2020
DOI: 10.15252/emmm.201911498
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Abstract: Despite impressive clinical benefit obtained with anti-HER2-targeted therapies, in advances stages, especially in the metastatic setting, HER2-positive tumors remain incurable. Therefore, it is important to develop novel strategies to fight these tumors, especially when they become resistant to available therapies. We show here that the anti-HER3 antibody-drug conjugate EV20/MMAF exerted potent antitumoral properties against several models of primary resistance and secondary resistance to common anti-HER2 avai… Show more

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Cited by 28 publications
(21 citation statements)
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“…In this context, ACNPs could overcome this limitation. Finally, polymeric NPs own the ability to release the payload when a specific pH, mainly acidic, is produced in the tumor, particularly in areas of poor vascularization, therefore acting on areas where cancer drugs have limited penetration [152].…”
Section: Challenges For Clinical Implementationmentioning
confidence: 99%
“…In this context, ACNPs could overcome this limitation. Finally, polymeric NPs own the ability to release the payload when a specific pH, mainly acidic, is produced in the tumor, particularly in areas of poor vascularization, therefore acting on areas where cancer drugs have limited penetration [152].…”
Section: Challenges For Clinical Implementationmentioning
confidence: 99%
“… 34 Recently, it was shown that an anti-HER3 ADC (EV20/MMAF), generated by coupling monomethyl auristatin F (MMAF) through a non-cleavable linker to the anti-HER3 antibody EV20, was highly potent in different HER2-positive tumor models including tumor cells resistant to trastuzumab treatment. 35 Bispecific antibodies targeting HER2 and HER3 might further improve the efficacy of ADCs in different tumor settings. Bispecific ADCs are already under development, for instance, targeting HER2 and CD63 to increase the lysosomal delivery mediated by binding to the shuttle protein CD63.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore PIK3CA and PTEN mutations may contribute to the acquisition of resistance to these agents [37,60,61]. Moreover, EGFR, HER3, HER4, IGF-1R, MET upregulation and heterodimerization may confer resistance to anti-HER2 therapies by restoring the original downstream signaling pathways activated by HER2-overexpression and amplification [61][62][63].…”
Section: Presence Of Compensatory Signaling Pathwaysmentioning
confidence: 99%