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Details on Person For the following EGFR-binding ERBB2 KD mutants that were sh...

Class:Id	Summation:9664945
_displayName	For the following EGFR-binding ERBB2 KD mutants that were sh...
_timestamp	2023-03-22 12:13:50
created	[InstanceEdit:9664944] Orlic-Milacic, Marija, 2019-10-28
literatureReference	[LiteratureReference:9649397] Differential sensitivity of ERBB2 kinase domain mutations towards lapatinib [LiteratureReference:9646787] Neratinib is effective in breast tumors bearing both amplification and mutation of ERBB2 (HER2) [LiteratureReference:9646445] Combined Blockade of Activating ERBB2 Mutations and ER Results in Synthetic Lethality of ER+/HER2 Mutant Breast Cancer [LiteratureReference:9646758] Intra-tumor genetic heterogeneity and alternative driver genetic alterations in breast cancers with heterogeneous HER2 gene amplification [LiteratureReference:9650849] Antitumor effect of afatinib, as a human epidermal growth factor receptor 2-targeted therapy, in lung cancers harboring HER2 oncogene alterations [LiteratureReference:9652195] Human breast cancer cells harboring a gatekeeper T798M mutation in HER2 overexpress EGFR ligands and are sensitive to dual inhibition of EGFR and HER2 [LiteratureReference:9647026] An Acquired HER2^T798I Gatekeeper Mutation Induces Resistance to Neratinib in a Patient with HER2 Mutant-Driven Breast Cancer [LiteratureReference:9646962] Phosphorylation of mutationally introduced tyrosine in the activation loop of HER2 confers gain-of-function activity [LiteratureReference:9646964] Tumor driven by gain-of-function HER2 H878Y mutant is highly sensitive to HER2 inhibitor [LiteratureReference:9646435] Activating HER2 mutations in HER2 gene amplification negative breast cancer
modified	[InstanceEdit:9665640] Orlic-Milacic, Marija, 2019-10-31 [InstanceEdit:9665666] Orlic-Milacic, Marija, 2019-10-31 [InstanceEdit:9831085] Orlic-Milacic, Marija, 2023-03-18 [InstanceEdit:9831504] Orlic-Milacic, Marija, 2023-03-22 [InstanceEdit:9831563] Orlic-Milacic, Marija, 2023-03-22
text	For the following EGFR-binding ERBB2 KD mutants that were shown to activate PI3K/AKT signaling, it is assumed that heterodimers of these mutants with EGFR, like the wild type ERBB2:EGFR heterodimer, bind to the PI3K complex through GRB2:GAB1, leading to conversion of PIP2 to PIP3: ERBB2 L755S (Kancha et al. 2011, Cocco et al. 2018, Croessmann et al. 2019); ERBB2 L755P (Kancha et al. 2011); ERBB2 I767M (Ng et al. 2015; heterodimerization with EGFR indirectly shown by Bose et al. 2013); ERBB2 V777L (Kancha et al. 2011); ERBB2 G778_P780dup (Suzawa et al. 2016); ERBB2 T798M (Kancha et al. 2011, Rexer et al. 2013); ERBB2 T798I (Hanker et al. 2017); ERBB2 T862A (Kancha et al. 2011); ERBB2 H878Y (Kancha et al. 2011, Hu, Hu et al. 2015, Hu, Wan et al. 2015); ERBB2 Y772_A775dup (Wang et al. 2006); Activation of PI3K/AKT signaling downstream of the following ERBB2 KD cancer mutants has not been studied and they are annotated as candidates: ERBB2 L755M ERBB2 L755W ERBB2 V777M ERBB2 V777E ERBB2 T733I ERBB2 H878R
(summation)	[Reaction:9664940] PI3K bound to phosphorylated heterodimers of ERBB2 KD mutants and EGFR converts PIP2 to PIP3 [Homo sapiens]
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