Julia Ketzer
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View article: The observational EURACAN prospective clinical registry dedicated to epithelioid hemangioendothelioma: The protocol of an international and collaborative effort on an ultra-rare entity
The observational EURACAN prospective clinical registry dedicated to epithelioid hemangioendothelioma: The protocol of an international and collaborative effort on an ultra-rare entity Open
Introduction Epithelioid hemangioendothelioma (EHE) is an ultra-rare sarcoma, marked by distinctive molecular and pathological features and with a variable clinical behavior. Its natural history is still partially understood, reliable prog…
View article: Evaluation of the Effect of Photodynamic Therapy on CAM-Grown Sarcomas
Evaluation of the Effect of Photodynamic Therapy on CAM-Grown Sarcomas Open
Resection margin adequacy plays a critical role in the local control of sarcomas. Fluorescence-guided surgery has increased complete resection rates and local recurrence-free survival in several oncological disciplines. The purpose of this…
View article: Data from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy
Data from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy Open
Sporadic gastrointestinal stromal tumors (GIST), characterized by activating mutations of KIT or PDGFRA, favorably respond to KIT inhibitory treatment but eventually become resistant. The development of effective salvage trea…
View article: Supplemental Methods and Supplemental Figures S1-S3 from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy
Supplemental Methods and Supplemental Figures S1-S3 from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy Open
Supplemental Methods; Supplemental Figure S1: Cancer-related mutations in the DKTK-Master patient cohort; Supplemental Figure S2: T1-PTEN cells were treated with increasing concentrations of approved KIT-inhibitors for 72h and analyzed by …
View article: Data from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy
Data from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy Open
Sporadic gastrointestinal stromal tumors (GIST), characterized by activating mutations of KIT or PDGFRA, favorably respond to KIT inhibitory treatment but eventually become resistant. The development of effective salvage trea…
View article: Supplemental Methods and Supplemental Figures S1-S3 from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy
Supplemental Methods and Supplemental Figures S1-S3 from KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy Open
Supplemental Methods; Supplemental Figure S1: Cancer-related mutations in the DKTK-Master patient cohort; Supplemental Figure S2: T1-PTEN cells were treated with increasing concentrations of approved KIT-inhibitors for 72h and analyzed by …
View article: Supplementary methods, patient information and figure legends from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Supplementary methods, patient information and figure legends from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Supplementary methods, patient information and figure legends
View article: Supplementary Tables from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Supplementary Tables from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Supplementary Tables. Table S1. In Vitro Kinase IC50 Values (nM) for Native and Mutant Recombinant KIT. Table S2. Summary of Ba/F3 KIT Cell Lines Generated in this Study. Table S3. Summary of IC50 Viability Values in Ba/F3 KIT Cells. Table…
View article: Supplementary methods, patient information and figure legends from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Supplementary methods, patient information and figure legends from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Supplementary methods, patient information and figure legends
View article: Supplementary Figures from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Supplementary Figures from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Supplementary Figures. Figure S1. Chemical structures of imatinib, sunitinib, regorafenib and ponatinib. Figure S2. Expression and activation of KIT in engineered Ba/F3 cells. Figure S3. Ponatinib inhibits the phosphorylation of exon 11pri…
View article: Data from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Data from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Purpose: KIT is the major oncogenic driver of gastrointestinal stromal tumors (GIST). Imatinib, sunitinib, and regorafenib are approved therapies; however, efficacy is often limited by the acquisition of polyclonal secondary resista…
View article: Supplementary Figures from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Supplementary Figures from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Supplementary Figures. Figure S1. Chemical structures of imatinib, sunitinib, regorafenib and ponatinib. Figure S2. Expression and activation of KIT in engineered Ba/F3 cells. Figure S3. Ponatinib inhibits the phosphorylation of exon 11pri…
