Jenny Y. Xue
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View article: Yours or Mine? Overwriting Attacks Against Neural Audio Watermarking
Yours or Mine? Overwriting Attacks Against Neural Audio Watermarking Open
As generative audio models are rapidly evolving, AI-generated audios increasingly raise concerns about copyright infringement and misinformation spread. Audio watermarking, as a proactive defense, can embed secret messages into audio for c…
View article: SpeechVerifier: Robust Acoustic Fingerprint against Tampering Attacks via Watermarking
SpeechVerifier: Robust Acoustic Fingerprint against Tampering Attacks via Watermarking Open
With the surge of social media, maliciously tampered public speeches, especially those from influential figures, have seriously affected social stability and public trust. Existing speech tampering detection methods remain insufficient: th…
View article: In vivo vulnerabilities to GPX4 and HDAC inhibitors in drug-persistent versus drug-resistant BRAFV600E lung adenocarcinoma
In vivo vulnerabilities to GPX4 and HDAC inhibitors in drug-persistent versus drug-resistant BRAFV600E lung adenocarcinoma Open
View article: Pan-KRAS inhibitor disables oncogenic signalling and tumour growth
Pan-KRAS inhibitor disables oncogenic signalling and tumour growth Open
KRAS is one of the most commonly mutated proteins in cancer, and efforts to directly inhibit its function have been continuing for decades. The most successful of these has been the development of covalent allele-specific inhibitors that t…
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary Composite Figure File
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary Table S8
View article: Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Despite decades of research, efforts to directly target KRAS have been challenging. MRTX849 was identified as a potent, selective, and covalent KRASG12C inhibitor that exhibits favorable drug-like properties, selectively modifie…
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary Composite Figure File
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary methods and Tables
View article: Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Despite decades of research, efforts to directly target KRAS have been challenging. MRTX849 was identified as a potent, selective, and covalent KRASG12C inhibitor that exhibits favorable drug-like properties, selectively modifie…
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary Table S8
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary Table S7
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary methods and Tables
View article: Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
Supplementary Data from The KRAS<sup>G12C</sup> Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients Open
Supplementary Table S7
View article: Supplementary Data Table 1 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 1 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S1 shows mutations in A375 VemR cells compared to the parental using exome sequencing.
View article: Supplementary Data Table 2 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 2 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S2 shows mutations in A375 CobiR cells compared to the parental using exome sequencing
View article: Supplementary Data Table 1 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 1 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S1 shows mutations in A375 VemR cells compared to the parental using exome sequencing.
View article: Supplementary Data Table 4 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 4 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S4 shows the moleculared used in the pharmacological screen and the corresponding IC50 values
View article: Data from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Data from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Purpose:Combined MAPK pathway inhibition using dual BRAF and MEK inhibitors has prolonged the duration of clinical response in patients with BRAFV600E-driven tumors compared with either agent alone. However, resistance frequentl…
View article: Data from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Data from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Purpose:Combined MAPK pathway inhibition using dual BRAF and MEK inhibitors has prolonged the duration of clinical response in patients with BRAFV600E-driven tumors compared with either agent alone. However, resistance frequentl…
View article: Supplementary Data Table 3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S3 shows unique mutations in A375 VCR cells compared to parental using exome sequencing
View article: Supplementary Data S1-S3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data S1-S3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Figure S1 shows the A375 VCR cells being resistant and addicted to dabrafenib and trametinib (A,B), that knockdown of STAT3 had no effect on drug resistance (C,D), Caspase-Glo assays of drug-treated cells (F), and time course of pFGFR1 and…
View article: Supplementary Figure Legends from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Figure Legends from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Supplementary Figure Legends
View article: Supplementary Data Table 4 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 4 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S4 shows the moleculared used in the pharmacological screen and the corresponding IC50 values
View article: Supplementary Data Table 5 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 5 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S5 shows the raw counts from RNA sequencing of paired non-small cell lung cancer samples with BRAF mutations pre- and post-treatment using BRAF/MEK inhibitor combinations
View article: Supplementary Figure Legends from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Figure Legends from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Supplementary Figure Legends
View article: Supplementary Data S1-S3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data S1-S3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Figure S1 shows the A375 VCR cells being resistant and addicted to dabrafenib and trametinib (A,B), that knockdown of STAT3 had no effect on drug resistance (C,D), Caspase-Glo assays of drug-treated cells (F), and time course of pFGFR1 and…
View article: Supplementary Data Table 2 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 2 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S2 shows mutations in A375 CobiR cells compared to the parental using exome sequencing
View article: Supplementary Data Table 3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 3 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S3 shows unique mutations in A375 VCR cells compared to parental using exome sequencing
View article: Supplementary Data Table 5 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Supplementary Data Table 5 from Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation Open
Table S5 shows the raw counts from RNA sequencing of paired non-small cell lung cancer samples with BRAF mutations pre- and post-treatment using BRAF/MEK inhibitor combinations