Charlotte Chan
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View article: Supplementary Fig. 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.
View article: Supplementary Fig. 3 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 3 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
View article: Supplementary Fig. 4 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 4 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental…
View article: Supplementary Fig. 5 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 5 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
View article: Supplementary Fig. 2 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 2 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 2 Tumor growth is inhibited by STING agonism and MEK inhibition in vivo.
View article: Supplementary Fig. 3 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 3 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
View article: Supplementary Fig. 2 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 2 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 2 Tumor growth is inhibited by STING agonism and MEK inhibition in vivo.
View article: Supplementary Data 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Data 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Resources and Table
View article: Supplementary Fig. 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.
View article: Data from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Data from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Purpose: STING (Stimulator of Interferon Genes) agonists are currently in development for treatment of solid tumors, including pancreatic ductal adenocarcinoma (PDAC). Response rates to STING agonists alone have been promising yet modest a…
View article: Supplementary Fig. 4 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 4 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental…
View article: Supplementary Data 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Data 1 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Resources and Table
View article: Supplementary Fig. 5 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 5 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling Open
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
View article: The scalar product formula for parahoric Deligne--Lusztig induction
The scalar product formula for parahoric Deligne--Lusztig induction Open
Parahoric Deligne--Lusztig induction gives rise to positive-depth representations of parahoric subgroups of $p$-adic groups. The most fundamental basic question about parahoric Deligne--Lusztig induction is whether it satisfies the scalar …
View article: Generic character sheaves on parahoric subgroups
Generic character sheaves on parahoric subgroups Open
We study parabolic induction producing $\ell$-adic sheaves on a parahoric subgroup scheme in the loop group of a reductive group. Under a genericity assumption on the input data, we prove that it produces conjugation equivariant perverse s…
View article: Geometric $L$-packets of Howe-unramified toral supercuspidal representations
Geometric $L$-packets of Howe-unramified toral supercuspidal representations Open
We show that L -packets of toral supercuspidal representations arising from unramified maximal tori of p -adic groups are realized by Deligne–Lusztig varieties for parahoric subgroups. We prove this by exhibiting a direct comparison betwee…
View article: Supplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.
View article: Supplementary Fig. 3 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 3 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
View article: Supplementary Fig. 3 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 3 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
View article: Data from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Data from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Purpose:Stimulator of interferon genes (STING) agonists are currently in development for treatment of solid tumors, including pancreatic ductal adenocarcinoma (PDAC). Response rates to STING agonists alone have been promising yet modest, a…
View article: Supplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental…
View article: Supplementary Data 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Data 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Resources and Table
View article: Supplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.
View article: Supplementary Data 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Data 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Resources and Table
View article: Supplementary Fig. 2 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 2 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 2 Tumor growth is inhibited by STING agonism and MEK inhibition in vivo.
View article: Supplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental…
View article: Supplementary Fig. 2 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 2 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 2 Tumor growth is inhibited by STING agonism and MEK inhibition in vivo.
View article: Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
View article: Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
View article: Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling Open
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.