View article: Supplementary Tables from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Supplementary Tables from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Supplementary Tables. Table S1. In Vitro Kinase IC50 Values (nM) for Native and Mutant Recombinant KIT. Table S2. Summary of Ba/F3 KIT Cell Lines Generated in this Study. Table S3. Summary of IC50 Viability Values in Ba/F3 KIT Cells. Table…
View article: Data from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients
Data from Ponatinib Inhibits Polyclonal Drug-Resistant KIT Oncoproteins and Shows Therapeutic Potential in Heavily Pretreated Gastrointestinal Stromal Tumor (GIST) Patients Open
Purpose: KIT is the major oncogenic driver of gastrointestinal stromal tumors (GIST). Imatinib, sunitinib, and regorafenib are approved therapies; however, efficacy is often limited by the acquisition of polyclonal secondary resista…
View article: Plasma Sequencing for Patients with GIST—Limitations and Opportunities in an Academic Setting
Plasma Sequencing for Patients with GIST—Limitations and Opportunities in an Academic Setting Open
Circulating tumor DNA (ctDNA) from circulating free DNA (cfDNA) in GIST is of interest for the detection of heterogeneous resistance mutations and treatment monitoring. However, methodologies for use in a local setting are not standardized…
View article: Late Sequelae after Neuroblastoma-Associated Paraneoplastic Anti-Hu Syndrome in a 4-Year-Old Boy
Late Sequelae after Neuroblastoma-Associated Paraneoplastic Anti-Hu Syndrome in a 4-Year-Old Boy Open
Anti-Hu syndrome is a rare autoantibody associated paraneoplastic disease of the central and peripheral nervous system resulting in a variety of neurological symptoms. In pediatric patients it is described in the context of (ganglio) neuro…
View article: Targeting Her2-insYVMA with Covalent Inhibitors—A Focused Compound Screening and Structure-Based Design Approach
Targeting Her2-insYVMA with Covalent Inhibitors—A Focused Compound Screening and Structure-Based Design Approach Open
Mutated or amplified Her2 serves as a driver of non-small cell lung cancer or mediates resistance toward the inhibition of its family member epidermal growth factor receptor with small-molecule inhibitors. To date, small-molecule inhibitor…
View article: CCDC 1876852: Experimental Crystal Structure Determination
CCDC 1876852: Experimental Crystal Structure Determination Open
View article: KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy
KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy Open
Sporadic gastrointestinal stromal tumors (GIST), characterized by activating mutations of KIT or PDGFRA, favorably respond to KIT inhibitory treatment but eventually become resistant. The development of effective salvage treatments is comp…
View article: Correction: Complementary activity of tyrosine kinase inhibitors against secondary kit mutations in imatinib-resistant gastrointestinal stromal tumours
Correction: Complementary activity of tyrosine kinase inhibitors against secondary kit mutations in imatinib-resistant gastrointestinal stromal tumours Open
View article: Complementary activity of tyrosine kinase inhibitors against secondary kit mutations in imatinib-resistant gastrointestinal stromal tumours
Complementary activity of tyrosine kinase inhibitors against secondary kit mutations in imatinib-resistant gastrointestinal stromal tumours Open
Our data highlight that heterogeneity of KIT secondary mutations is the main mechanism of tumour progression to KIT inhibitors in imatinib-resistant GIST patients. Therapeutic combinations of TKIs with complementary activity against resist…
View article: Inhibition of osimertinib-resistant epidermal growth factor receptor EGFR-T790M/C797S
Inhibition of osimertinib-resistant epidermal growth factor receptor EGFR-T790M/C797S Open
We present inhibitors of drug resistant mutants of EGFR including T790M and C797S. In addition, we present the first X-ray crystal structures of covalent inhibitors in complex with C797S-mutated EGFR to gain insight into their binding mode.
View article: Inhibitors to Overcome Secondary Mutations in the Stem Cell Factor Receptor KIT
Inhibitors to Overcome Secondary Mutations in the Stem Cell Factor Receptor KIT Open
In modern cancer therapy, the use of small organic molecules against receptor tyrosine kinases (RTKs) has been shown to be a valuable strategy. The association of cancer cells with dysregulated signaling pathways linked to RTKs represents …
View article: Indazole-Based Covalent Inhibitors To Target Drug-Resistant Epidermal Growth Factor Receptor
Indazole-Based Covalent Inhibitors To Target Drug-Resistant Epidermal Growth Factor Receptor Open
The specific targeting of oncogenic mutant epidermal growth factor receptor (EGFR) is a breakthrough in targeted cancer therapy and marks a drastic change in the treatment of non-small cell lung cancer (NSCLC). The recurrent emergence of r…