creatorIndovina, P
dc.creatorForte, IM
dc.creatorPentimalli, F
dc.creatorGiordano, A
dc.date.accessioned2020-12-15T20:31:59Z
dc.date.available2020-12-15T20:31:59Z
dc.date.issued2020-07-01
dc.identifier.issn2072-6694
dc.identifier.issn2072-6694
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/4453
dc.identifier.otherMS2MA (isidoc)
dc.identifier.other32664483 (pubmed)
dc.identifier.urihttp://hdl.handle.net/20.500.12613/4471
dc.description.abstract© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Malignant mesothelioma (MM) is a deadly tumor mainly caused by exposure to asbestos. Unfortunately, no current treatment is able to change significantly the natural history of the disease, which has a poor prognosis in the majority of patients. The non-receptor tyrosine kinase SRC and other SRC family kinase (SFK) members are frequently hyperactivated in many cancer types, including MM. Several works have indeed suggested that SFKs underlie MM cell proliferation, survival, motility, and invasion, overall affecting multiple oncogenic pathways. Consistently, SFK inhibitors effectively counteracted MM cancerous features at the preclinical level. Dasatinib, a multi-kinase inhibitor targeting SFKs, was also assessed in clinical trials either as second-line treatment for patients with unresectable MM or, more recently, as a neoadjuvant agent in patients with resectable MM. Here, we provide an overview of the molecular mechanisms implicating SFKs in MM progression and discuss possible strategies for a more successful clinical application of SFK inhibitors. Our aim is to stimulate discussion and further consideration of these agents in better designed preclinical and clinical studies to make the most of another class of powerful antitumoral drugs, which too often are lost in translation when applied to MM.
dc.format.extent1-21
dc.language.isoen
dc.relation.haspartCancers
dc.relation.isreferencedbyMDPI AG
dc.rightsCC BY
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectSRC family kinases
dc.subjectmalignant mesothelioma
dc.subjectreceptor tyrosine kinases
dc.subjectp27
dc.subjectAKT
dc.subjectinvasion
dc.subjectdasatinib
dc.subjecttreatment resistance
dc.subjectpredictive signature
dc.subjectdrug combination
dc.titleTargeting SRC family kinases in mesothelioma: Time to upgrade
dc.typeArticle
dc.type.genreReview
dc.type.genreJournal
dc.relation.doi10.3390/cancers12071866
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.creator.orcidGiordano, Antonio|0000-0002-5959-016X
dc.date.updated2020-12-15T20:31:56Z
refterms.dateFOA2020-12-15T20:32:00Z


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