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Cited by 4 publications
(5 citation statements)
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References 7 publications
(7 reference statements)
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“…This antibody has been shown to block HER3/AKT signaling (Sala et al, 2012) and to be rapidly and efficiently internalized by cells expressing HER3 (Sala et al, 2013). Moreover, the antibody impaired ligand-induced signaling and clonogenic growth in vitro and tumor growth in BRAF-V600E mutant colon cancer (Prasetyanti et al, 2015). We show that EV20/ MMAF exerts a potent and efficient anti-tumoral effect in different HER2 + models including cells resistant to classical anti-HER2 therapeutics.…”
Section: Introductionmentioning
confidence: 81%
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“…This antibody has been shown to block HER3/AKT signaling (Sala et al, 2012) and to be rapidly and efficiently internalized by cells expressing HER3 (Sala et al, 2013). Moreover, the antibody impaired ligand-induced signaling and clonogenic growth in vitro and tumor growth in BRAF-V600E mutant colon cancer (Prasetyanti et al, 2015). We show that EV20/ MMAF exerts a potent and efficient anti-tumoral effect in different HER2 + models including cells resistant to classical anti-HER2 therapeutics.…”
Section: Introductionmentioning
confidence: 81%
“…Together, these evidences indicate that acting on HER3 may be of therapeutic value for HER2 + tumors, particularly in circumstances in which these tumors become refractory to the action of approved anti-HER2 drugs. Indeed, dysregulation of HER3 trafficking, as well as the ability of this receptor to interact with other receptor tyrosine kinases to modulate the sensitivity of targeted therapeutics in different cancers, has prompted the use of anti-HER3 antibodies, both as single agent or in combination with anti-cancer drugs to overcome resistance (Chakrabarty et al, 2012;Abel et al, 2013;Ma et al, 2014;Capone et al, 2015;Gaborit et al, 2016;Black et al, 2019). Several naked antibodies have been developed and tested in clinical trials.…”
Section: Introductionmentioning
confidence: 99%
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“…Historically, TKIs required reshaping to newer generations targeting novel mutations, illustrating the need for complementary therapies focused beyond the main mutation driver. Inhibition of EGFR family members can lead to compensatory activation of other tyrosine kinases [ 42 ], including ErbB family members such as HER3 [ 43 , 44 ]. Reportedly, HER3 is upregulated by targeting HER2 [ 45 , 46 ], and by targeting double-mutant EGFR L858R–T790M with osimertinib [ 13 , 14 ].…”
Section: Discussionmentioning
confidence: 99%
“…Over the past two decades, there has been a significant increase in interest in developing new cancer therapeutic agents specifically targeting and hampering the HER-3 receptor [ 6 ]. There are essentially two reasons behind this therapeutic strategy: first, HER-3 is overexpressed in many cancers [ 5 ]; second, the receptor acts as the main hub for escape mechanisms during the emergence of resistance to anticancer drugs [ 22 , 23 , 24 ]. In addition, somatic HER-3 oncogenic mutations have been identified in gastric and colorectal cancer patients [ 25 ].…”
Section: Discussionmentioning
confidence: 99%