Andreas Bräuninger
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View article: Increase in Alveolar Septal Width Is a Histological Predictor of Chronic Lung Allograft Dysfunction and Survival in Lung Transplant Recipients—A Longitudinal Study
Increase in Alveolar Septal Width Is a Histological Predictor of Chronic Lung Allograft Dysfunction and Survival in Lung Transplant Recipients—A Longitudinal Study Open
Background: Chronic lung allograft dysfunction (CLAD) occurs in up to 50% of patients within the first five years after lung transplantation (LuTX) and represents the main complication and cause of death regarding this surgery. Alveolar se…
View article: Treatment outcome of NSCLC patients with BRAF mutations: a retrospective, multicentre analysis within the national Network Genomic Medicine (nNGM) Lung Cancer in Germany
Treatment outcome of NSCLC patients with BRAF mutations: a retrospective, multicentre analysis within the national Network Genomic Medicine (nNGM) Lung Cancer in Germany Open
Patients with activating BRAFnon-V600E mutations respond to BRAF/MEK inhibitor or (chemo-)immunotherapy, while those with non-activating mutations do not benefit from targeted therapy, but may benefit from (chemo-)immune therapy. Correlati…
View article: Circulating Tumor DNA (ctDNA) Assessment in Pediatric Patients with Newly Diagnosed High-Risk Classic Hodgkin Lymphoma (cHL): Exploratory Analysis from the Phase 2 Keynote-667 Study
Circulating Tumor DNA (ctDNA) Assessment in Pediatric Patients with Newly Diagnosed High-Risk Classic Hodgkin Lymphoma (cHL): Exploratory Analysis from the Phase 2 Keynote-667 Study Open
Introduction: KEYNOTE-667 (NCT03407144) evaluated pembrolizumab (pembro) plus chemotherapy consolidation in children and young adults with cHL and slow early response to frontline chemotherapy. We present an exploratory analysis of ctDNA i…
View article: Detection of multiple activating NRAS variants under BRAF/MEK-inhibitor therapy in BRAF positive malignant melanoma using liquid biopsy
Detection of multiple activating NRAS variants under BRAF/MEK-inhibitor therapy in BRAF positive malignant melanoma using liquid biopsy Open
Malignant melanoma is one of the most common skin cancers worldwide.1 The most frequent driver mutation is BRAF V600E, observed in about 50% of patients and a target for kinase inhibitor therapy.2 In addition, activating mutations in NRAS …
View article: Development, testing and validation of a targeted NGS-panel for the detection of actionable mutations in lung cancer (NSCLC) using anchored multiplex PCR technology in a multicentric setting
Development, testing and validation of a targeted NGS-panel for the detection of actionable mutations in lung cancer (NSCLC) using anchored multiplex PCR technology in a multicentric setting Open
Lung cancer is a paradigm for a genetically driven tumor. A variety of drugs were developed targeting specific biomarkers requiring testing for tumor genetic alterations in relevant biomarkers. Different next-generation sequencing technolo…
View article: Supplementary Methods from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Methods from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 65K
View article: Data from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Data from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
Hodgkin-Reed/Sternberg (HRS) cells of classical Hodgkin lymphoma show aberrant expression and activation of several receptor tyrosine kinases (RTK) in the majority of cases. Therefore, we tested whether tyrosine kinase inhibitors (TKI) alr…
View article: Supplementary Figure 1 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure 1 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 28K, Supplementary Figure S1. Effect of sorafenib treatment on GADD34 and GADD153 mRNA expression in different cell lines.
View article: Supplementary Figure 2 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure 2 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 29K, Supplementary Figure S2. Effect of lestaurtinib treatment on TNFSF8 mRNA expression in HRS and ALCL cell lines.
View article: Supplementary Figure 2 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure 2 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 29K, Supplementary Figure S2. Effect of lestaurtinib treatment on TNFSF8 mRNA expression in HRS and ALCL cell lines.
View article: Supplementary Figure Legend from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure Legend from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 46K
View article: Supplementary Tables 1 - 8 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Tables 1 - 8 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - Supplementary Table S1. Primary antibodies for Western blot analysis. Supplementary Table S2. Primer sequences for qRT-PCR. Supplementary Table S3. TKIs and conventional chemotherapeutics used in this study. Supplementary Table …
View article: Supplementary Figure 3 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure 3 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 322K, Supplementary Figure S3. Effect of lestaurtinib and sorafenib combined with conventional chemotherapeutic drugs.
