Daniel Rauh
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View article: Targeting KRASG13C with cyclic linker based inhibitors to explore warhead orientation
Targeting KRASG13C with cyclic linker based inhibitors to explore warhead orientation Open
The small GTPase KRAS is a key driver of carcinogenesis when mutated, and significant progress has been made in targeting KRAS G12C and other oncogenic variants. Building on our previous work demonstrating the potential of nucleotide-based…
View article: Supplementary Table S4 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Table S4 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
Cell line Screen
View article: Supplementary Table S1 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Table S1 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
Representativeness of Study participants
View article: Supplementary Figure S3 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Figure S3 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
Structural Analyses of sunitinib, regorafenib and ripretinib in T670I-mutant KIT
View article: Supplementary Table S2 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Table S2 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
ddPCR primer and probe sequences
View article: Supplementary Table S3 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Table S3 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
Efficacy Assessment: CBR, best response
View article: Supplementary Figure S2 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Figure S2 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
PFS by primary mutation
View article: Data from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Data from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
Purpose:Imatinib resistance is conferred by secondary mutations within the ATP-binding pocket or the activation loop of KIT in gastrointestinal stromal tumors (GIST). Ponatinib is active against KIT secondary activation loop and the gateke…
View article: Supplementary Figure S1 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial)
Supplementary Figure S1 from Phase II Trial of Ponatinib in Patients with Metastatic Gastrointestinal Stromal Tumor following Failure or Intolerance of Prior Therapy with Imatinib (POETIG Trial) Open
CONSORT Diagram
View article: Computational Design of Lysine Targeting Covalent Binders Using Rosetta
Computational Design of Lysine Targeting Covalent Binders Using Rosetta Open
Chemical probes that form a covalent bond with their target protein have been established as a powerful tool for investigating proteins and modulating their activity, but until recently were mostly targeting cysteine residues. Covalent bin…
View article: Targeting KRASG13C: Exploring Warhead Orientation with Cyclic Linker-Based Inhibitors
Targeting KRASG13C: Exploring Warhead Orientation with Cyclic Linker-Based Inhibitors Open
The small GTPase KRAS is a key driver of carcinogenesis when mutated, and significant progress has been made in targeting KRAS G12C and other oncogenic variants. Building on our previous work demonstrating the potential of nucleotide-based…
View article: Akt Inhibitor Advancements: From Capivasertib Approval to Covalent-Allosteric Promises
Akt Inhibitor Advancements: From Capivasertib Approval to Covalent-Allosteric Promises Open
Akt kinase is vital in cell growth, survival, metabolism, and migration. Dysregulation of Akt signaling is implicated in cancer and metabolic disorders. In the context of cancer, overactive Akt promotes cell survival and proliferation. Thi…
View article: KIT ATP-Binding Pocket/Activation Loop Mutations in GI Stromal Tumor: Emerging Mechanisms of Kinase Inhibitor Escape
KIT ATP-Binding Pocket/Activation Loop Mutations in GI Stromal Tumor: Emerging Mechanisms of Kinase Inhibitor Escape Open
PURPOSE Imatinib resistance in GI stromal tumors (GISTs) is primarily caused by secondary KIT mutations, and clonal heterogeneity of these secondary mutations represents a major treatment obstacle. KIT inhibitors used after imatinib have c…
View article: Avapritinib-based SAR studies unveil a binding pocket in KIT and PDGFRA
Avapritinib-based SAR studies unveil a binding pocket in KIT and PDGFRA Open
Avapritinib is the only potent and selective inhibitor approved for the treatment of D842V-mutant gastrointestinal stromal tumors (GIST), the most common primary mutation of the platelet-derived growth factor receptor α (PDGFRA). The appro…
View article: Correction: A high-throughput effector screen identifies a novel small molecule scaffold for inhibition of ten-eleven translocation dioxygenase 2
Correction: A high-throughput effector screen identifies a novel small molecule scaffold for inhibition of ten-eleven translocation dioxygenase 2 Open
Correction for ‘A high-throughput effector screen identifies a novel small molecule scaffold for inhibition of ten-eleven translocation dioxygenase 2’ by Shubhendu Palei et al. , RSC Med. Chem. , 2022, 13 , 1540–1548, https://doi.org/10.10…
View article: Addressing the Osimertinib Resistance Mutation EGFR-L858R/C797S with Reversible Aminopyrimidines
Addressing the Osimertinib Resistance Mutation EGFR-L858R/C797S with Reversible Aminopyrimidines Open
Drug resistance mutations emerging during the treatment of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) inhibitors represent a major challenge in personalized cancer treatment and require constant develop…
View article: Supplementary Figures 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Supplementary Figures 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
Supplementary Figures 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
View article: Supplementary Figure Legends 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Supplementary Figure Legends 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
Supplementary Figure Legends 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
View article: Interview with Dr. Meyerson from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Interview with Dr. Meyerson from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
mp3 file (6.8 MB). In the inaugural edition of the Cancer Discovery podcast, Executive Editor Mark Landis talks with Matthew Meyerson about his paper, which describes the identification of the DDR2 kinase as a therapeutic target in squamou…
View article: Supplementary Figure Legends 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Supplementary Figure Legends 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
Supplementary Figure Legends 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
View article: Supplementary Figures 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Supplementary Figures 1-7 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
Supplementary Figures 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
View article: Data from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer
Data from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer Open
The 8p12 locus (containing the FGFR1 tyrosine kinase gene) is frequently amplified in squamous cell lung cancer. However, it is currently unknown which of the 8p12-amplified tumors are also sensitive to fibroblast growth factor receptor (F…
View article: Supplementary Figures S1-S14 from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer
Supplementary Figures S1-S14 from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer Open
PDF file 34156K, Table of genes from 16 recurrent amplified genomic regions (Figure S1), amplicon focality on TCGA copy number aberrations (Figure S2), hierarchical clustering of CLCGP copy number data (Figure S3), centrality frequencies o…
View article: Supplementary Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain
Supplementary Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain Open
Contains: Supplemental Figures 1-7; Supplemental Tables 1 -3; Supplemental Methods
View article: Supplementary Table 1 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Supplementary Table 1 from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
Supplementary Table 1 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
View article: Supplementary Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain
Supplementary Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain Open
Contains: Supplemental Figures 1-7; Supplemental Tables 1 -3; Supplemental Methods
View article: Supplementary Figures S1-S14 from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer
Supplementary Figures S1-S14 from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer Open
PDF file 34156K, Table of genes from 16 recurrent amplified genomic regions (Figure S1), amplicon focality on TCGA copy number aberrations (Figure S2), hierarchical clustering of CLCGP copy number data (Figure S3), centrality frequencies o…
View article: Supplementary Methods and Legends from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer
Supplementary Methods and Legends from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified <i>FGFR1</i> in Lung Cancer Open
PDF file 136K,Methods: Additional information on experimental techniques and data analysis. Legends: describing supplementary figures S1-S14
View article: Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain
Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain Open
Gastrointestinal stromal tumors (GIST) harboring activating mutations of PDGFRA respond to imatinib, with the notable exception of the most common mutation, D842V. Avapritinib is a novel, potent KIT/PDGFRA inhibitor with substantial clinic…
View article: Data from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
Data from Mutations in the <i>DDR2</i> Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer Open
Although genomically targeted therapies have improved outcomes for patients with lung adenocarcinoma, little is known about the genomic alterations that drive squamous cell cancer (SCC) of the lung. Sanger sequencing of the tyrosine kinome…