Daniel Zingg
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View article: PI3Kα Inhibitor and Degrader Inavolisib Can Co-opt FGFR2 to Enhance Responses in Patients with <i>PIK3CA</i> -Mutated Solid Tumors and in Preclinical Models
PI3Kα Inhibitor and Degrader Inavolisib Can Co-opt FGFR2 to Enhance Responses in Patients with <i>PIK3CA</i> -Mutated Solid Tumors and in Preclinical Models Open
Purpose: PIK3CA mutations frequently drive solid tumors, particularly hormone receptor–positive breast cancer. Inavolisib, an ATP-competitive p110α inhibitor, also promotes the degradation of mutated p110α. PI3K inhibitors have generally s…
View article: Supplementary Figure S1 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S1 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Isolation and analysis of GFPhi NMuMG cells expressing Fgfr2-GFP variants using FACS (includes gating strategy) and western blotting.
View article: Supplementary Table S1 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Table S1 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Key resources. List of antibodies, commercial assays, experimental models, reagents, and software used in this study.
View article: Supplementary Methods from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Methods from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Supplementary Methods related to FLAG and HALO tag constructs.
View article: Supplementary Figure S9 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S9 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Data supporting the functional analysis of C-terminal F703–S704 combination Fgfr2 variants using in vitro and in vivo methods.
View article: Supplementary Figure S7 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S7 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Data supporting the functional analysis of the C-terminal F703–S704 Fgfr2 motif using in vitro and in vivo methods.
View article: Supplementary Table S2 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Table S2 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Exact P values corresponding to Fig. 4B.
View article: Supplementary Figure S4 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S4 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Data supporting the mapping of the F703–S704 motif in the Fgfr2 C-tail using FACS (gating strategy shown) and RNA-seq.
View article: Supplementary Figure S8 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S8 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Histological examination of mammary glands injected with C-terminal F703–S704 Fgfr2 motif variants.
View article: Supplementary Table S3 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Table S3 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Proteins identified in Fgfr2-GFP immunoprecipitation samples using MS-based proteomics. The table shows all proteins identified using global proteomics on GFP-immunoprecipitation samples using NMuMG cells expressing GFP, Fgfr2FL-GFP, or Fg…
View article: Supplementary Figure S3 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S3 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Histological examination of mammary glands injected with Fgfr2-E18 C-tail motif variants
View article: Data from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Data from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Genetic alterations in receptor tyrosine kinase genes can generate potent oncogenic drivers. Truncation of the FGFR2 gene by its last exon 18 (E18) is caused by structural alterations, such as focal amplifications and gene fusions/rearrang…
View article: Supplementary Figure S5 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S5 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
FACS data incl. gating strategy supporting the HALO Fgfr2 internalization analysis and data supporting the biochemical Fgfr2-CT assays
View article: Supplementary Figure S2 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S2 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Data supporting the in vitro and in vivo Fgfr2-E18 C-tail motif analyses.
View article: Supplementary Figure S6 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Figure S6 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Alignments of C-tail sequences of Fgfr2 orthologs and human Fgfr paralogs.
View article: Supplementary Table S4 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2
Supplementary Table S4 from The C-Terminal Kinase Domain–Binding and Suppression Motif Prevents Constitutive Activation of FGFR2 Open
Differentially expressed genes identified in Fgfr2-GFP samples using RNA-seq. The table shows all genes identified using RNA-seq on NMuMG cells expressing GFP, Fgfr2FL-GFP, Fgfr2DE18-GFP, Fgfr2DVFSPD702-6-GFP, or Fgfr2F703A/S704A-GFP.
Clinical evidence of venoactive drugs in diabetic microvascular complications: a scoping review Open
Diabetic microvascular complications (DmVCs) and chronic venous disease (CVD) share common risk factors and pathophysiological features. However, they are often assessed and managed as separate conditions. The study objective was to map th…
Evaluating the Role of Calcium Dobesilate in COVID-19-Related Pulmonary Vascular Endotheliitis and Thrombosis: A Retrospective Analysis of Real-World Data Open
Background SARS-CoV-2 (COVID-19) infection is known to cause acute inflammatory pulmonary microangiopathy, leading to alveolar-capillary thrombosis, severe respiratory failure, and potential mortality. This study aims to evaluate the effic…
Enhancing identification and treatment of patients with concomitant chronic venous insufficiency and diabetes mellitus. A modified Delphi study from the CODAC (ChrOnic venous disease and Diabetes Advisory Council) group Open
The high level of agreement shows that healthcare professionals are aware of the gaps in identification and treatment of patients with concomitant CVI and DM, and of the need to approach this as a combined therapy area. An algorithm is pro…
MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer Open
Targeting the PI3K–AKT–mTOR pathway is a promising therapeutic strategy for breast cancer treatment. However, low response rates and development of resistance to PI3K–AKT–mTOR inhibitors remain major clinical challenges. Here, we show that…
DOBESILATE AN OLD DRUG AS A POSSIBLE NEW TREATMENT OPTION FOR COVID-19 INFECTION Open
COVID-19 pandemic is responsible for near to two million deaths worldwide. Because of the lack of any specific treatment option, repurposing of existing drugs continues worldwide in order to find immediate therapeutic strategies for deadly…
View article: Response of metastatic mouse invasive lobular carcinoma to mTOR inhibition is partly mediated by the adaptive immune system
Response of metastatic mouse invasive lobular carcinoma to mTOR inhibition is partly mediated by the adaptive immune system Open
Effective treatment of invasive lobular carcinoma (ILC) of the breast is hampered by late detection, invasive growth, distant metastasis, and poor response to chemotherapy. Phosphoinositide 3-kinase (PI3K) signaling, one of the major drugg…
SMAD signaling promotes melanoma metastasis independently of phenotype switching Open
The development of metastatic melanoma is thought to require the dynamic shifting of neoplastic cells between proliferative and invasive phenotypes. Contrary to this conventional "phenotype switching" model, we now show that disease progre…
Rare, yet relevant tumor cells – A new twist to melanoma cell plasticity Open
Metastatic cancers, including malignant cutaneous melanoma, have remained an incurable disease for most patients. Major advancements in the fields of targeted therapies and immunotherapies have brought some breakthrough to successfully era…
The Histone Methyltransferase Ezh2 Controls Mechanisms of Adaptive Resistance to Tumor Immunotherapy Open
Immunotherapy and particularly immune checkpoint inhibitors have resulted in remarkable clinical responses in patients with immunogenic tumors, although most cancers develop resistance to immunotherapy. The molecular mechanisms of tumor re…