View article: Supplementary Figure 1 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure 1 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 28K, Supplementary Figure S1. Effect of sorafenib treatment on GADD34 and GADD153 mRNA expression in different cell lines.
View article: Supplementary Tables 1 - 8 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Tables 1 - 8 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - Supplementary Table S1. Primary antibodies for Western blot analysis. Supplementary Table S2. Primer sequences for qRT-PCR. Supplementary Table S3. TKIs and conventional chemotherapeutics used in this study. Supplementary Table …
View article: Supplementary Methods from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Methods from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 65K
View article: Supplementary Figure Legend from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure Legend from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 46K
View article: Data from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Data from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
Hodgkin-Reed/Sternberg (HRS) cells of classical Hodgkin lymphoma show aberrant expression and activation of several receptor tyrosine kinases (RTK) in the majority of cases. Therefore, we tested whether tyrosine kinase inhibitors (TKI) alr…
View article: Supplementary Figure 3 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines
Supplementary Figure 3 from Induction of Endoplasmic Reticulum Stress by Sorafenib and Activation of NF-κB by Lestaurtinib as a Novel Resistance Mechanism in Hodgkin Lymphoma Cell Lines Open
PDF file - 322K, Supplementary Figure S3. Effect of lestaurtinib and sorafenib combined with conventional chemotherapeutic drugs.
View article: Supplementary information from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells
Supplementary information from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells Open
Supplementary information. Supplementary Table S1. Antibodies used in the study. Supplementary Table S2. Primer sequences for Sanger sequencing and site-directed mutagenesis. Supplementary Table S3. SNP array analysis of 8 primary cardiac …
View article: Data from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells
Data from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells Open
Primary cardiac angiosarcomas are rare tumors with unfavorable prognosis. Pathogenic driver mutations are largely unknown. We therefore analyzed a collection of cases for genomic aberrations using SNP arrays and targeted next-generation se…
View article: Data from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells
Data from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells Open
Primary cardiac angiosarcomas are rare tumors with unfavorable prognosis. Pathogenic driver mutations are largely unknown. We therefore analyzed a collection of cases for genomic aberrations using SNP arrays and targeted next-generation se…
View article: Supplementary information from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells
Supplementary information from A Recurrent Activating <i>PLCG1</i> Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells Open
Supplementary information. Supplementary Table S1. Antibodies used in the study. Supplementary Table S2. Primer sequences for Sanger sequencing and site-directed mutagenesis. Supplementary Table S3. SNP array analysis of 8 primary cardiac …
View article: Upregulation of mesothelial genes in ovarian carcinoma cells is associated with an unfavorable clinical outcome and the promotion of cancer cell adhesion
Upregulation of mesothelial genes in ovarian carcinoma cells is associated with an unfavorable clinical outcome and the promotion of cancer cell adhesion Open
A hallmark of ovarian high‐grade serous carcinoma (HGSC) is its early and massive peritoneal dissemination via the peritoneal fluid. It is generally believed that tumor cells must breach the mesothelium of peritoneal organs to adhere to th…
View article: Genetic Alterations in HPV-associated Oropharyngeal Squamous Cell Carcinoma of Patients with Treatment Failure
Genetic Alterations in HPV-associated Oropharyngeal Squamous Cell Carcinoma of Patients with Treatment Failure Open
An increasing number of oropharyngeal squamous cell carcinoma (OPSCC) is associated with human papillomavirus (HPV). Despite different biological and clinical features HPV+ and HPV- OPSCC are treated equally. Due to improved survival rates…
View article: Detection of Tumor-Specific Genetic Aberrations in Liquid Biopsies of Patients with HPV-associated Oropharyngeal Squamous Cell Carcinoma
Detection of Tumor-Specific Genetic Aberrations in Liquid Biopsies of Patients with HPV-associated Oropharyngeal Squamous Cell Carcinoma Open
In addition to tobacco and alcohol, infection with HPV is recognized as major risk factor for the development of oropharyngeal squamous cell carcinoma (OPSCC). Although HPV-associated OPSCC have a more favorable prognosis and differ in the…